qseqid VFDB_internal_id pident evalue bitscore VFID VFCID gene protein_name Organism VF_Name VF_FullName Bacteria VFcategory Characteristics Structure Function Mechanism Reference C2_00025 VFG021557 40.3 5.950000000000001e-29 105.0 VF0958 VFC0001 stfA fimbrial major subunit StfA Salmonella enterica subsp. enterica serovar Enteritidis str. P125109 C2_00026 VFG021563 56.9 0.0 1067.0 VF0958 VFC0001 stfC fimbrial biogenesis outer membrane usher protein Salmonella enterica subsp. enterica serovar Agona str. SL483 C2_00027 VFG018314 63.6 2.5200000000000004e-103 300.0 VF0958 VFC0001 stfD fimbrial chaperone StfD Salmonella enterica subsp. enterica serovar Paratyphi B str. SPB7 C2_00028 VFG021584 49.7 1.6800000000000002e-47 152.0 VF0958 VFC0001 stfE fimbrial protein Salmonella enterica subsp. enterica serovar Newport str. SL254 C2_00029 VFG021592 53.8 1.5699999999999995e-54 169.0 VF0958 VFC0001 stfF fimbrial minor subunit StfF Salmonella enterica subsp. enterica serovar Newport str. SL254 C2_00030 VFG018311 41.7 2.65e-36 124.0 VF0958 VFC0001 stfG fimbrial protein Salmonella enterica subsp. enterica serovar Paratyphi B str. SPB7 C2_00042 VFG043120 99.4 2.8100000000000003e-226 617.0 VF1154 VFC0204 flk flagella biosynthesis regulator Flk Escherichia coli O157:H7 str. EDL933 C2_00055 VFG002901 78.1 3.97e-122 345.0 VF0392 VFC0258 YPA_RS10790 histidine ABC transporter permease HisQ Yersinia pestis Antiqua O-antigen Yersinia enterocolitica Immune modulation "Clinical Y. enterocolitica isolates from humans predominantly belong to serotypes O:3, O:9, O:8 and O:5,27; Y. enterocolitica O antigen expression is temperature regulated." LPS O antigen mutants were severely impaired in their ability to colonize the Peyer's patches and did not colonize spleen and liver. The absence of O antigen in the outer membrane affects the expression of other Yersinia virulence factors. Abstract(s) in PubMed C2_00107 VFG011158 42.0 2.71e-95 290.0 VF0033 VFC0258 bplF lipopolysaccharide biosynthesis protein Bordetella avium 197N LPS Bordetella pertussis Immune modulation B. pertussis LPS lacks a repetitive O-antigen due to the deletion of the wbm cluster; two types, band A and B. The band A trisaccharide from B. pertussis 1414 is composed of N-acetyl-D-glucosamine (D-GlcNAc), 2,3-diacetamido-2,3-dideoxy-D-mannuronic acid (D-ManNAc3NAcA), and 2-acetamido-4-methylaminofucose (FucNAc4NMe); The B. pertussis bpl locus is required for the biosynthesis of trisaccharide to generate band A LPS Prevents clearance of the organism by host surfactant protein; confers protection to the bacterium from complement-mediated cell lysis Abstract(s) in PubMed C2_00108 VFG042525 43.2 6.25e-40 134.0 AF/R1 VFC0001 afrS transcriptional activator precursor AfrS Escherichia coli str. RDEC-1 C2_00122 VFG015921 48.9 1.32e-06 50.8 VF0920 VFC0325 hcnB cyanide-forming glycine dehydrogenase subunit HcnB Pseudomonas aeruginosa PA7 C2_00128 VFG003391 42.2 7.03e-12 58.9 VF0392 VFC0258 YPTB_RS05510 CDP-6-deoxy-delta-3,4-glucoseen reductase Yersinia pseudotuberculosis IP 32953 O-antigen Yersinia enterocolitica Immune modulation "Clinical Y. enterocolitica isolates from humans predominantly belong to serotypes O:3, O:9, O:8 and O:5,27; Y. enterocolitica O antigen expression is temperature regulated." LPS O antigen mutants were severely impaired in their ability to colonize the Peyer's patches and did not colonize spleen and liver. The absence of O antigen in the outer membrane affects the expression of other Yersinia virulence factors. Abstract(s) in PubMed C2_00141 VFG049010 98.1 3.32e-147 408.0 VF0571 VFC0301 rcsB transcriptional regulator RcsB Klebsiella oxytoca E718 RcsAB Regulation of capsule synthesis Klebsiella pneumoniae Regulation RcsB combined with the unstable auxiliary regulator RcsA to bind to an RcsAB box in the promoter region to upregulate the cps genes expression Abstract(s) in PubMed C2_00159 VFG045716 40.3 1.22e-34 122.0 VF0292 VFC0272 ccmB ABC transporter involved in cytochrome c biogenesis, CcmB subunit Legionella longbeachae NSW150 CcmC Legionella pneumophila Nutritional/Metabolic factor Required for cytochrome c production, promotes iron assimilation and intracellular infection Abstract(s) in PubMed C2_00160 VFG001856 49.0 1.22e-83 250.0 VF0292 VFC0272 ccmC cytochrome c-type biogenesis protein CcmC, putative heme lyase for CcmE Legionella pneumophila subsp. pneumophila str. Philadelphia 1 CcmC Legionella pneumophila Nutritional/Metabolic factor Required for cytochrome c production, promotes iron assimilation and intracellular infection Abstract(s) in PubMed C2_00162 VFG010881 48.3 1.74e-36 122.0 VF0292 VFC0272 ccmE cytochrome c-type biogenesis protein CcmE, heme chaperone Legionella pneumophila str. Corby CcmC Legionella pneumophila Nutritional/Metabolic factor Required for cytochrome c production, promotes iron assimilation and intracellular infection Abstract(s) in PubMed C2_00163 VFG045720 53.1 6.479999999999999e-225 640.0 VF0292 VFC0272 ccmF cytochrome c heme lyase subunit CcmF Legionella longbeachae NSW150 CcmC Legionella pneumophila Nutritional/Metabolic factor Required for cytochrome c production, promotes iron assimilation and intracellular infection Abstract(s) in PubMed C2_00223 VFG038248 42.9 1.77e-56 185.0 VF0468 VFC0258 pbpG D-alanyl-D-alanine endopeptidase PBP7/8 Acinetobacter baumannii AB307-0294 PbpG Penicillin-binding protein Acinetobacter baumannii Immune modulation Penicillin-binding proteins (PBPs) are most commonly associated with binding to and inactivating b-lactam antibiotics; PBPs also participate in the final steps of the biosynthesis of the peptidoglycan layer and thus contribute to bacterial cell stability Abstract(s) in PubMed C2_00233 VFG024200 40.5 4.55e-11 60.5 VF0317 VFC0301 devR/dosR response regulator transcription factor Mycobacterium indicus pranii MTCC 9506 DevRS Mycobacterium tuberculosis Regulation A two-component system consists of a histidine sensor kinase and a response regulator; phosphorylation-based signalling has been established for five of eleven systems in M. tuberculosis, RegX3-SenX3, TrcR-TrcS, MprA-MprB, PrrA-PrrB and DevR-DevS (DosR-DosS) Controls the global response to oxidative stress and low oxygen repsonse, key regulator in the oxygen starvation-induced mycobacterial dormancy response Abstract(s) in PubMed C2_00244 VFG007583 42.5 2.49e-07 51.6 VF0519 VFC0204 fleN/flhG MinD-like ATPase Vibrio vulnificus CMCP6 Flagella Vibrio cholerae Motility Single polar flagellum Contributes to the virulence of pathogenic Vibrio through adhesion or biofilm formation The flagellar regulatory system positively mediates the transcription of diguanylate cyclase CdgD which results in the transcription of a hemagglutinin that enhances intestinal colonization; c-di-GMP directly bound to YcgR interacts with components of the flagellar motor to disrupt flagellar rotation, thereby leading to decreased motility and inducing the biofilm formation Abstract(s) in PubMed C2_00247 VFG004271 64.7 2.99e-104 300.0 VF0955 VFC0001 stcB fimbrial biogenesis chaperone StcB Salmonella enterica subsp. enterica serovar Typhi str. CT18 C2_00248 VFG004269 75.5 0.0 1321.0 VF0955 VFC0001 stcC fimbrial biogenesis outer membrane usher protein Salmonella enterica subsp. enterica serovar Choleraesuis str. SC-B67 C2_00249 VFG004261 50.4 2.87e-102 304.0 VF0955 VFC0001 stcD putative fimbrial-like adhesin protein Salmonella enterica subsp. enterica serovar Typhi str. CT18 C2_00292 VFG048962 56.3 1.24e-55 171.0 VF0560 VFC0258 KP1_RS17335 protein-tyrosine-phosphatase Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00293 VFG048951 51.1 1.59e-246 700.0 VF0560 VFC0258 KP1_RS17330 polysaccharide biosynthesis tyrosine autokinase Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00294 VFG046745 40.2 4.59e-15 73.9 VF0543 VFC0258 FTM_RS05910 glycosyltransferase family 2 protein Francisella tularensis subsp. mediasiatica FSC147 Capsule Francisella tularensis Immune modulation Group 4 capsule; high molecular weight (HMW) O-antigen capsule A polymer of the tetrasaccharide repeat, 4)-a-D-GalNAcAN-(1-.4)-a-D-GalNAcAN-(1-.3)-b-D-QuiNAc-(1-.2)-b-D-Qui4NFm-(1-, which is identical to F. tularensis O-antigen subunit; F. tularensis synthesizes an O-antigen capsule containing approximately 125 to 300 or more O-antigen repeating units Providing a stealth shield that prevents the host immune system from detecting this potent pathogen Abstract(s) in PubMed C2_00298 VFG008744 43.8 2.63e-08 53.1 VF0309 VFC0258 OEM_RS14570 glycosyltransferase Mycobacterium yongonense 05-1390 PDIM Phthiocerol dimycocerosate Mycobacterium tuberculosis Immune modulation Major lipid, also referred as ball of wax; mas (mycocerosic acid synthase catalyzing the synthesis of long-chain, multiply methylated branched fatty acid, called mycocerosic acid), fadD26 and fadD28 (long-chain fatty acyl-AMP ligases) are essential for the biosynthesis of PDIM; drrC and mmpL7 gene are necessary for the proper localization of PDIM Play a mainly structural role in providing a stable base for the insertion of other lipid and also play a role as a fluidity modifier, whose function could be to modulate cell wall viscosity;PDIM is crucial for infection by masking pathogen-associated molecular patterns (PAMP) of the cell wall from the innate immune system Abstract(s) in PubMed C2_00300 VFG048885 88.9 2.2000000000000002e-249 679.0 VF0560 VFC0258 gmd GDP-mannose 4,6-dehydratase Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00301 VFG048868 77.7 1.11e-186 516.0 VF0560 VFC0258 A79E_RS08235 GDP-L-fucose synthase Klebsiella pneumoniae subsp. pneumoniae 1084 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00302 VFG048863 47.0 3.03e-54 168.0 VF0560 VFC0258 KP1_RS17300 GDP-mannose mannosyl hydrolase Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00303 VFG048852 61.7 1.87e-180 508.0 VF0560 VFC0258 KP1_RS17295 glycosyltransferase WbuB Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00304 VFG023783 62.9 6.529999999999999e-216 603.0 VF0392 VFC0258 YE105_RS07900 mannose-1-phosphate guanylyltransferase/mannose-6-phosphate isomerase Yersinia enterocolitica subsp. palearctica 105.5R(r) O-antigen Yersinia enterocolitica Immune modulation "Clinical Y. enterocolitica isolates from humans predominantly belong to serotypes O:3, O:9, O:8 and O:5,27; Y. enterocolitica O antigen expression is temperature regulated." LPS O antigen mutants were severely impaired in their ability to colonize the Peyer's patches and did not colonize spleen and liver. The absence of O antigen in the outer membrane affects the expression of other Yersinia virulence factors. Abstract(s) in PubMed C2_00305 VFG019017 74.3 3.11e-261 716.0 VF0392 VFC0258 cpsG phosphomannomutase CpsG Yersinia pseudotuberculosis YPIII O-antigen Yersinia enterocolitica Immune modulation "Clinical Y. enterocolitica isolates from humans predominantly belong to serotypes O:3, O:9, O:8 and O:5,27; Y. enterocolitica O antigen expression is temperature regulated." LPS O antigen mutants were severely impaired in their ability to colonize the Peyer's patches and did not colonize spleen and liver. The absence of O antigen in the outer membrane affects the expression of other Yersinia virulence factors. Abstract(s) in PubMed C2_00306 VFG048942 66.2 3.77e-231 641.0 VF0560 VFC0258 wcaJ undecaprenyl-phosphate glucose phosphotransferase Klebsiella variicola At-22 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00307 VFG048850 48.6 2e-136 402.0 VF0560 VFC0258 KPN2242_RS16275 MOP flippase family protein Klebsiella pneumoniae KCTC 2242 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00311 VFG019018 49.2 1.31e-101 301.0 VF0392 VFC0258 YPK_RS15930 NAD-dependent epimerase/dehydratase family protein Yersinia pseudotuberculosis YPIII O-antigen Yersinia enterocolitica Immune modulation "Clinical Y. enterocolitica isolates from humans predominantly belong to serotypes O:3, O:9, O:8 and O:5,27; Y. enterocolitica O antigen expression is temperature regulated." LPS O antigen mutants were severely impaired in their ability to colonize the Peyer's patches and did not colonize spleen and liver. The absence of O antigen in the outer membrane affects the expression of other Yersinia virulence factors. Abstract(s) in PubMed C2_00312 VFG048990 89.2 6.6e-194 533.0 VF0560 VFC0258 galF GalU regulator GalF Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00317 VFG005939 46.0 3.45e-67 208.0 VF0144 VFC0258 STU_RS14575 exopolysaccharide biosynthesis protein Streptococcus thermophilus LMG 18311 Capsule Streptococcus pneumoniae Immune modulation Ninety different capsule types have been identified. Each has a structurally distinct capsule, composed of repeating oligosaccharide units joined by glycosidic linkages Resistant to complement deposition and masks cell wall-associated complement from being recognized by the complement receptors on phagocytes Abstract(s) in PubMed C2_00320 VFG001967 59.9 2.5900000000000003e-164 464.0 VF0323 VFC0258 glf UDP-galactopyranose mutase Campylobacter jejuni subsp. jejuni NCTC 11168 Capsule Campylobacter jejuni Immune modulation Major antigenic component of the classic Penner serotyping system; Variation in the capsule structure may cause by multiple mechanisms, such as exchange of capsular genes and entire clusters by horizontal transfer, gene duplication, deletion, fusion and the presence of homopolymeric G tracts in several cps genes The capsule consists of repeating oligosaccharide units attached to a dipalmitoyl-glycerophosphate lipid anchor; The CPS is extensively substituted with variable O-methylphosphoramidate, methyl, ethanolamine, and N-glycerol groups Play an important role in bacterial survival and persistence in the environment and evasion of host immune response; the presence of heptose residues in the capsule may be important for virulence. Heptose residues found in some cell surface-located glycoconjugates are required for adhesion Abstract(s) in PubMed C2_00322 VFG048959 95.1 0.0 883.0 VF0560 VFC0258 gndA NADP-dependent phosphogluconate dehydrogenase Klebsiella pneumoniae JM45 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00323 VFG048789 83.8 8.9e-238 651.0 VF0560 VFC0258 ugd UDP-glucose 6-dehydrogenase Klebsiella oxytoca E718 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_00328 VFG014106 43.3 4.73e-46 150.0 VF0085 VFC0258 hisH2 imidazole glycerol phosphate synthase subunit HisH Pseudomonas aeruginosa PAO1 LPS Pseudomonas aeruginosa Immune modulation Two distinct forms of LPS: A-band and B-band. A-band is a homopolymer of -linked D-rhamnose, whereas B-band LPS is a heteropolymer Mediates biological effects including resistance to serum killing and phagocytosis; the binding to normal CFTR (cystic fibrosis transmembrane conductance regulator) and invasion of host cells may make a contribution to virulence in the human eye; internalization by binding to normal CFTR protein expressed by airway epithelial cells followed by desquamation of bacteria-laden epithelial cells, constitutes a host defense mechanism. If this mechanism fails to function properly, abnormally high bacterial carriage would promote the establishment of chronic bacterial infection Binding interaction occurs between the first extracellular loop of CFTR (predicted to be in amino acids 108-117 of the mature protein) and the complete outer portion of the core polysaccharide of the LPS Abstract(s) in PubMed C2_00356 VFG042725 100.0 1.08e-196 538.0 VF1138 VFC0001 csgG curli production assembly/transport protein CsgG Escherichia coli O157:H7 str. EDL933 Curli fibers Escherichia coli (UPEC) Adherence "Many commensal E. coli strains and the commonly studied lab strains express curli at temperatures of <30°C. In contrast, pathogenic E. coli strains like UPECs, EAECs including the 2012 German outbreak strain and S. Typhimurium, have been shown to express curli at 37°C" In E. coli, curli fibers compose up to 85% of the biofilm biomass. Curli acts in vitro as an essential scaffold protein during biofilm formation.;In vivo, curli also directly regulates the immune system and is known to induce inflammation by activating the immune Toll-like receptors (TLRs). Abstract(s) in PubMed C2_00357 VFG046069 100.0 4.96e-95 270.0 VF1138 VFC0001 cgsF curli production assembly/transport protein CsgF Escherichia coli VR50 Curli fibers Escherichia coli (UPEC) Adherence "Many commensal E. coli strains and the commonly studied lab strains express curli at temperatures of <30°C. In contrast, pathogenic E. coli strains like UPECs, EAECs including the 2012 German outbreak strain and S. Typhimurium, have been shown to express curli at 37°C" In E. coli, curli fibers compose up to 85% of the biofilm biomass. Curli acts in vitro as an essential scaffold protein during biofilm formation.;In vivo, curli also directly regulates the immune system and is known to induce inflammation by activating the immune Toll-like receptors (TLRs). Abstract(s) in PubMed C2_00358 VFG045790 100.0 5.96e-94 266.0 VF1138 VFC0001 cgsE curli production assembly/transport protein CsgE Escherichia coli O25b:H4-ST131 Curli fibers Escherichia coli (UPEC) Adherence "Many commensal E. coli strains and the commonly studied lab strains express curli at temperatures of <30°C. In contrast, pathogenic E. coli strains like UPECs, EAECs including the 2012 German outbreak strain and S. Typhimurium, have been shown to express curli at 37°C" In E. coli, curli fibers compose up to 85% of the biofilm biomass. Curli acts in vitro as an essential scaffold protein during biofilm formation.;In vivo, curli also directly regulates the immune system and is known to induce inflammation by activating the immune Toll-like receptors (TLRs). Abstract(s) in PubMed C2_00359 VFG045791 100.0 9.61e-156 429.0 VF1138 VFC0001 cgsD transcriptional regulator CsgD Escherichia coli O25b:H4-ST131 Curli fibers Escherichia coli (UPEC) Adherence "Many commensal E. coli strains and the commonly studied lab strains express curli at temperatures of <30°C. In contrast, pathogenic E. coli strains like UPECs, EAECs including the 2012 German outbreak strain and S. Typhimurium, have been shown to express curli at 37°C" In E. coli, curli fibers compose up to 85% of the biofilm biomass. Curli acts in vitro as an essential scaffold protein during biofilm formation.;In vivo, curli also directly regulates the immune system and is known to induce inflammation by activating the immune Toll-like receptors (TLRs). Abstract(s) in PubMed C2_00360 VFG045792 100.0 1.26e-38 128.0 VF1138 VFC0001 csgB curlin minor subunit CsgB Escherichia coli O25b:H4-ST131 Curli fibers Escherichia coli (UPEC) Adherence "Many commensal E. coli strains and the commonly studied lab strains express curli at temperatures of <30°C. In contrast, pathogenic E. coli strains like UPECs, EAECs including the 2012 German outbreak strain and S. Typhimurium, have been shown to express curli at 37°C" In E. coli, curli fibers compose up to 85% of the biofilm biomass. Curli acts in vitro as an essential scaffold protein during biofilm formation.;In vivo, curli also directly regulates the immune system and is known to induce inflammation by activating the immune Toll-like receptors (TLRs). Abstract(s) in PubMed C2_00361 VFG046073 93.3 3.47e-18 75.9 VF1138 VFC0001 csgA curlin major subunit CsgA Escherichia coli VR50 Curli fibers Escherichia coli (UPEC) Adherence "Many commensal E. coli strains and the commonly studied lab strains express curli at temperatures of <30°C. In contrast, pathogenic E. coli strains like UPECs, EAECs including the 2012 German outbreak strain and S. Typhimurium, have been shown to express curli at 37°C" In E. coli, curli fibers compose up to 85% of the biofilm biomass. Curli acts in vitro as an essential scaffold protein during biofilm formation.;In vivo, curli also directly regulates the immune system and is known to induce inflammation by activating the immune Toll-like receptors (TLRs). Abstract(s) in PubMed C2_00362 VFG045794 98.2 4.36e-69 202.0 VF1138 VFC0001 csgC curli assembly protein CsgC Escherichia coli O25b:H4-ST131 Curli fibers Escherichia coli (UPEC) Adherence "Many commensal E. coli strains and the commonly studied lab strains express curli at temperatures of <30°C. In contrast, pathogenic E. coli strains like UPECs, EAECs including the 2012 German outbreak strain and S. Typhimurium, have been shown to express curli at 37°C" In E. coli, curli fibers compose up to 85% of the biofilm biomass. Curli acts in vitro as an essential scaffold protein during biofilm formation.;In vivo, curli also directly regulates the immune system and is known to induce inflammation by activating the immune Toll-like receptors (TLRs). Abstract(s) in PubMed C2_00372 VFG013437 56.5 3.01e-121 350.0 VF0044 VFC0258 htrB lipid A biosynthesis lauroyl acyltransferase Haemophilus influenzae 86-028NP LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_00388 VFG043072 97.8 1.12e-91 261.0 VF1154 VFC0204 flgN flagella biosynthesis chaperone FlgN Escherichia coli O157:H7 str. EDL933 C2_00389 VFG043020 81.3 1.43e-43 136.0 VF0967 VFC0204 flgM anti-sigma-28 factor FlgM Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 C2_00390 VFG043073 96.3 2.31e-144 401.0 VF1154 VFC0204 flgA flagellar basal body P-ring formation protein FlgA Escherichia coli O157:H7 str. EDL933 C2_00391 VFG043074 99.3 9.249999999999999e-91 259.0 VF1154 VFC0204 flgB flagellar basal body rod protein FlgB Escherichia coli O157:H7 str. EDL933 C2_00392 VFG043075 100.0 1.89e-88 253.0 VF1154 VFC0204 flgC flagellar basal body rod protein FlgC Escherichia coli O157:H7 str. EDL933 C2_00393 VFG043076 99.1 1.14e-150 418.0 VF1154 VFC0204 flgD flagellar hook assembly protein FlgD Escherichia coli O157:H7 str. EDL933 C2_00394 VFG043077 98.8 4.01e-275 747.0 VF1154 VFC0204 flgE flagellar hook protein FlgE Escherichia coli O157:H7 str. EDL933 C2_00395 VFG043078 98.4 1.14e-169 468.0 VF1154 VFC0204 flgF flagellar basal-body rod protein FlgF Escherichia coli O157:H7 str. EDL933 C2_00396 VFG043079 100.0 7.22e-182 499.0 VF1154 VFC0204 flgG flagellar basal-body rod protein FlgG Escherichia coli O157:H7 str. EDL933 C2_00397 VFG043080 100.0 1.7100000000000002e-166 458.0 VF1154 VFC0204 flgH flagellar basal body L-ring protein FlgH Escherichia coli O157:H7 str. EDL933 C2_00398 VFG043081 99.7 5.41e-248 675.0 VF1154 VFC0204 flgI flagellar basal body P-ring protein FlgI Escherichia coli O157:H7 str. EDL933 C2_00399 VFG043082 99.4 2.49e-220 601.0 VF1154 VFC0204 flgJ flagellar assembly peptidoglycan hydrolase FlgJ Escherichia coli O157:H7 str. EDL933 C2_00400 VFG043083 99.3 0.0 1003.0 VF1154 VFC0204 flgK flagellar hook-associated protein FlgK Escherichia coli O157:H7 str. EDL933 C2_00401 VFG043084 97.5 8.75e-207 567.0 VF1154 VFC0204 flgL flagellar hook-associated protein FlgL Escherichia coli O157:H7 str. EDL933 C2_00410 VFG038840 77.9 4.53e-129 364.0 VF0473 VFC0204 flmH short chain dehydrogenase/reductase family oxidoreductase Aeromonas hydrophila ML09-119 Polar flagella Aeromonas hydrophila Motility Types of bacterial movement: swimming, swarming, gliding, twitching and sliding. Only swimming and swarming are correlated with the presence of flagella. Swimming is an individual endeavour, while swarming is the movement of a group of bacteria; constitutively expressed for motility in liquid environments Necessary for motility, adhesion and invasion; glycosylation of the flagellin may play a role in provoking a proinflammatory response Abstract(s) in PubMed C2_00411 VFG011430 63.5 1.02e-23 85.1 VF0367 VFC0258 acpXL acyl carrier protein Brucella melitensis bv. 1 str. 16M LPS Lipopolysaccharide Brucella melitensis Immune modulation Brucella possesses a non-classical LPS as compared with the so-called classical LPS from enterobacteria such as Escherichia coli. B. abortus lipid A possesses a diaminoglucose backbone (rather than glucosamine), and acyl groups are longer (C28 rather than C12 and C16) and are only linked to the core by amide bounds (rather than ester and amide bonds).; In contrast to enterobacterial LPSs, Brucella LPS is several-hundred-times less active and toxic than E. coli LPS.; this is an evolutionary adaptation to an intracellular lifestyle, low endotoxic activity is shared by other intracellular pathogens such as Bartonella and Legionella. Plays a role in entry and early survival inside macrophages; Resistance to innate-immunity anti-bacterial responses; a modulator of the immune response The entry and early survival stages of smooth Brucella are lipid-raft-dependent. The entry-gateway seems to include Brucella surface-exposed HSP60-PrPc (cellular prion protein) interaction but also a SR-A (class A scavenger)-lipid-A interaction and is also dependent on the LPS O-chain. And the LPS O-chain ensures the Brucella containing vacuole (BCV) aviodance of fusion with lysosomes transiently; The chemical structure of Brucella LPS permits the bacteria to become highly resistant to anti-bacterial effectors of the innate immune system. Long O-chains at the bacterial surface should provoke a steric hindrance leading to the formation of a protecting barrier. The presence of long O-chains at the surface of Brucella prevents the deposition of complement at the bacterial surface. The O-chains also could prevent a specific recognition of the Pathogen-associated molecular patterns (PAMPs) and as a consequence impair expression of any cytokines or iNOS, both of which are known to be involved in the clearance of intracellular Brucella. The low number of anionic groups in the core lipid A, especially charged phosphate groups could both remove anionic targets and facilitate a tighter aggregation of LPS molecules via their hydrophobic fatty acids, leading to less binding and penetration of antibacterial cationic peptides.;The Brucella LPS forms stable large clusters with MHC-II named macrodomians in the cell surface, interfering with MHC-II presentation of peptides to specific CD4+ T cells. Abstract(s) in PubMed C2_00412 VFG009135 42.1 6.33e-93 285.0 VF0809 VFC0272 kasB 3-oxoacyl-(acyl carrier protein) synthase II Mycobacterium tuberculosis RGTB327 C2_00434 VFG035924 40.6 7.06e-33 118.0 VF0215 VFC0346 aatC ATP-binding protein AatC Escherichia coli O78:H11:K80 str. H10407 Dispersin Anti-aggregation protein Escherichia coli (EAEC) Others Encoded by a gene called aap lying immediately upstream of that encoding the AggR transcriptional activator, and that app is under AggR control; Dispersin's position on the bacterial surface (where it is accessible to immune cells) and its presence in the vast majority of EAEC strains make it a potential candidate for vaccine development; exported by a putative ABC transporter complex encoded by a gene cluster designated aatPABCD Typical signal sequence, secreted to the extracellular milieu, where it remains noncovalently attached to the surface of the bacterium Promotes dispersal of EAEC on the intestinal mucosa to establish new foci of infection and facilitate efficient colonization via bacterial dispersal Abstract(s) in PubMed C2_00446 VFG021077 85.6 4.85e-301 820.0 VF0111 VFC0301 phoQ two-component system sensor histidine kinase PhoQ Salmonella enterica subsp. enterica serovar Agona str. SL483 PhoPQ Salmonella enterica (serovar typhimurium) Regulation Activated by low divalent cations magnesium and calcium levels; control expression of more than 40 genes; required for intracellular survival, cationic antimicrobial peptides (CAMPs) resistance, stimulation of cytokine secretion PhoQ contains distinct binding sites for Mg2+ and Ca2+, and is maximally repressed in the presence of both cations. PhoP-PO4 activates expression of pags (for PhoP-activated genes), including cation transporter, outer membrane proteins, nonspecific acid phosphatase, enzymes important for LPS modification, and pmrAB (a second two-component system that are activated in response to mildly acidic environment. PmrAB leads to an increased substitution of phosphates with 4-amino-4-deoxy-L-arabinose in both the core oligosaccharide and the lipid A components of LPS, these cations stabilize the outer membrane by neutralizing the negative charge of phosphate groups, PmrAB induced modification of LPS composition may be vital to maintenance of outer membrane integrity); represses transcription of prgs (for PhoP-repressed genes) required for epithelial cell invasion, including hilA, prgHIJKorgA operon; regulate acid tolerance response (ATR) Abstract(s) in PubMed C2_00447 VFG004063 93.7 2.51e-150 416.0 VF0111 VFC0301 phoP two-component system response regulator PhoP Salmonella enterica subsp. enterica serovar Paratyphi A str. ATCC 9150 PhoPQ Salmonella enterica (serovar typhimurium) Regulation Activated by low divalent cations magnesium and calcium levels; control expression of more than 40 genes; required for intracellular survival, cationic antimicrobial peptides (CAMPs) resistance, stimulation of cytokine secretion PhoQ contains distinct binding sites for Mg2+ and Ca2+, and is maximally repressed in the presence of both cations. PhoP-PO4 activates expression of pags (for PhoP-activated genes), including cation transporter, outer membrane proteins, nonspecific acid phosphatase, enzymes important for LPS modification, and pmrAB (a second two-component system that are activated in response to mildly acidic environment. PmrAB leads to an increased substitution of phosphates with 4-amino-4-deoxy-L-arabinose in both the core oligosaccharide and the lipid A components of LPS, these cations stabilize the outer membrane by neutralizing the negative charge of phosphate groups, PmrAB induced modification of LPS composition may be vital to maintenance of outer membrane integrity); represses transcription of prgs (for PhoP-repressed genes) required for epithelial cell invasion, including hilA, prgHIJKorgA operon; regulate acid tolerance response (ATR) Abstract(s) in PubMed C2_00475 VFG036051 99.6 6.07e-159 442.0 VF1134 VFC0235 hlyE/clyA hemolysin HlyE Escherichia coli O111:H- str. 11128 C2_00506 VFG013196 48.3 1.04e-127 375.0 VF0758 VFC0272 hemA glutamyl-tRNA reductase Haemophilus somnus 2336 C2_00511 VFG013466 82.0 2.11e-170 472.0 VF0044 VFC0258 kdsA 2-dehydro-3-deoxyphosphooctonate aldolase Haemophilus influenzae 86-028NP LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_00524 VFG009599 48.6 0.0 1197.0 VF0302 VFC0272 narG nitrate reductase subunit alpha Mycobacterium sp. KMS Nitrate reductase Mycobacterium tuberculosis Nutritional/Metabolic factor NarX function as a respiratory fused nitrate reductase (three different domains present in this protein encode the difference subunits of nitrate reductase: the N-terminal domain showing similarity to narG, the central domain showing homology with narJ and the C-terminus showing homology to narI); NarGHJI is a membrane-bound nitrate reductase complex; NarK2, a putative nitrite-extrusion protein Nitrate respiration helps the bacteria to survive in O2-depleted areas of inflammatory or necrotic tissue Abstract(s) in PubMed C2_00534 VFG013348 73.6 2.27e-149 420.0 VF0044 VFC0258 galU glucosephosphate uridylyltransferase Haemophilus influenzae PittEE LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_00539 VFG006719 48.6 1.89e-273 781.0 VF0444 VFC0001 lap Listeria adhesion protein Lap Listeria innocua Clip11262 Lap Listeria adhesion protein Listeria monocytogenes Adherence Originally named surface protein p104, is a 104 kDa adhesion protein, present in every Listeria spp. except L. grayi Promotes bacterial adhesion to intestinal cells Host cell receptor is Hsp60 Abstract(s) in PubMed C2_00547 VFG016532 51.1 2.2e-40 144.0 VF0881 VFC0258 oppF oligopeptide ABC transporter permease Mycoplasma mycoides subsp. mycoides SC str. PG1 C2_00576 VFG026700 43.6 1.05e-77 253.0 VF0299 VFC0272 mbtI Isochorismate synthase MbtI Mycobacterium tuberculosis str. Haarlem/NITR202 Mycobactin Mycobacterium tuberculosis Nutritional/Metabolic factor Mycobacteria produce two classes of siderophores, mycobactins and the exochelins. Pathogenic mycobacteria solely produce mycobactins, whereas saprophytic mycobacteria such as M. smegmatis and Mycobacterium neoarum produce both mycobactins and exochelins; Mycobactins are salicylate containing siderophores, and exochelins are peptidic molecules; Mycobactins are found in two forms that differ in the length of an alkyl substitution and hence in polarity and solubility. The less polar form remains cell associated (mycobactin), whereas the more polar one (carboxymycobactin) is secreted into the medium. Cell-association mycobactin participates in iron internalization and/or to serve as a temporary iron-holding molecule to prevent sudden influx of excess iron if the metal suddenly becomes available after a period of iron limitation Abstract(s) in PubMed C2_00633 VFG030724 48.2 1.08e-112 333.0 VF0842 VFC0272 sugC sn-glycerol-3-phosphate ABC transporter ATP-binding protein UgpC Mycobacterium smegmatis JS623 C2_00638 VFG043148 43.2 3.95e-72 236.0 VF0625 VFC0271 VP_RS22515 sigma-54 dependent transcriptional regulator Vibrio parahaemolyticus RIMD 2210633 C2_00723 VFG043139 40.2 1.04e-12 70.5 VF0625 VFC0271 VP_RS22390 bifunctional diguanylate cyclase/phosphodiesterase Vibrio parahaemolyticus RIMD 2210633 C2_00731 VFG037105 50.8 1.09e-37 133.0 VF0456 VFC0282 msrA/B(pilB ) trifunctional thioredoxin/methionine sulfoxide reductase A/B protein Neisseria meningitidis WUE 2594 MsrAB Methionine sulphoxide reductase Neisseria meningitidis Stress survival Methionine sulfoxide reductases (Msr) are enzymes that catalyze the reduction of free and protein-bound methionine sulfoxide (MetSO) back to Met. Two structurally unrelated classes of Msrs have been described so far. MsrAs are stereo specific toward the S isomer on the sulfur of the sulfoxide function, whereas MsrBs are specific toward the R isomer Repairs oxidized proteins Abstract(s) in PubMed C2_00778 VFG037032 41.8 6.930000000000001e-118 364.0 VF0454 VFC0282 katA catalase Neisseria gonorrhoeae NCCP11945 KatA Neisseria meningitidis Stress survival Detoxifies H2O2; Protects against ROS (Reactive oxygen species), a family of chemical that are oxidized version of molecular oxygen, including hydrogen peroxide, superoxide and hydroxyl radicals Abstract(s) in PubMed C2_00791 VFG034754 95.4 1.06e-299 825.0 VF1110 VFC0086 espL1 Type III secretion system effector espL1 Escherichia coli O157:H7 str. EDL933 TTSS secreted effectors Escherichia coli (EHEC) Effector delivery system Cif (Deamidase. Induces cytopathic effects of actin stress fiber formation and cell cycle arrest. ); EspB (Pore formation, actin disruption, microvilli effacement, anti-phagocytosis. ); EspF (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspFu/tccP (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspG (TBC-like GTPase activating protein. Efficiently catalyzes GTP hydrolysis in Rab1 to disrupt of Rab1-mediated ER-to-Golgi trafficking. ); EspH (First bacterial effector acting directly on RhoGEFs, EspH directly binds to the DH-PH domain in RhoGEFs to disrupt RhoGEF-Rho signaling; critical for inhibiting macrophage phagocytosis. ); EspJ (Inhibit both IgG- and complement receptor-mediated phagocytosis. ); EspK; EspL1; EspL2 (Cysteine protease. Bounds F-actin-aggregating annexin 2 directly to increase annexin 2's ability to aggregate Tir-induced F-actin; block necroptosis and in flammation. ); EspL4; EspM1 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspM2 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspN; EspO1-1; EspO1-2; EspR1; EspR3; EspR4; EspT (GEF. Activates Rac1 and Cdc42 leading to formation of membrane ruffles and lamellipodia; induces membrane ruffles to facilitate bacterial invasion into non-phagocytic cells in a process involving Rac1 and Wave2. ); EspW; EspX1; EspX2; EspX4; EspX5; EspX6; EspX7/nleL (E3 ubiquitin ligase, HECT-like. Modulates pedestal formation. ); EspY1; EspY2; EspY3; EspY4; EspY5; Map (GEF. Mimics the host Dbl and catalyses the exchange of GDP for GTP in Cdc42, involved in effacement, SGLT1 inhibition, formation of filopodia and disruption of mitochondrial function. ); NleA/espI (Disruption of tight junctions by inhibition of host cell protein trafficking through COPII-dependent pathways. ); NleB1 (Blocks translocation of the p65 and to the host cell nucleus to inhibit NF-B pathway, but NleE and NleB act at different points in the NF-B signaling pathway. ); NleB2 (May also have anti-inflammatory activity. ); NleC (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate RelA (p65), thus blocking NF-B pathway. ); NleD (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate JNK and p38, thus blocking AP-1 pathway. ); NleE (PMN tran-epithelial migration; blocks translocation of the p65 to the host cell nucleus by preventing IB degradation to inhibit NF-B pathway. ); NleF; NleG-1; NleG2-2; NleG2-3; NleG2-4; NleG5-1; NleG5-2; NleG6-1; NleG6-2; NleG6-3; NleG7 (U-box type E3 ubiquitin ligases. ); NleG8-2; NleH1 (Ser/Thr protein kinase. Binds directly to a subunit of NF-B, the ribosomal protein S3 (RPS3), reducing the nuclear abundance of RPS3 to dampen host transcriptional outputs; interact with Bax inhibitor-1 to block apoptosis. ); NleH2 (Putative kinase. Attenuates NF-B pathway. ); SepZ/espZ (EspZ interacts with CD98 in host cell membranes to promote host cell survival, therefore provide the pathogen with valuable time to colonize efficiently prior to dissemination. ); TccP2; Tir (Mimics host immunoreceptor tyrosine-based inhibition motifs (ITIMs), also see helicobacter CagA. EHEC Tir lacks the Nck binding site. Conserved NPY (Asn-Pro-Tyr) motif recruits the adaptor protein IRTKS and/or IRSp53. IRTKS/IRSp53 link Tir and TccP/EspFu, which in turn activates N-WASP; Receptor for intimin; effacement; SGLT1 inhibition; recruits SHIP2 to control actin-pedestal morphology; maintains the integrity of the epithelium by keeping the destructive activity of EspG and EspG2 in check. ) Abstract(s) in PubMed C2_00799 VFG044101 47.2 2.38e-66 211.0 VF0941 VFC0272 PA4707 ABC transporter permease Pseudomonas aeruginosa PAO1 C2_00805 VFG044241 55.6 4.41e-07 42.4 VF1031 VFC0272 YE_RS01740 hemin uptake protein HemP Yersinia enterocolitica subsp. enterocolitica 8081 C2_00806 VFG044185 55.3 2.79e-116 340.0 VF0626 VFC0272 BJE04_RS21750 3-deoxy-7-phosphoheptulonate synthase Vibrio vulnificus YJ016 C2_00856 VFG001867 67.5 1.33e-98 283.0 VF0169 VFC0282 sodB superoxide dismutase Legionella pneumophila subsp. pneumophila str. Philadelphia 1 SodB Legionella pneumophila Stress survival A cytoplasmic iron superoxide dismutase; important for intracellular survival and transmission Abstract(s) in PubMed C2_00866 VFG000463 58.3 7.03e-57 176.0 VF0109 VFC0282 sodCI Gifsy-2 prophage: superoxide dismutase precursor (Cu-Zn) Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 SodCI Salmonella enterica (serovar typhimurium) Stress survival Encoded on the lysogenic phage Gifsy-2 Contribute to survival during systemic phase of infection Abstract(s) in PubMed C2_00905 VFG038216 44.8 2.97e-64 199.0 VF0463 VFC0301 bfmR biofilm-controlling response regulator Acinetobacter baumannii 1656-2 C2_01041 VFG001864 42.6 3.58e-47 154.0 VF0153 VFC0315 mip macrophage infectivity potentiator Mip Legionella pneumophila subsp. pneumophila str. Philadelphia 1 Mip Macrophage infectivity potentiator Legionella pneumophila Post-translational modification 24-kDa surface protein forms a nonglobular, V-shaped homodimer. Each monomer of the homodimeric protein consists of an N-terminal dimerization module, a long connecting -helix and a C-terminal PPIase domain; PDB code :1FD9 Necessary for intracellular survival Belongs to the enzyme family of FK-506 binding proteins that exhibit the peptidyl-prolyl-cis/trans isomerase (PPIase) activity, catalyzes the isomerization of peptide bonds N-terminal to Pro residues Abstract(s) in PubMed C2_01052 VFG038902 59.6 7.13e-180 509.0 VF0646 VFC0235 hlyA Hemolysin A Aeromonas salmonicida subsp. salmonicida A449 C2_01066 VFG045476 41.2 4.08e-28 102.0 VF0798 VFC0086 LPG_RS00105 ribosome-associated protein Legionella pneumophila subsp. pneumophila str. Philadelphia 1 Dot/Icm T4SS secreted effectors Legionella pneumophila Effector delivery system AnkB/legAU13/ceg27 (E3 Ubiquitin Ligase Activity, bounds Skp1, targets host protein parvin B. ); AnkC/legA12 (Ankyrin repeat. ); AnkD/legA15 (Ankyrin repeat. ); AnkF/legA14/ceg31 (Ankyrin repeat. ); AnkG/ankZ/legA7 (Ankyrin repeat. ); AnkH/legA3/ankW (Ankyrin repeat, NF-B inhibitor. ); AnkI/legAS4 (Ankyrin repeat. ); AnkJ/legA11 (Ankyrin repeat. ); AnkK/legA5 (Ankyrin repeat. ); AnkN/ankX/legA8 (Phosphocholination of Rab1 and Rab35 to regulate their activity; modulation of endosomal trafficking. ); AnkQ/legA10; AnkY/legA9 (Ankyrin repeat, STPK, Enhancer of autophagy. ); Ceg10; Ceg14/sidL (Inhibition of host protein synthesis leading to activation of the NF-B pathway. ); Ceg15; Ceg17; Ceg18; Ceg19 (Vesicle trafficking. ); Ceg23; Ceg25; Ceg28; Ceg29; Ceg3; Ceg30; Ceg32/sidI (Interacts with eEF1A to inhibit host protein synthesis. ); Ceg33; Ceg34; Ceg4; Ceg5; Ceg7; Ceg8; Ceg9 (Vesicle trafficking. ); CegC1 (Zinc metallophospholipase C. Zinc metallophospholipase C. ); CegC2 (Ninein domain. ); CegC3; CegC4; DrrA/sidM (Rab1-GEF and GDF (RabGDI displacement factor) activity responsible for Rab1 recruitment to LCV, C-terminal PI4P binding domain responsible for membrane binding; N-terminal AMPylation activity. ); LaiE (SidE paralog. ); LegA1; LegA2; LegA6; LegA7; LegC1; LegC3/ppeA (Vesicle trafficking. ); LegC4 (Coiled-coil. ); LegC6 (Coiled-coil. ); LegD1; LegD2; LegG2 (Ras GEF. ); LegK1 (Eukaryotic-like Ser/Thr kinase activity, directly activates NF-B pathway by phosphorylating the IB family of inhibitors. ); LegK2 (Ser/Thr kinase. ); LegK3 (STPK. ); LegL1 (Leucine-rich repeats. ); LegL2 (Leucine-rich repeats. ); LegL3 (Leucine-rich repeats. ); LegL5 (Leucine-rich repeats. ); LegL6 (Leucine-rich repeats. ); LegL7 (Leucine-rich repeats. ); LegLC4 (Leucine-rich repeats, coiled-coil. ); LegLC8 (Leucine-rich repeats, coiled-coil. ); LegN; LegP (Astacin protease. ); LegS1; LegS2 (Putative Sphingosine-1-phosphate lyase 1 (SP-lyase). ); LegT (Thaumatin domain. ); LegU1 (E3 Ubiquitin Ligase, targets host chaperone protein BAT3. ); LegY; Lem1; Lem10; Lem11; Lem12; Lem14; Lem15; Lem16; Lem17; Lem19; Lem2; Lem20; Lem21; Lem22; Lem23; Lem24; Lem25; Lem26; Lem27; Lem28; Lem29; Lem3 (Dephosphoryl-cholinase relieving the AnkX-mediated modification on Rab1. ); Lem4/smdA (PI4P-binding protein. ); Lem5; Lem6; Lem7; Lem8; Lem9; LepA (Nonlytic release from protozoa. ); LepB (Rab1 GAP, vesicle trafficking and bacterial egress. ); Lgt2/legC8 (Glucosyltransferase, inhibits host protein systhesis by glucosylating mammalian elongation factor eEF1A at serine-53. ); Lgt3/legC5 (Glucosyltransferase, inhibits host protein systhesis by glucosylating mammalian elongation factor eEF1A at serine-53. ); LidA (Promotion of Rab1 recruitment and tethering of ER derived vesicles to the LCV; stabilization of Rab guanosine nucleotide complex. ); LidL (EnhC paralogue. ); LirA; LirB (Peptidyl-prolyl cis-trans isomerase A (rotamase A). ); Lpg0045; Lpg0081; Lpg0294; Lpg0365; Lpg0518; Lpg0634; Lpg0963; Lpg1148; Lpg1158; Lpg1273; Lpg1689; Lpg1717; Lpg1751; Lpg2160 (Associates with BAT3 independently of LegU1; LegU1 and Lpg2160 may function redundantly or in concert to modulate BAT3 activity during the course of infection. ); Lpg2327; Lpg2407; Lpg2525 (F-box protein. ); Lpg2527; Lpg2744; LpnE (Putative Beta-lactamase. ); LubX/legU2 (E3 ubiquitin ligase, targets another effector protein SidH to proteasome-mediated protein degradation in the host cells; cell cycle modulation via Clk1. ); MavA; MavB; MavC; MavE; MavF; MavG; MavH; MavI; MavJ; MavL; MavM; MavN; MavV; PieA/lirC; PieB/lirD; PieC/lirE; PieD/lirF; PieE; PieF; PieG/legG1 (Regulator of chromosome condensation RCC. ); PpeB; PpgA (Regulator of chromosome condensation. ); RalF (Arf-GEF; Arf1 recuitment to LCV. ); RavE; RavF; RavG; RavH; RavI; RavJ; RavK; RavL; RavM; RavN; RavO; RavP; RavQ; RavR; RavS; RavT; RavW; RavX; RavY; RavZ (Cysteine protease. Inhibits host autophagy by cleaving and deconjugating LC3-PE. ); RvfA; SdbA (Contributes to sustained NF-B activation. ); SdbB (SidB paralog. ); SdbC (SidB paralog. ); SdcA (SidC paralog, anchors to PtdIns(4)P on LCVs. ); SdeA/laiA (Adherence and/or uptake. ); SdeB/laiB; SdeC/laiC; SdeD/laiF (SidE paralog. ); SdhA (Maintenance of LCV integrity preventing cell death and type I interferon induction. ); SdhB (Paralog of sidH, ANTH domain. ); SdjA; SetA (Vesicle trafficking. ); SidA; SidB (Rtx toxin, lipase. ); SidC (ER recuitment. ); SidD; SidE/laiD; SidF (Anti-apoptosis by targeting pro-death members of the Bcl2 protein family. ); SidG (Coiled-coil. ); SidH (A substrate of LubX E3 ubiquitin ligase. ); SidJ (ER recuitment. ); SidK (Interacting with VatA, a key component of the proton pump. Inhibition of LCV acidification. ); VipA (Actin nucleator contributing to modulate organelle trafficking. ); VipD (Phospholipase A1, removes PI(3)P from early endosomes. ); VipE; VipF (N-terminal acetyltransferase, GNAT family. ); VpdA/vipD2 (VipD paralog, Acyl transferase/acyl hydrolase/lysophospholipase. ); VpdB/vipD3 (VipD paralog, phospholipase. ); VpdC; WipA; WipB; YlfA/legC7 (Vesicle trafficking. ); YlfB/legC2 (Vesicle trafficking. ); CegC4; MesI; LPG_RS00040; LPG_RS00105; LPG_RS00150; LPG_RS00200; LPG_RS00235; LPG_RS00300; LPG_RS00665 (PI-3-phosphatase. ); LPG_RS00825; LPG_RS00870; LPG_RS00880; LPG_RS00925; LPG_RS01290; LPG_RS01305; LPG_RS01820; LPG_RS01880; LPG_RS02025; LPG_RS03550; LPG_RS03935; LPG_RS04800; LPG_RS05365; LPG_RS05490; LPG_RS05590; LPG_RS05660; LPG_RS05710; LPG_RS05830; LPG_RS07260; LPG_RS07280; LPG_RS07435; LPG_RS07905; LPG_RS08210; LPG_RS08285; LPG_RS08320; LPG_RS08345; LPG_RS08350; LPG_RS08370; LPG_RS08445; LPG_RS08450; LPG_RS08485; LPG_RS08595; LPG_RS08775; LPG_RS08895; LPG_RS09040; LPG_RS09470; LPG_RS09565; LPG_RS09650; LPG_RS09825; LPG_RS09915; LPG_RS09965; LPG_RS10290; LPG_RS10795; LPG_RS10800; LPG_RS11170; LPG_RS11255; LPG_RS11415; LPG_RS11860; LPG_RS11920; LPG_RS11940; LPG_RS11990; LPG_RS12190; LPG_RS12265; LPG_RS12310; LPG_RS12405; LPG_RS12815; LPG_RS12820; LPG_RS12830; LPG_RS12855; LPG_RS12885; LPG_RS12900; LPG_RS13265; LPG_RS13310; LPG_RS13590; LPG_RS13860; LPG_RS14265; LPG_RS14285; LPG_RS14345; LPG_RS14500; LPG_RS14525; LPG_RS14550; LPG_RS14555; LPG_RS14570; LPG_RS14710; LPG_RS14840; LPG_RS15050; LPG_RS15170 Abstract(s) in PubMed C2_01076 VFG018402 52.6 2.52e-307 869.0 VF0106 VFC0272 mgtB Mg2+ transport protein Salmonella enterica subsp. arizonae serovar 62:z4,z23:-- str. RSK2980 MgtBC Salmonella enterica (serovar typhimurium) Nutritional/Metabolic factor Hypothesized to be a magnesium transporter MgtA and MgtB are not required for intracellular survival or for virulence, MgtC is essential for both functions Abstract(s) in PubMed C2_01079 VFG047692 43.9 5.12e-71 222.0 VF0558 VFC0272 pyrB aspartate carbamoyltransferase Francisella cf. tularensis subsp. novicida 3523 Pyrimidine biosynthesis Francisella tularensis Nutritional/Metabolic factor CarB, CarA, and PyrB encode the large and small subunits of carbamoylphosphate synthetase and aspartate carbamoyl transferase, respectively. These enzymes catalyze the first two steps in the pyrimidine nucleotide biosynthetic pathway in many bacteria, including Francisella, and are required for the virulence of several pathogens, including Salmonella and E. coli Mediating bacterial resistance to reactive oxygen species (ROS) that is important for phagosomal escape Abstract(s) in PubMed C2_01085 VFG015903 44.6 6.37e-86 261.0 VF0917 VFC0235 argK ornithine carbamoyltransferase Pseudomonas syringae pv. phaseolicola 1448A C2_01120 VFG000871 99.5 1.06e-151 418.0 VF0221 VFC0001 fimB Type 1 fimbriae Regulatory protein fimB Escherichia coli CFT073 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_01121 VFG000872 100.0 8.02e-146 403.0 VF0221 VFC0001 fimE Type 1 fimbriae Regulatory protein fimE Escherichia coli CFT073 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_01122 VFG033211 100.0 3.52e-114 322.0 VF0221 VFC0001 fimA Type-1 fimbrial protein, A chain precursor Escherichia coli O111:H- str. 11128 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_01123 VFG033232 98.8 2.19e-121 339.0 VF0221 VFC0001 fimI Fimbrin-like protein fimI precursor Escherichia coli O111:H- str. 11128 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_01124 VFG033256 99.2 1.3e-170 469.0 VF0221 VFC0001 fimC Chaperone protein fimC precursor Escherichia coli O103:H2 str. 12009 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_01125 VFG000876 99.7 0.0 1769.0 VF0221 VFC0001 fimD Outer membrane usher protein fimD precursor Escherichia coli CFT073 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_01126 VFG012305 99.4 5.55e-124 346.0 VF0221 VFC0001 fimF FimF protein precursor Escherichia coli str. K-12 substr. MG1655 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_01127 VFG012313 98.2 1.43e-108 306.0 VF0221 VFC0001 fimG FimG protein precursor Escherichia coli O157:H7 str. EDL933 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_01128 VFG033355 100.0 6.85e-216 588.0 VF0221 VFC0001 fimH FimH protein precursor Escherichia coli O55:H7 str. CB9615 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_01135 VFG041219 47.6 2.11e-26 95.5 VF1264 VFC0086 iraD anti-adapter protein IraD Citrobacter rodentium ICC168 C2_01141 VFG035937 40.5 1.14e-310 979.0 VF1124 VFC0001 air/eaeX inverse autotransporter adhesin EaeX/Air Escherichia coli O44:H18 042 C2_01144 VFG034884 79.6 8.73e-272 764.0 VF1110 VFC0086 espX6 Type III secretion system effector EspX6 Escherichia coli O157:H7 str. EC4115 TTSS secreted effectors Escherichia coli (EHEC) Effector delivery system Cif (Deamidase. Induces cytopathic effects of actin stress fiber formation and cell cycle arrest. ); EspB (Pore formation, actin disruption, microvilli effacement, anti-phagocytosis. ); EspF (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspFu/tccP (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspG (TBC-like GTPase activating protein. Efficiently catalyzes GTP hydrolysis in Rab1 to disrupt of Rab1-mediated ER-to-Golgi trafficking. ); EspH (First bacterial effector acting directly on RhoGEFs, EspH directly binds to the DH-PH domain in RhoGEFs to disrupt RhoGEF-Rho signaling; critical for inhibiting macrophage phagocytosis. ); EspJ (Inhibit both IgG- and complement receptor-mediated phagocytosis. ); EspK; EspL1; EspL2 (Cysteine protease. Bounds F-actin-aggregating annexin 2 directly to increase annexin 2's ability to aggregate Tir-induced F-actin; block necroptosis and in flammation. ); EspL4; EspM1 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspM2 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspN; EspO1-1; EspO1-2; EspR1; EspR3; EspR4; EspT (GEF. Activates Rac1 and Cdc42 leading to formation of membrane ruffles and lamellipodia; induces membrane ruffles to facilitate bacterial invasion into non-phagocytic cells in a process involving Rac1 and Wave2. ); EspW; EspX1; EspX2; EspX4; EspX5; EspX6; EspX7/nleL (E3 ubiquitin ligase, HECT-like. Modulates pedestal formation. ); EspY1; EspY2; EspY3; EspY4; EspY5; Map (GEF. Mimics the host Dbl and catalyses the exchange of GDP for GTP in Cdc42, involved in effacement, SGLT1 inhibition, formation of filopodia and disruption of mitochondrial function. ); NleA/espI (Disruption of tight junctions by inhibition of host cell protein trafficking through COPII-dependent pathways. ); NleB1 (Blocks translocation of the p65 and to the host cell nucleus to inhibit NF-B pathway, but NleE and NleB act at different points in the NF-B signaling pathway. ); NleB2 (May also have anti-inflammatory activity. ); NleC (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate RelA (p65), thus blocking NF-B pathway. ); NleD (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate JNK and p38, thus blocking AP-1 pathway. ); NleE (PMN tran-epithelial migration; blocks translocation of the p65 to the host cell nucleus by preventing IB degradation to inhibit NF-B pathway. ); NleF; NleG-1; NleG2-2; NleG2-3; NleG2-4; NleG5-1; NleG5-2; NleG6-1; NleG6-2; NleG6-3; NleG7 (U-box type E3 ubiquitin ligases. ); NleG8-2; NleH1 (Ser/Thr protein kinase. Binds directly to a subunit of NF-B, the ribosomal protein S3 (RPS3), reducing the nuclear abundance of RPS3 to dampen host transcriptional outputs; interact with Bax inhibitor-1 to block apoptosis. ); NleH2 (Putative kinase. Attenuates NF-B pathway. ); SepZ/espZ (EspZ interacts with CD98 in host cell membranes to promote host cell survival, therefore provide the pathogen with valuable time to colonize efficiently prior to dissemination. ); TccP2; Tir (Mimics host immunoreceptor tyrosine-based inhibition motifs (ITIMs), also see helicobacter CagA. EHEC Tir lacks the Nck binding site. Conserved NPY (Asn-Pro-Tyr) motif recruits the adaptor protein IRTKS and/or IRSp53. IRTKS/IRSp53 link Tir and TccP/EspFu, which in turn activates N-WASP; Receptor for intimin; effacement; SGLT1 inhibition; recruits SHIP2 to control actin-pedestal morphology; maintains the integrity of the epithelium by keeping the destructive activity of EspG and EspG2 in check. ) Abstract(s) in PubMed C2_01165 VFG043209 67.3 2.7399999999999998e-189 542.0 VF0394 VFC0204 cheD methyl-accepting chemotaxis protein CheD Yersinia enterocolitica subsp. enterocolitica 8081 Flagella Yersinia enterocolitica Motility Required for efficient cellular invasion.; YplA, a phospholipase is secreted by this type III flagellum secretion system. YplA is required for survival of Y. enterocolitica in the Peyer's patches and for stimulation of the acute inflammatory response of the host to the infection;contributed to the initiation of biofilm formation Abstract(s) in PubMed C2_01175 VFG042668 49.1 7.3e-06 45.8 VF0700 VFC0001 QU43_RS68240 response regulator transcription factor Burkholderia cenocepacia J2315 C2_01222 VFG037678 52.8 3.7e-145 420.0 VF0472 VFC0271 pgaC poly-beta-1,6 N-acetyl-D-glucosamine synthase Acinetobacter baumannii ACICU PNAG Acinetobacter baumannii Biofilm PNAG is produced by the Pga machinery consisting of PgaABCD proteins. Pga complex probably spans the inner and outer bacterial membrane. PgaC and PgaD form an inner membrane-intergrated complex. PgaC is the cataytic glycosyltransferase containing 4-5 predicted transmembrane helices (TMHs). PgaD probably contains two TMHs with a short periplasmic loop and small cytosolic C terminus. PgaA is an outer membrane porin and might associate with PgaB, a periplasmic lipoprotein that is probably anchored to the outer membrane. PgaB deacetylates a small fraction of the polymer's NAG units. -(1-->6)-Poly-N-acetyl-D-glucosamine (PNAG) is a surface polysaccharide produced by many pathogens, including S. aureus, E. coli, Y. pestis, B. pertussis, A. baumannii and others Critical for biofilm formation Abstract(s) in PubMed C2_01260 VFG048984 76.4 9.08e-219 602.0 VF0560 VFC0258 KPN_RS13510 polysaccharide export protein Klebsiella pneumoniae subsp. pneumoniae MGH 78578 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_01261 VFG048820 63.9 1.55e-64 193.0 VF0560 VFC0258 KPR_RS08965 protein-tyrosine-phosphatase Klebsiella pneumoniae subsp. rhinoscleromatis SB3432 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_01262 VFG048831 60.8 2.87e-302 842.0 VF0560 VFC0258 KPR_RS08970 polysaccharide biosynthesis tyrosine autokinase Klebsiella pneumoniae subsp. rhinoscleromatis SB3432 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_01287 VFG043544 96.0 3.14e-243 662.0 VF1158 VFC0001 ompA porin OmpA Escherichia coli O157:H7 str. EDL933 C2_01300 VFG018351 44.5 5.84e-60 188.0 VF0950 VFC0001 bcfG fimbrial chaparone Salmonella enterica subsp. arizonae serovar 62:z4,z23:-- str. RSK2980 C2_01301 VFG042403 98.8 2.74e-119 334.0 ELF VFC0001 ycbV type 1 fimbrial protein Escherichia coli O157:H7 str. EDL933 C2_01302 VFG042402 100.0 2.11e-122 342.0 ELF VFC0001 ycbU fimbrial protein Escherichia coli O157:H7 str. EDL933 C2_01303 VFG045923 100.0 1.95e-266 721.0 ELF VFC0001 elfG fimbrial protein Escherichia coli O103:H2 str. 12009 C2_01304 VFG045904 99.9 0.0 1717.0 ELF VFC0001 elfC fimbrial biogenesis usher protein Escherichia coli O111:H- str. 11128 C2_01305 VFG045887 100.0 5.53e-168 462.0 ELF VFC0001 elfD molecular chaperone Escherichia coli O103:H2 str. 12009 C2_01306 VFG045865 100.0 8.089999999999999e-119 333.0 ELF VFC0001 elfA fimbrial protein Escherichia coli O103:H2 str. 12009 C2_01326 VFG038845 69.9 1.47e-121 346.0 VF0473 VFC0204 nueA NeuA protein Aeromonas hydrophila ML09-119 Polar flagella Aeromonas hydrophila Motility Types of bacterial movement: swimming, swarming, gliding, twitching and sliding. Only swimming and swarming are correlated with the presence of flagella. Swimming is an individual endeavour, while swarming is the movement of a group of bacteria; constitutively expressed for motility in liquid environments Necessary for motility, adhesion and invasion; glycosylation of the flagellin may play a role in provoking a proinflammatory response Abstract(s) in PubMed C2_01329 VFG013244 51.0 1.29e-103 306.0 VF0044 VFC0258 lpxK tetraacyldisaccharide 4'-kinase Haemophilus influenzae PittEE LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_01330 VFG013253 67.1 3.16e-275 762.0 VF0044 VFC0258 msbA lipid transporter ATP-binding/permease Haemophilus somnus 129PT LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_01358 VFG016185 40.5 2.11e-46 171.0 VF0923 VFC0272 ybtQ ABC transporter ATP-binding protein/permease Pseudomonas syringae pv. phaseolicola 1448A C2_01374 VFG015379 40.1 1.69e-32 125.0 VF0334 VFC0086 tagT type VI secretion associated protein TagT, ATP-binding component of ABC transporter Pseudomonas aeruginosa PA7 HSI-1 Hcp secretion island I Pseudomonas aeruginosa Effector delivery system HSI-1 is highly homologous to a group of genes found in many Gram-negative proteobacteria that have been termed the IcmF-associated homologous protein (IAHP) cluster and encodes a secretory system that may play a general role in mediating host interaction Play role in chronic P. aeruginosa infections Encoding a protein secretion apparatus for exporting Hcp1, a hexameric protein that forms rings with 40 angstrom internal diameter; a ClpB-like AAA+ family protein, ClpV1, forms a core component of this secretion apparatus and is likely to provide the energy for translocation of Hcp1 Abstract(s) in PubMed C2_01398 VFG036559 45.4 2.61e-64 208.0 VF0272 VFC0272 fbpC iron(III) ABC transporter, ATP-binding protein Neisseria lactamica 020-06 FbpABC Neisseria meningitidis Nutritional/Metabolic factor Encodes a periplasmic-binding protein-dependent iron transport system necessary for the utilization of iron bound to transferrin or iron chelates, FbpA is the periplasmic Fe3+ binding protein Abstract(s) in PubMed C2_01427 VFG044378 43.1 3.2199999999999995e-54 179.0 VF0937 VFC0272 qbsC QbsC Pseudomonas fluorescens ATCC 17400 C2_01488 VFG013573 42.5 1.03e-58 193.0 VF0268 VFC0272 hitC iron(III) ABC transporter, ATP-binding protein Haemophilus somnus 129PT HitABC Haemophilus influenzae Nutritional/Metabolic factor HitA encodes a periplasmic ferric-binding protein A (FbpA), a high-affinity iron-binding protein belonging to the transferrin superfamily. hitB encodes a cytoplasmic permease. hitC encodes ATP-binding protein HitABC(fbpABC) operon encodes a periplasmic-binding protein-dependent iron transport system necessary for the utilization of iron bound to transferrin or iron chelates Abstract(s) in PubMed C2_01527 VFG037726 40.3 7.18e-245 720.0 VF0504 VFC0271 adeG cation/multidrug efflux pump Acinetobacter baumannii D1279779 AdeFGH efflux pump Acinetobacter baumannii Biofilm Belongs to resistance-nodulation-cell division (RND)-type efflux system; RND efflux systems, composed of an inner membrane protein (RND pump) linked by a periplasmic adaptor protein (PAP) to an outer membrane factor (OMF), can extrude a wide range of substrates often unrelated in structure; To date, three Acinetobacter drug efflux (Ade) RND systems, AdeABC, AdeFGH, and AdeIJK, have been characterized in A. baumannii Play a potential role in the synthesis and transport of autoinducer molecules during biofilm formation Abstract(s) in PubMed C2_01555 VFG038764 45.2 2.25e-85 276.0 VF0473 VFC0204 flrA FleQ protein Aeromonas hydrophila ML09-119 Polar flagella Aeromonas hydrophila Motility Types of bacterial movement: swimming, swarming, gliding, twitching and sliding. Only swimming and swarming are correlated with the presence of flagella. Swimming is an individual endeavour, while swarming is the movement of a group of bacteria; constitutively expressed for motility in liquid environments Necessary for motility, adhesion and invasion; glycosylation of the flagellin may play a role in provoking a proinflammatory response Abstract(s) in PubMed C2_01563 VFG047558 44.8 1.18e-88 270.0 VF0559 VFC0272 purM phosphoribosylaminoimidazole synthetase Francisella philomiragia subsp. philomiragia ATCC 25017 Purine biosynthesis Francisella tularensis Nutritional/Metabolic factor The purMCD locus encodes three enzymes (phosphoribosylaminoimidazol synthetase, SAICAR synthetase, and phosphoribosylamine-glycine ligase) required for the de novo synthesis of purine nucleotides. Required for bacterial cytosolic replication Abstract(s) in PubMed C2_01583 VFG031464 48.9 1.98e-37 124.0 VF0851 VFC0258 ndk nucleoside-diphosphate kinase Mycobacterium gilvum PYR-GCK C2_01619 VFG043345 42.7 1.11e-110 333.0 VF0157 VFC0204 fleR/flrC sigma 54-dependent response regulator Legionella pneumophila subsp. pneumophila str. Philadelphia 1 Flagella Legionella pneumophila Motility Flagella expression is associated with the cellular cycle in L. pneumophila, the bacteria are not motile while multiplying in host cells, but become motile in the later stages of the infection process Not required for intracellular growth but enhance the invasion capacity Abstract(s) in PubMed C2_01638 VFG000121 66.0 1.56e-85 250.0 VF0091 VFC0271 algU alginate biosynthesis protein AlgZ/FimS Pseudomonas aeruginosa PAO1 Alginate Mucoid exopolysaccharide Pseudomonas aeruginosa Biofilm Alginate production is frequently referred to as mucoidy because colonies producing alginate have a wet glistening (mucoid) appearance, which is very different from that of colonies not producing alginate; most of the alginate biosynthetic genes are clustered in the algD operon; Alginate production is highly regulated. Regulatory genes are located in two areas far removed from the biosynthetic genes, with one exception algC Alginate is a linear polymer of high molecular weight composed of the uronic acids -D-mannuronate and its C-5 epimer, -L-guluronate, which are linked by -1,4 glycosidic bonds; The early steps in the biosynthesis of alginate to form GDP mannuronic acid require the products of algA and algC to convert fructose-6-phosphate to GDP-mannose and then require the product of algD to convert this to the uronic acid form, GDP-mannuronate Allows the bacteria form biofilm; contributes to the persistence of the bacteria in the CF lung: act as an adhesin, preventing the bacteria from being expelled from the lung, and alginate slime layer makes it more difficult for phagocytes to ingest and kill the bacteria Abstract(s) in PubMed C2_01653 VFG013384 63.9 2.08e-167 473.0 VF0044 VFC0258 lpxB lipid-A-disaccharide synthase Haemophilus influenzae Rd KW20 LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_01654 VFG013393 63.7 3.89e-104 303.0 VF0044 VFC0258 lpxA UDP-N-acetylglucosamine acyltransferase Haemophilus ducreyi 35000HP LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_01655 VFG011402 46.0 1.85e-39 130.0 VF0367 VFC0258 fabZ (3R)-hydroxymyristoyl ACP dehydratase Brucella suis 1330 LPS Lipopolysaccharide Brucella melitensis Immune modulation Brucella possesses a non-classical LPS as compared with the so-called classical LPS from enterobacteria such as Escherichia coli. B. abortus lipid A possesses a diaminoglucose backbone (rather than glucosamine), and acyl groups are longer (C28 rather than C12 and C16) and are only linked to the core by amide bounds (rather than ester and amide bonds).; In contrast to enterobacterial LPSs, Brucella LPS is several-hundred-times less active and toxic than E. coli LPS.; this is an evolutionary adaptation to an intracellular lifestyle, low endotoxic activity is shared by other intracellular pathogens such as Bartonella and Legionella. Plays a role in entry and early survival inside macrophages; Resistance to innate-immunity anti-bacterial responses; a modulator of the immune response The entry and early survival stages of smooth Brucella are lipid-raft-dependent. The entry-gateway seems to include Brucella surface-exposed HSP60-PrPc (cellular prion protein) interaction but also a SR-A (class A scavenger)-lipid-A interaction and is also dependent on the LPS O-chain. And the LPS O-chain ensures the Brucella containing vacuole (BCV) aviodance of fusion with lysosomes transiently; The chemical structure of Brucella LPS permits the bacteria to become highly resistant to anti-bacterial effectors of the innate immune system. Long O-chains at the bacterial surface should provoke a steric hindrance leading to the formation of a protecting barrier. The presence of long O-chains at the surface of Brucella prevents the deposition of complement at the bacterial surface. The O-chains also could prevent a specific recognition of the Pathogen-associated molecular patterns (PAMPs) and as a consequence impair expression of any cytokines or iNOS, both of which are known to be involved in the clearance of intracellular Brucella. The low number of anionic groups in the core lipid A, especially charged phosphate groups could both remove anionic targets and facilitate a tighter aggregation of LPS molecules via their hydrophobic fatty acids, leading to less binding and penetration of antibacterial cationic peptides.;The Brucella LPS forms stable large clusters with MHC-II named macrodomians in the cell surface, interfering with MHC-II presentation of peptides to specific CD4+ T cells. Abstract(s) in PubMed C2_01656 VFG013165 60.5 1.14e-112 330.0 VF0044 VFC0258 lpxD UDP-3-O-(3-hydroxymyristoyl) glucosamine N-acyltransferase Haemophilus somnus 2336 LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_01659 VFG015004 48.1 8.47e-137 400.0 VF0091 VFC0271 mucP metalloprotease protease Pseudomonas syringae pv. syringae B728a Alginate Mucoid exopolysaccharide Pseudomonas aeruginosa Biofilm Alginate production is frequently referred to as mucoidy because colonies producing alginate have a wet glistening (mucoid) appearance, which is very different from that of colonies not producing alginate; most of the alginate biosynthetic genes are clustered in the algD operon; Alginate production is highly regulated. Regulatory genes are located in two areas far removed from the biosynthetic genes, with one exception algC Alginate is a linear polymer of high molecular weight composed of the uronic acids -D-mannuronate and its C-5 epimer, -L-guluronate, which are linked by -1,4 glycosidic bonds; The early steps in the biosynthesis of alginate to form GDP mannuronic acid require the products of algA and algC to convert fructose-6-phosphate to GDP-mannose and then require the product of algD to convert this to the uronic acid form, GDP-mannuronate Allows the bacteria form biofilm; contributes to the persistence of the bacteria in the CF lung: act as an adhesin, preventing the bacteria from being expelled from the lung, and alginate slime layer makes it more difficult for phagocytes to ingest and kill the bacteria Abstract(s) in PubMed C2_01662 VFG045688 46.1 5.71e-70 216.0 VF0361 VFC0258 cpsA/uppS undecaprenyl diphosphate synthase Enterococcus faecium Aus0004 Capsule Enterococcus faecalis Immune modulation The biosynthesis of capsular polysaccharides by E. faecalis is encoded by the csp operon, which includes 11 open reading frames (cpsA to cpsK). However, only 7 open reading frames in the cps operon are essential for capsule production (cpsC, cpsD, cpsE, cpsG, cpsI, cpsJ, and cpsK); Previous genetic evidence demonstrated that E. faecalis isolates can be classified in 1 of 3 capsule operon polymorphisms. CPS 1 presents only cpsA and cpsB. CPS 2 presents all 11 genes in the cps operon. CPS 5 presents all genes except for cpsF. Furthermore, CPS 2 and 5 express the capsular polysaccharide, whereas CPS 1 does not. Contributes to host immune evasion Masks bound C3 from detection on the surface of E. faecalis; masks lipoteichoic acid from detection Abstract(s) in PubMed C2_01673 VFG014960 40.6 4.02e-84 267.0 VF0091 VFC0271 mucD serine protease MucD precursor Pseudomonas fluorescens Pf0-1 Alginate Mucoid exopolysaccharide Pseudomonas aeruginosa Biofilm Alginate production is frequently referred to as mucoidy because colonies producing alginate have a wet glistening (mucoid) appearance, which is very different from that of colonies not producing alginate; most of the alginate biosynthetic genes are clustered in the algD operon; Alginate production is highly regulated. Regulatory genes are located in two areas far removed from the biosynthetic genes, with one exception algC Alginate is a linear polymer of high molecular weight composed of the uronic acids -D-mannuronate and its C-5 epimer, -L-guluronate, which are linked by -1,4 glycosidic bonds; The early steps in the biosynthesis of alginate to form GDP mannuronic acid require the products of algA and algC to convert fructose-6-phosphate to GDP-mannose and then require the product of algD to convert this to the uronic acid form, GDP-mannuronate Allows the bacteria form biofilm; contributes to the persistence of the bacteria in the CF lung: act as an adhesin, preventing the bacteria from being expelled from the lung, and alginate slime layer makes it more difficult for phagocytes to ingest and kill the bacteria Abstract(s) in PubMed C2_01680 VFG013618 69.7 1.05e-224 622.0 VF0758 VFC0272 hemL glutamate-1-semialdehyde 2,1-aminomutase Haemophilus somnus 129PT C2_01683 VFG013728 45.3 5.37e-66 206.0 VF0740 VFC0272 ciuD ABC transporter ATP-binding protein Corynebacterium jeikeium K411 C2_01694 VFG018336 61.4 6.05e-102 296.0 VF0953 VFC0001 staB fimbrial chaperone Salmonella enterica subsp. enterica serovar Paratyphi B str. SPB7 C2_01695 VFG021422 62.3 0.0 1104.0 VF0953 VFC0001 staC outer membrane usher protein Salmonella enterica subsp. enterica serovar Schwarzengrund str. CVM19633 C2_01696 VFG021420 48.2 2.3999999999999997e-38 130.0 VF0953 VFC0001 staD fimbrial protein Salmonella enterica subsp. enterica serovar Schwarzengrund str. CVM19633 C2_01697 VFG018339 45.1 7.209999999999999e-38 129.0 VF0953 VFC0001 staE fimbrial protein StaE Salmonella enterica subsp. enterica serovar Paratyphi B str. SPB7 C2_01701 VFG009302 48.2 1.23e-71 223.0 VF0319 VFC0272 panC pantoate--beta-alanine ligase Mycobacterium gilvum PYR-GCK PanC/PanD Mycobacterium tuberculosis Nutritional/Metabolic factor Lipid biosynthesis and metabolism play a pivotal role in the intracellular replication and persistence of M. tuberculosis. Pantothenic acid (vitamin B5) is an essential molecule required for the synthesis of coenzyme A and acyl carrier protein (ACP). PanC (pantothenate synthetase) and PanD (aspartate-1-decarboxylase) involved in pantothenate biosynthesis. Abstract(s) in PubMed C2_01703 VFG022623 51.8 2.77e-38 125.0 VF0319 VFC0272 panD aspartate 1-decarboxylase Mycobacterium sp. JDM601 PanC/PanD Mycobacterium tuberculosis Nutritional/Metabolic factor Lipid biosynthesis and metabolism play a pivotal role in the intracellular replication and persistence of M. tuberculosis. Pantothenic acid (vitamin B5) is an essential molecule required for the synthesis of coenzyme A and acyl carrier protein (ACP). PanC (pantothenate synthetase) and PanD (aspartate-1-decarboxylase) involved in pantothenate biosynthesis. Abstract(s) in PubMed C2_01726 VFG045950 100.0 1.8300000000000002e-103 291.0 HCP VFC0001 hcpA prepilin peptidase-dependent pilin Escherichia coli O104:H4 str. 2009EL-2050 C2_01727 VFG045987 99.8 0.0 912.0 HCP VFC0001 hcpB type II secretion system protein GspE Escherichia coli O104:H4 str. 2009EL-2050 C2_01728 VFG046022 100.0 1.18e-287 778.0 HCP VFC0001 hcpC protein transport protein HofC Escherichia coli O103:H2 str. 12009 C2_01736 VFG013414 77.3 1.09e-171 477.0 VF0044 VFC0258 lpxC UDP-3-O-(R-3-hydroxymyristoyl)-N-acetylglucosamine deacetylase Haemophilus influenzae PittEE LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_01759 VFG009376 46.7 1.47e-55 174.0 VF0814 VFC0272 leuD 3-isopropylmalate dehydratase small subunit Mycobacterium smegmatis str. MC2 155 C2_01797 VFG047710 57.8 0.0 1154.0 VF0558 VFC0272 carB carbamoyl phosphate synthase large subunit Francisella cf. tularensis subsp. novicida 3523 Pyrimidine biosynthesis Francisella tularensis Nutritional/Metabolic factor CarB, CarA, and PyrB encode the large and small subunits of carbamoylphosphate synthetase and aspartate carbamoyl transferase, respectively. These enzymes catalyze the first two steps in the pyrimidine nucleotide biosynthetic pathway in many bacteria, including Francisella, and are required for the virulence of several pathogens, including Salmonella and E. coli Mediating bacterial resistance to reactive oxygen species (ROS) that is important for phagosomal escape Abstract(s) in PubMed C2_01798 VFG047720 49.2 9.88e-126 367.0 VF0558 VFC0272 carA carbamoyl phosphate synthase small subunit Francisella philomiragia subsp. philomiragia ATCC 25017 Pyrimidine biosynthesis Francisella tularensis Nutritional/Metabolic factor CarB, CarA, and PyrB encode the large and small subunits of carbamoylphosphate synthetase and aspartate carbamoyl transferase, respectively. These enzymes catalyze the first two steps in the pyrimidine nucleotide biosynthetic pathway in many bacteria, including Francisella, and are required for the virulence of several pathogens, including Salmonella and E. coli Mediating bacterial resistance to reactive oxygen species (ROS) that is important for phagosomal escape Abstract(s) in PubMed C2_01808 VFG034852 92.6 1.04e-104 310.0 VF1111 VFC0086 espX1 Type III secretion system effector EspX1 Escherichia coli O55:H7 str. RM12579 TTSS secreted effectors Escherichia coli (EPEC) Effector delivery system EspF (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspFu/tccP (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspG (TBC-like GTPase activating protein. Efficiently catalyzes GTP hydrolysis in Rab1 to disrupt of Rab1-mediated ER-to-Golgi trafficking. ); EspH (First bacterial effector acting directly on RhoGEFs, EspH directly binds to the DH-PH domain in RhoGEFs to disrupt RhoGEF-Rho signaling; critical for inhibiting macrophage phagocytosis. ); EspJ (Inhibit both IgG- and complement receptor-mediated phagocytosis. ); EspL1; EspL2 (Cysteine protease. Bounds F-actin-aggregating annexin 2 directly to increase annexin 2's ability to aggregate Tir-induced F-actin; block necroptosis and in flammation. ); EspM1 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspM2 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspO1-1; EspR1; EspR3; EspR4; EspV (Inducing radical morphological changes in host cells. ); EspW; EspX1; EspX2; EspX4; EspX5; EspX6; EspY1; EspY2; EspY3; EspY4; Map (GEF. Mimics the host Dbl and catalyses the exchange of GDP for GTP in Cdc42, involved in effacement, SGLT1 inhibition, formation of filopodia and disruption of mitochondrial function. ); NleA/espI (Disruption of tight junctions by inhibition of host cell protein trafficking through COPII-dependent pathways. ); NleB2 (May also have anti-inflammatory activity. ); NleB2-2; NleC (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate RelA (p65), thus blocking NF-B pathway. ); NleD (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate JNK and p38, thus blocking AP-1 pathway. ); NleE (PMN tran-epithelial migration; blocks translocation of the p65 to the host cell nucleus by preventing IB degradation to inhibit NF-B pathway. ); NleF; NleG-1; NleG-2; NleG-3; NleG2-2; NleG2-4; NleG5-1; NleG6-1; NleG7 (U-box type E3 ubiquitin ligases. ); NleG8-2; NleH1 (Ser/Thr protein kinase. Binds directly to a subunit of NF-B, the ribosomal protein S3 (RPS3), reducing the nuclear abundance of RPS3 to dampen host transcriptional outputs; interact with Bax inhibitor-1 to block apoptosis. ); NleH2 (Putative kinase. Attenuates NF-B pathway. ); SepZ/espZ (EspZ interacts with CD98 in host cell membranes to promote host cell survival, therefore provide the pathogen with valuable time to colonize efficiently prior to dissemination. ); Tir (Mimics host immunoreceptor tyrosine-based inhibition motifs (ITIMs), also see helicobacter CagA. EHEC Tir lacks the Nck binding site. Conserved NPY (Asn-Pro-Tyr) motif recruits the adaptor protein IRTKS and/or IRSp53. IRTKS/IRSp53 link Tir and TccP/EspFu, which in turn activates N-WASP; Receptor for intimin; effacement; SGLT1 inhibition; recruits SHIP2 to control actin-pedestal morphology; maintains the integrity of the epithelium by keeping the destructive activity of EspG and EspG2 in check. ) Abstract(s) in PubMed C2_01815 VFG015291 49.2 7.25e-09 56.6 VF0911 VFC0086 hopI1 DnaJ domain-containing protein Pseudomonas syringae pv. syringae B728a C2_01816 VFG043573 60.4 9.23e-243 685.0 VF0713 VFC0001 dnaK chaperone protein DnaK Chlamydia trachomatis D/UW-3/CX C2_01824 VFG042879 48.9 3.4e-101 301.0 VF0609 VFC0001 VV1_RS07215 type IV pilus twitching motility protein PilT Vibrio vulnificus CMCP6 ChiRP Chitin-regulated pilus Vibrio vulnificus Adherence Also known as PilA pilus PilA is involved in biofilm formation, adherence to human epithelial cells. Abstract(s) in PubMed C2_01828 VFG013266 58.5 1.13e-75 225.0 VF0044 VFC0258 orfM deoxyribonucleotide triphosphate pyrophosphatase Haemophilus influenzae 86-028NP LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_01829 VFG013626 67.0 4.24e-195 543.0 VF0758 VFC0272 hemN radical SAM family heme chaperone HemW Haemophilus influenzae 86-028NP C2_01845 VFG040946 95.5 2.33e-117 329.0 VF1177 VFC0086 yghD GspM family type II secretion system protein YghD Escherichia coli E24377A C2_01846 VFG040947 99.0 2.36e-283 767.0 VF1177 VFC0086 gspL type II secretion system protein GspL Escherichia coli E24377A C2_01847 VFG012910 99.4 2.2999999999999998e-222 607.0 VF0333 VFC0086 gspK general secretion pathway protein K Shigella boydii Sb227 T2SS Type II secretion system Shigella dysenteriae Effector delivery system T2SS encoded by genes of the general secretion pathway (gsp) is widely distributed in Gram-negative bacteria. The known E.coli T2SS, responsible for chitinase secretion, encoded by the yhe genes at 74.5 min of the MG1655 chromosome is absent in all four sequenced Shigella genomes; A novel set of gsp genes are located on the S. dysenteriae Sd197 and S. boydii Sb227 chromosomes. The Sb227 T2SS is likely to be inactive due to a frameshift in gspC and a nonsense mutation in gspD. Those genes show significant similarity to those from ETEC and Vibrio cholerae responsible for secreting the E.coli heat labile toxin (Ltx) and cholera toxin (Ctx), respectively. While Shiga toxin has an overall similar structure to Ctx and Ltx. Still unknown. Abstract(s) in PubMed C2_01848 VFG040949 100.0 2.79e-142 394.0 VF1177 VFC0086 gspJ type II secretion system minor pseudopilin GspJ Escherichia coli E24377A C2_01849 VFG012906 98.4 2.9000000000000004e-80 231.0 VF0333 VFC0086 gspI general secretion pathway protein I Shigella boydii Sb227 T2SS Type II secretion system Shigella dysenteriae Effector delivery system T2SS encoded by genes of the general secretion pathway (gsp) is widely distributed in Gram-negative bacteria. The known E.coli T2SS, responsible for chitinase secretion, encoded by the yhe genes at 74.5 min of the MG1655 chromosome is absent in all four sequenced Shigella genomes; A novel set of gsp genes are located on the S. dysenteriae Sd197 and S. boydii Sb227 chromosomes. The Sb227 T2SS is likely to be inactive due to a frameshift in gspC and a nonsense mutation in gspD. Those genes show significant similarity to those from ETEC and Vibrio cholerae responsible for secreting the E.coli heat labile toxin (Ltx) and cholera toxin (Ctx), respectively. While Shiga toxin has an overall similar structure to Ctx and Ltx. Still unknown. Abstract(s) in PubMed C2_01850 VFG040951 100.0 2.14e-131 365.0 VF1177 VFC0086 gspH type II secretion system minor pseudopilin GspH Escherichia coli E24377A C2_01851 VFG002050 98.7 5.599999999999999e-105 296.0 VF0333 VFC0086 gspG general secretion pathway protein G Shigella dysenteriae Sd197 T2SS Type II secretion system Shigella dysenteriae Effector delivery system T2SS encoded by genes of the general secretion pathway (gsp) is widely distributed in Gram-negative bacteria. The known E.coli T2SS, responsible for chitinase secretion, encoded by the yhe genes at 74.5 min of the MG1655 chromosome is absent in all four sequenced Shigella genomes; A novel set of gsp genes are located on the S. dysenteriae Sd197 and S. boydii Sb227 chromosomes. The Sb227 T2SS is likely to be inactive due to a frameshift in gspC and a nonsense mutation in gspD. Those genes show significant similarity to those from ETEC and Vibrio cholerae responsible for secreting the E.coli heat labile toxin (Ltx) and cholera toxin (Ctx), respectively. While Shiga toxin has an overall similar structure to Ctx and Ltx. Still unknown. Abstract(s) in PubMed C2_01852 VFG040953 100.0 1.5e-273 743.0 VF1177 VFC0086 gspF type II secretion system inner membrane protein GspF Escherichia coli E24377A C2_01853 VFG040954 99.8 0.0 953.0 VF1177 VFC0086 gspE type II secretion system ATPase GspE Escherichia coli E24377A C2_01854 VFG040955 100.0 0.0 1297.0 VF1177 VFC0086 gspD type II secretion system secretin GspD Escherichia coli E24377A C2_01855 VFG040956 95.6 2.48e-181 501.0 VF1177 VFC0086 gspC type II secretion system protein GspC Escherichia coli E24377A C2_01857 VFG006914 46.1 3.04e-71 220.0 VF0609 VFC0001 pilD/vcpD A24 family peptidase Vibrio cholerae O1 biovar El Tor str. N16961 ChiRP Chitin-regulated pilus Vibrio vulnificus Adherence Also known as PilA pilus PilA is involved in biofilm formation, adherence to human epithelial cells. Abstract(s) in PubMed C2_01858 VFG000106 49.2 0.0 1373.0 VF0127 VFC0346 acfD accessory colonization factor AcfD Vibrio cholerae O1 biovar El Tor str. N16961 ACF Accessory colonization factor Vibrio cholerae Others Regulated by the same system that controls expression of cholera toxin; AcfB exhibits sequence similarity with chemotaxis regulatory proteins found in other Gram-negative species. Play a role in chemotaxis, thereby assisting in intestinal colonization Abstract(s) in PubMed C2_01860 VFG043448 57.6 2.07e-296 828.0 VF0864 VFC0001 glcB malate synthase Mycobacterium tuberculosis H37Rv C2_01912 VFG041842 46.1 2.97e-60 188.0 SPI-1 like VFC0086 CV_RS12900 response regulator Chromobacterium violaceum ATCC 12472 C2_01922 VFG044140 74.1 1.25e-227 633.0 VF1029 VFC0272 tolC outer membrane channel protein TolC Yersinia pestis CO92 C2_01931 VFG021496 41.9 2.6200000000000003e-213 624.0 VF0956 VFC0001 stdB fimbrial outer membrane usher protein StdB Salmonella enterica subsp. enterica serovar Newport str. SL254 C2_01937 VFG000331 71.0 5.4e-237 657.0 VF0044 VFC0258 rfaE ADP-heptose synthase Haemophilus influenzae Rd KW20 LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_01952 VFG009718 60.3 1.3199999999999998e-89 285.0 VF0257 VFC0301 sigA/rpoV RNA polymerase sigma factor Mycobacterium smegmatis str. MC2 155 SigA Mycobacterium tuberculosis Regulation In M. tuberculosis, 13 sigma factor genes have been annotated in the genome, 9 of which belong to a special subfamily thought to direct extracytoplasmic functions and various other stress responses (temperature, oxidative stress, pH, and infection of macrophages); sigma A also known as RpoV, is the essential principal mycobacterial sigma factors, necessary for most mycobacterial housekeeping gene transcription; It was the first mycobacterial sigma factor to be associated with virulence Sigma A interacts with a transcriptional activator WhiB3 to allow the expression of genes necessary for virulence Abstract(s) in PubMed C2_01978 VFG034648 99.7 9.43e-277 748.0 VF0213 VFC0001 cfaD/cfaE minor pilin and initiator Escherichia coli E24377A Adhesive fimbriae Escherichia coli (ETEC) Adherence Adherence is mediated by proteinaceous surface structures that are referred to as colonization factors (CFs), colonization factor antigens (CFAs), coli surface antigens (CSAs), or putative colonization factors (PCFs); ETEC strains are host-specific. The CFs confer host specificity on the strain. In human-specific ETEC strains, 21 different CFs have been identified. Approximately 75% of human ETEC express either CFA/I, CFA/II or CFA/IV. Animal-specific ETEC strains produce a variety of CFs that are distinct from those produced by human-specific isolates, such as K88 and K99; ETEC strains typically possess multiple plasmids with a wide range of molecular masses. The genes encoding CFs generally are found on a plasmid that also encodes ST and/or LT ETEC CFs can be classified as fimbriae or fibrillae depending on their structure. The fimbrial CFs are rigid filamentous, rodlike structures, whereas the fibrillar CFs are thinner, more flexible, and have fewer subunits in each helical turn than do fimbrial CFs Adhesin, receptor is the oligosaccharide components of glycolipids and glycoproteins Abstract(s) in PubMed C2_01979 VFG034636 99.9 0.0 1751.0 VF0213 VFC0001 cfaC colonisation factor antigen c, usher Escherichia coli E24377A Adhesive fimbriae Escherichia coli (ETEC) Adherence Adherence is mediated by proteinaceous surface structures that are referred to as colonization factors (CFs), colonization factor antigens (CFAs), coli surface antigens (CSAs), or putative colonization factors (PCFs); ETEC strains are host-specific. The CFs confer host specificity on the strain. In human-specific ETEC strains, 21 different CFs have been identified. Approximately 75% of human ETEC express either CFA/I, CFA/II or CFA/IV. Animal-specific ETEC strains produce a variety of CFs that are distinct from those produced by human-specific isolates, such as K88 and K99; ETEC strains typically possess multiple plasmids with a wide range of molecular masses. The genes encoding CFs generally are found on a plasmid that also encodes ST and/or LT ETEC CFs can be classified as fimbriae or fibrillae depending on their structure. The fimbrial CFs are rigid filamentous, rodlike structures, whereas the fibrillar CFs are thinner, more flexible, and have fewer subunits in each helical turn than do fimbrial CFs Adhesin, receptor is the oligosaccharide components of glycolipids and glycoproteins Abstract(s) in PubMed C2_01980 VFG034624 100.0 3.79e-108 305.0 VF0213 VFC0001 cfaB colonization factor antigen 1 Escherichia coli E24377A Adhesive fimbriae Escherichia coli (ETEC) Adherence Adherence is mediated by proteinaceous surface structures that are referred to as colonization factors (CFs), colonization factor antigens (CFAs), coli surface antigens (CSAs), or putative colonization factors (PCFs); ETEC strains are host-specific. The CFs confer host specificity on the strain. In human-specific ETEC strains, 21 different CFs have been identified. Approximately 75% of human ETEC express either CFA/I, CFA/II or CFA/IV. Animal-specific ETEC strains produce a variety of CFs that are distinct from those produced by human-specific isolates, such as K88 and K99; ETEC strains typically possess multiple plasmids with a wide range of molecular masses. The genes encoding CFs generally are found on a plasmid that also encodes ST and/or LT ETEC CFs can be classified as fimbriae or fibrillae depending on their structure. The fimbrial CFs are rigid filamentous, rodlike structures, whereas the fibrillar CFs are thinner, more flexible, and have fewer subunits in each helical turn than do fimbrial CFs Adhesin, receptor is the oligosaccharide components of glycolipids and glycoproteins Abstract(s) in PubMed C2_01981 VFG034605 100.0 9.89e-169 464.0 VF0213 VFC0001 cfaA colonisation factor antigen a, chaperone Escherichia coli O111:H- str. 11128 Adhesive fimbriae Escherichia coli (ETEC) Adherence Adherence is mediated by proteinaceous surface structures that are referred to as colonization factors (CFs), colonization factor antigens (CFAs), coli surface antigens (CSAs), or putative colonization factors (PCFs); ETEC strains are host-specific. The CFs confer host specificity on the strain. In human-specific ETEC strains, 21 different CFs have been identified. Approximately 75% of human ETEC express either CFA/I, CFA/II or CFA/IV. Animal-specific ETEC strains produce a variety of CFs that are distinct from those produced by human-specific isolates, such as K88 and K99; ETEC strains typically possess multiple plasmids with a wide range of molecular masses. The genes encoding CFs generally are found on a plasmid that also encodes ST and/or LT ETEC CFs can be classified as fimbriae or fibrillae depending on their structure. The fimbrial CFs are rigid filamentous, rodlike structures, whereas the fibrillar CFs are thinner, more flexible, and have fewer subunits in each helical turn than do fimbrial CFs Adhesin, receptor is the oligosaccharide components of glycolipids and glycoproteins Abstract(s) in PubMed C2_02073 VFG020187 69.9 6.46e-166 464.0 VF0981 VFC0346 msbB2 lauroyl-Kdo(2)-lipid IV(A) myristoyltransferase Shigella boydii CDC 3083-94 C2_02082 VFG039536 59.3 1.83e-98 287.0 VF0696 VFC0086 CBU_1566 Coxiella Dot/Icm type IVB secretion system translocated effector Coxiella burnetii RSA 493 T4SS secreted effectors Coxiella burnetii Effector delivery system CBUA0020; CBU_0012*; CBU_0113; CBU_0122; CBU_0183; CBU_0201; CBU_0270; CBU_0295; CBU_0344*; CBU_0372; CBU_0375*; CBU_0469; CBU_0513; CBU_0534; CBU_0590; CBU_0635; CBU_0637; CBU_0820*; CBU_1048*; CBU_1079; CBU_1107*; CBU_1150*; CBU_1198; CBU_1268; CBU_1349; CBU_1370; CBU_1409; CBU_1434; CBU_1493; CBU_1495*; CBU_1525*; CBU_1530; CBU_1566; CBU_1576; CBU_1594; CBU_1607; CBU_1614; CBU_1639; CBU_1665; CBU_1677; CBU_1685; CBU_1752; CBU_1754; CBU_1789; CBU_1790; CBU_1794; CBU_1818; CBU_1819; CBU_1863; CBU_2016; CBU_2028; CBU_2056; CBU_2059*; CBU_2076; AnkA; AnkB; AnkF; AnkG (Interacts with host protein p32 to block apoptosis. ); AnkH; AnkI; AnkM/cig58; AnkP; Cem1; Cem12; Cem13; Cem3; Cem4; Cem6; Cem9; CetCb1; CetCb2; CetCb3; CetCB4; CetCb5; CetCb6; CirA/coxCC1 (Phosphate transporter family protein. ); CirB; CirC/coxDFB1; CoxCC10/cig49; CoxCC11; CoxCC12; CoxCC14; CoxCC15; CoxCC3; CoxCC4; CoxCC5; CoxCC6; CoxCC7/cig44; CoxCC8; CoxDFB3; CoxDFB4 (Surface antigen. ); CoxDFB5/cig57; CoxDFB6; CoxFIC1; CoxH2/rimL (Acetyltransferase. ); CoxH3; CoxH4/cig61; CoxK1 (Protein kinase, putative. ); CoxK2; CoxTPR1 (Conserved domain protein. ); CoxU1; CoxU2; CpeA; CpeB; CpeC/coxU3 (Hypothetical protein plasmid QpH1. ); CpeD; CpeE; CpeF; CpeG; CpeH; CvpA; MceA; PhnB; CBUD_RS05145; CBUD_RS06720*; CBUD_RS08635; CBUD_RS11275; CBUD_RS12405; CBUG_RS02435; CBUK_RS06760 Abstract(s) in PubMed C2_02096 VFG043085 97.7 1.99e-88 252.0 VF1154 VFC0204 flhe flagellar protein FlhE Escherichia coli O157:H7 str. EDL933 C2_02097 VFG043086 99.7 0.0 1293.0 VF1154 VFC0204 flhA flagellar biosynthesis protein FlhA Escherichia coli O157:H7 str. EDL933 C2_02098 VFG043087 98.7 3.65e-266 723.0 VF1154 VFC0204 flhB flagellar type III secretion system protein FlhB Escherichia coli O157:H7 str. EDL933 C2_02099 VFG043088 99.5 4.53e-144 400.0 VF1154 VFC0204 cheZ protein phosphatase CheZ Escherichia coli O157:H7 str. EDL933 C2_02100 VFG043089 100.0 1.52e-87 250.0 VF1154 VFC0204 cheY chemotaxis response regulator CheY Escherichia coli O157:H7 str. EDL933 C2_02101 VFG043090 99.1 1.1799999999999998e-243 663.0 VF1154 VFC0204 cheB protein-glutamate methylesterase/protein glutamine deamidase Escherichia coli O157:H7 str. EDL933 C2_02102 VFG043091 99.0 1.96e-208 568.0 VF1154 VFC0204 cheR protein-glutamate O-methyltransferase CheR Escherichia coli O157:H7 str. EDL933 C2_02103 VFG014046 41.7 5.21e-19 90.5 VF0082 VFC0001 pilJ twitching motility protein PilJ Pseudomonas syringae pv. syringae B728a Type IV pili Pseudomonas aeruginosa Adherence PilA, B, C, D, E, F, M, N, O, P, Q, T, U, V, W, X, Y1, Y2, Z, and fimT, U, V are involved in the biogenesis and mechanical function of pili, pilG, H, I, K, chpA, B, C, D, E, pilS, R, fimS, rpoN, algR, algU, and vfr are involved in transcriptional regulation and chemosensory pathways that control the expression or activity of the twitching motility of the pili Attaches to host cells, but not to mucin, causing a twitching motility that allows the bacteria to move along the cell surface; biofilm formation The C-terminal receptor-binding domain of pilin binds to asialoGM1 gangliosides on host cells. Generally, GM1 gangliosides contain a sialic acid moiety. P.aeruginosa produces a neuraminidase which removes sialic acid residues from the GM1 to form the asialoGM1, which is a better receptor for the pili; The asialoGM1 is present in increased abundance on the surface of cystic fibrosis respiratory epithelial cells Abstract(s) in PubMed C2_02104 VFG043092 98.0 1.24e-309 847.0 VF1154 VFC0204 tar methyl-accepting chemotaxis protein II Escherichia coli O157:H7 str. EDL933 C2_02105 VFG043093 99.4 3.500000000000001e-109 308.0 VF1154 VFC0204 cheW chemotaxis protein CheW Escherichia coli O157:H7 str. EDL933 C2_02106 VFG043094 99.7 0.0 1222.0 VF1154 VFC0204 cheA chemotaxis protein CheA Escherichia coli O157:H7 str. EDL933 C2_02107 VFG043095 100.0 3.13e-216 590.0 VF1154 VFC0204 motB flagellar motor protein MotB Escherichia coli O157:H7 str. EDL933 C2_02108 VFG043096 99.7 9.500000000000001e-200 547.0 VF1154 VFC0204 motA flagellar motor stator protein MotA Escherichia coli O157:H7 str. EDL933 C2_02109 VFG043097 100.0 1.83e-139 386.0 VF1154 VFC0204 flhC flagellar transcriptional regulator FlhC Escherichia coli O157:H7 str. EDL933 C2_02110 VFG043098 99.1 1.32e-75 219.0 VF1154 VFC0204 flhD flagellar transcriptional regulator FlhD Escherichia coli O157:H7 str. EDL933 C2_02129 VFG015080 60.4 1.8900000000000002e-86 254.0 VF0908 VFC0301 gacA response regulator GacA Pseudomonas aeruginosa PAO1 C2_02131 VFG000152 40.8 1.34e-55 177.0 VF0093 VFC0271 rhlR transcriptional regulator RhlR Pseudomonas aeruginosa PAO1 Quorum sensing Pseudomonas aeruginosa Biofilm Consists of two separate but interrelated systems, las and rhl. The autoinducer signal molecules produced by P.aeruginosa are N-(3-oxododencanoyl) homeserine lactone(3O-C12-HSL) and N-butyryl homoserine lactone(C4-HSL); a novel, additional autoinducer has recently been demonstrated to be involved in quorum sensing. It is 2-heptyl-3-hydroxy-4-quinolone, an additional link between the Las and Rhl circuits Both the las and rhl systems regulate the production of multiple virulence factors; crucial for proper biofilm formation; 3O-C12-HSL also directly acts as a virulence factor:; activates extracellular-signal-regulated kinases(ERKs) that subsequently induced the activation of the transcription factor NF-B. This activation of NF-B was essential for maximal production of IL-8; a potent inducer of IFN- production in T cells; upregulate the expression of cyclooxygenase-2(Cox-2), which results in the increased production of PGE2. PGE2 has many functions, one of which is the induction of endothelial permeability. This vasorelaxant activity might lead to increased local blood flow, edema and cellular migration to the site of infection Abstract(s) in PubMed C2_02132 VFG006259 40.7 5.62e-42 146.0 VF0272 VFC0272 fbpC iron(III) ABC transporter, ATP-binding protein Neisseria gonorrhoeae FA 1090 FbpABC Neisseria meningitidis Nutritional/Metabolic factor Encodes a periplasmic-binding protein-dependent iron transport system necessary for the utilization of iron bound to transferrin or iron chelates, FbpA is the periplasmic Fe3+ binding protein Abstract(s) in PubMed C2_02135 VFG043099 99.6 1.45e-189 520.0 VF1154 VFC0204 tcyJ cystine ABC transporter substrate-binding protein Escherichia coli O157:H7 str. EDL933 C2_02136 VFG043100 100.0 6.21e-138 382.0 VF1154 VFC0204 fliZ flagella biosynthesis regulatory protein FliZ Escherichia coli O157:H7 str. EDL933 C2_02137 VFG043101 100.0 6.92e-165 454.0 VF1154 VFC0204 fliA RNA polymerase sigma factor FliA Escherichia coli O157:H7 str. EDL933 C2_02138 VFG043102 58.1 9.24e-139 415.0 VF1154 VFC0204 Z_RS14145 FliC/FljB family flagellin Escherichia coli O157:H7 str. EDL933 C2_02139 VFG043103 98.7 1.4e-276 756.0 VF1154 VFC0204 fliD flagellar filament capping protein FliD Escherichia coli O157:H7 str. EDL933 C2_02140 VFG043104 97.1 7.06e-85 244.0 VF1154 VFC0204 fliS flagellar export chaperone FliS Escherichia coli O157:H7 str. EDL933 C2_02141 VFG043105 100.0 4.32e-81 233.0 VF1154 VFC0204 fliT flagella biosynthesis regulatory protein FliT Escherichia coli O157:H7 str. EDL933 C2_02148 VFG034833 93.3 3.35e-187 522.0 VF1111 VFC0086 espR4 Type III secretion system effector espR4 Escherichia coli O55:H7 str. RM12579 TTSS secreted effectors Escherichia coli (EPEC) Effector delivery system EspF (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspFu/tccP (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspG (TBC-like GTPase activating protein. Efficiently catalyzes GTP hydrolysis in Rab1 to disrupt of Rab1-mediated ER-to-Golgi trafficking. ); EspH (First bacterial effector acting directly on RhoGEFs, EspH directly binds to the DH-PH domain in RhoGEFs to disrupt RhoGEF-Rho signaling; critical for inhibiting macrophage phagocytosis. ); EspJ (Inhibit both IgG- and complement receptor-mediated phagocytosis. ); EspL1; EspL2 (Cysteine protease. Bounds F-actin-aggregating annexin 2 directly to increase annexin 2's ability to aggregate Tir-induced F-actin; block necroptosis and in flammation. ); EspM1 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspM2 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspO1-1; EspR1; EspR3; EspR4; EspV (Inducing radical morphological changes in host cells. ); EspW; EspX1; EspX2; EspX4; EspX5; EspX6; EspY1; EspY2; EspY3; EspY4; Map (GEF. Mimics the host Dbl and catalyses the exchange of GDP for GTP in Cdc42, involved in effacement, SGLT1 inhibition, formation of filopodia and disruption of mitochondrial function. ); NleA/espI (Disruption of tight junctions by inhibition of host cell protein trafficking through COPII-dependent pathways. ); NleB2 (May also have anti-inflammatory activity. ); NleB2-2; NleC (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate RelA (p65), thus blocking NF-B pathway. ); NleD (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate JNK and p38, thus blocking AP-1 pathway. ); NleE (PMN tran-epithelial migration; blocks translocation of the p65 to the host cell nucleus by preventing IB degradation to inhibit NF-B pathway. ); NleF; NleG-1; NleG-2; NleG-3; NleG2-2; NleG2-4; NleG5-1; NleG6-1; NleG7 (U-box type E3 ubiquitin ligases. ); NleG8-2; NleH1 (Ser/Thr protein kinase. Binds directly to a subunit of NF-B, the ribosomal protein S3 (RPS3), reducing the nuclear abundance of RPS3 to dampen host transcriptional outputs; interact with Bax inhibitor-1 to block apoptosis. ); NleH2 (Putative kinase. Attenuates NF-B pathway. ); SepZ/espZ (EspZ interacts with CD98 in host cell membranes to promote host cell survival, therefore provide the pathogen with valuable time to colonize efficiently prior to dissemination. ); Tir (Mimics host immunoreceptor tyrosine-based inhibition motifs (ITIMs), also see helicobacter CagA. EHEC Tir lacks the Nck binding site. Conserved NPY (Asn-Pro-Tyr) motif recruits the adaptor protein IRTKS and/or IRSp53. IRTKS/IRSp53 link Tir and TccP/EspFu, which in turn activates N-WASP; Receptor for intimin; effacement; SGLT1 inhibition; recruits SHIP2 to control actin-pedestal morphology; maintains the integrity of the epithelium by keeping the destructive activity of EspG and EspG2 in check. ) Abstract(s) in PubMed C2_02149 VFG043106 100.0 3.04e-64 189.0 VF1154 VFC0204 fliE flagellar hook-basal body complex protein FliE Escherichia coli O157:H7 str. EDL933 C2_02150 VFG043107 99.1 0.0 1030.0 VF1154 VFC0204 fliF flagellar M-ring protein FliF Escherichia coli O157:H7 str. EDL933 C2_02151 VFG043108 99.7 6.599999999999999e-225 614.0 VF1154 VFC0204 fliG flagellar motor switch protein FliG Escherichia coli O157:H7 str. EDL933 C2_02152 VFG043109 99.6 2.89e-131 369.0 VF1154 VFC0204 fliH flagellar assembly protein FliH Escherichia coli O157:H7 str. EDL933 C2_02153 VFG043110 100.0 0.0 880.0 VF1154 VFC0204 fliI flagellum-specific ATP synthase FliI Escherichia coli O157:H7 str. EDL933 C2_02154 VFG043111 100.0 2.49e-97 276.0 VF1154 VFC0204 fliJ flagella biosynthesis chaperone FliJ Escherichia coli O157:H7 str. EDL933 C2_02155 VFG043112 95.2 3.99e-239 654.0 VF1154 VFC0204 fliK flagellar hook length control protein FliK Escherichia coli O157:H7 str. EDL933 C2_02156 VFG043113 100.0 1.21e-105 298.0 VF1154 VFC0204 fliL flagellar basal body-associated protein FliL Escherichia coli O157:H7 str. EDL933 C2_02157 VFG043114 99.7 8.61e-243 659.0 VF1154 VFC0204 fliM flagellar motor switch protein FliM Escherichia coli O157:H7 str. EDL933 C2_02158 VFG043115 99.3 1.22e-90 258.0 VF1154 VFC0204 fliN flagellar motor switch protein FliN Escherichia coli O157:H7 str. EDL933 C2_02159 VFG043116 99.2 4.67e-76 220.0 VF1154 VFC0204 fliO flagellar type III secretion system protein FliO Escherichia coli O157:H7 str. EDL933 C2_02160 VFG043117 100.0 5.44e-165 455.0 VF1154 VFC0204 fliP flagellar type III secretion system pore protein FliP Escherichia coli O157:H7 str. EDL933 C2_02161 VFG043118 100.0 6.72e-52 157.0 VF1154 VFC0204 fliQ flagellar biosynthesis protein FliQ Escherichia coli O157:H7 str. EDL933 C2_02162 VFG043119 99.2 8.95e-172 474.0 VF1154 VFC0204 fliR flagellar type III secretion system protein FliR Escherichia coli O157:H7 str. EDL933 C2_02163 VFG049008 67.6 1.05e-95 277.0 VF0571 VFC0301 rcsA transcriptional activator for ctr capsule biosynthesis Klebsiella pneumoniae subsp. rhinoscleromatis SB3432 RcsAB Regulation of capsule synthesis Klebsiella pneumoniae Regulation RcsB combined with the unstable auxiliary regulator RcsA to bind to an RcsAB box in the promoter region to upregulate the cps genes expression Abstract(s) in PubMed C2_02180 VFG006826 41.4 5.880000000000001e-56 179.0 VF0792 VFC0301 lisR two-component response regulator Listeria monocytogenes EGD-e C2_02199 VFG006042 43.2 5.74e-12 65.1 VF0274 VFC0258 SAK_RS06335 LysR family transcriptional regulator Streptococcus agalactiae A909 Capsule Streptococcus agalactiae Immune modulation GBS can be subclassified into serotypes according to the immunologic type of the polysaccharide capsule. Of the nine serotypes described so far, the type Ia, Ib, II, III and V are responsible for the majority of invasive human GBS disease; serotype III is particularly important because it causes the majority of infection to neonates The different capsular polysaccharides consists of high-molecular-weight polymers with a repeating unit composed of glucose, galactose, N-acetylglucosamine and sialic acid; sialic acid plays important role in virulence Inhibits the binding of the activated complement factor C3b to the surface of S. agalactiae, preventing the activation of the alternative complement pathway and inhibits complement-mediated opsonophagocytosis Abstract(s) in PubMed C2_02233 VFG036944 44.1 1.7699999999999998e-95 290.0 VF0450 VFC0325 farA fatty acid efflux system protein FarA Neisseria meningitidis 8013 FarAB Fatty acid resistance system Neisseria meningitidis Antimicrobial activity/Competitive advantage The far efflux system is composed of the FarA membrane fusion protein, the FarB cytoplasmic membrane transporter protein, and the MtrE protein as the outer membrane channel to export antibacterial fatty acids from inside the cell; belongs to Major Facilitator Superfamily (MFS) of efflux pumps and uses the proton motive force as an energy source for export of toxic agents Mediates the resistance to antimicrobial long-chain fatty acids Abstract(s) in PubMed C2_02234 VFG036972 57.5 1.15e-207 585.0 VF0450 VFC0325 farB fatty acid efflux system protein FarB Neisseria lactamica 020-06 FarAB Fatty acid resistance system Neisseria meningitidis Antimicrobial activity/Competitive advantage The far efflux system is composed of the FarA membrane fusion protein, the FarB cytoplasmic membrane transporter protein, and the MtrE protein as the outer membrane channel to export antibacterial fatty acids from inside the cell; belongs to Major Facilitator Superfamily (MFS) of efflux pumps and uses the proton motive force as an energy source for export of toxic agents Mediates the resistance to antimicrobial long-chain fatty acids Abstract(s) in PubMed C2_02235 VFG018243 76.6 8.53e-94 269.0 VF0406 VFC0271 luxS S-ribosylhomocysteinase Vibrio parahaemolyticus RIMD 2210633 AI-2 Autoinducer-2 Vibrio cholerae Biofilm AI-2 is produced and detected by a wide variety of bacteria and is presumed to facilitate interspecies communications. Furanosyl borate diester (2S,4S)-2-methyl-2,3,3,4-tetrahydroxytetrahydrofuran borate LuxPQ receptor complex responds to the AI-2 molecule. Information from AI-2 is transduced through the LuxO protein to control the levels of the master transcription factor HapR. At low cell density, in the absence of autoinducers, HapR is not produced, so virulence factors are expressed and biofilms are formed. At high cell density, in the presence of autoinducers, LuxO is inactivated, HapR is produced, and it represses genes for virulence factor production and biofilm formation. These events are proposed to allow V. cholerae to leave the host, re-enter the environment in large numbers and initiate a new cycle of infection. Abstract(s) in PubMed C2_02244 VFG010906 76.7 1.27e-26 91.3 VF0261 VFC0301 csrA carbon storage regulator CsrA Legionella pneumophila subsp. pneumophila str. Philadelphia 1 CsrA Legionella pneumophila Regulation Belongs to a highly conserved family of global regulators that typically control stationary phase traits post-transcriptionally Post-transcriptional repression of the transmission regulon Binds to particular mRNAs at a consensus sequence encompassing the ribosome binding site (RBS), destabilizing the mRNAs and preventing their translation Abstract(s) in PubMed C2_02256 VFG013476 40.7 6.31e-73 227.0 VF0044 VFC0258 kpsF KpsF/GutQ family sugar isomerase Haemophilus influenzae Rd KW20 LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_02257 VFG041021 43.2 1.15e-69 231.0 VF0943 VFC0086 PA1663 transcriptional regulator Pseudomonas aeruginosa PAO1 HSI-2 Pseudomonas aeruginosa Effector delivery system P. aeruginosa encodes three distinct T6SS loci, H1- to H3-T6SS. While H1-T6SS has only been involved in antibacterial activity so far, H2-T6SS and H3-T6SS can target both bacterial and eukaryotic cells possessing even as said earlier trans-kingdom effectors. The effectors PldA and PldB of Pseudomonas aeruginosa H2-T6SS target the Akt pathway to facilitate bacterial internalization;involved in the secretion of ModA that mediates molybdate uptake for P. aeruginosa in bacterium-bacterium competition under anaerobic conditions Abstract(s) in PubMed C2_02289 VFG015355 44.8 6.81e-112 335.0 VF0911 VFC0086 hopAN1 four-carbon acid sugar kinase family protein Pseudomonas syringae pv. syringae B728a C2_02298 VFG000477 99.4 3.16e-227 620.0 VF0112 VFC0301 rpoS RNA polymerase sigma factor RpoS Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 RpoS Salmonella enterica (serovar typhimurium) Regulation Necessary for sustaining a log-phase acid tolerance response (ATR), induction a stationary-phase acid survival system, production of thin aggregative fimbriae and expression of spv gene during stationary phase Abstract(s) in PubMed C2_02307 VFG015885 55.9 1.36e-64 197.0 VF0917 VFC0235 cysC1 adenylyl-sulfate kinase Pseudomonas syringae pv. phaseolicola 1448A C2_02321 VFG005579 58.9 1.79e-165 472.0 VF1060 VFC0251 eno phosphopyruvate hydratase Streptococcus pneumoniae D39 C2_02326 VFG010925 45.1 3.4700000000000004e-222 640.0 VF0260 VFC0301 relA GTP diphosphokinase Legionella pneumophila str. Corby RelA Legionella pneumophila Regulation Dispensable for intracellular growth within amoebae or the alveolar macrophages, but dedicate to convert from a replicated to a virulent state The ribosome-associated RelA, ppGpp synthetase, converts GTP to (p)ppGpp in response to amino acid depletion. The alarmone ppGpp stimulates the two-component system LetA/S, the transmission trait enhancer LetE, the alternative sigma factor RpoS and perhaps the putative master flagellar regulator RpoN, which together promote the expression of transmission traits: cytotoxic, motile, and infectious form Abstract(s) in PubMed C2_02383 VFG011805 45.7 6.66e-79 236.0 VF0326 VFC0258 CFF8240_RS06905 aspartate/glutamate racemase family protein Campylobacter fetus subsp. fetus 82-40 LOS Lipooligosaccharide Campylobacter jejuni Immune modulation LOS diversity is important for the ability to colonize a wide variety of hosts and intestinal niches; the ability to generate variation at high frequency, the molecular mimicry evident in LOS structure support a role in the avoidance of host defences; the similarity of LOS structures to host gangliosides and the subsequent ability to generate crossreacting antibodies forms the pathological basis for the association of preceding C. jejuni infection with Guillain-Barre syndrome Abstract(s) in PubMed C2_02414 VFG047265 50.7 9.05e-152 439.0 VF0542 VFC0258 lpxA/glmU UDP-N-acetylglucosamine pyrophosphorylase/glucosamine-1-phosphate N-acetyltransferase Francisella noatunensis subsp. orientalis str. Toba 04 LPS Francisella tularensis Immune modulation The structure of Francisella spp. lipid A is unique in that it is modified by various carbohydrates that greatly reduce TLR4 activation and allow for immune evasion A key virulence factor does not signal through, and is not an agonist of, toll like receptor 4 (TLR-4) and has little endotoxic activity Francisella lipid A is a very poor stimulant of the host's innate immunity. The lack of immune recognition of Franciscella lipid A has been attributed to several structural differences compared to E. coli lipid A. These include (1) the absence of phosphate at the 40 position as well as the modification of 1-phosphate with GalN and (2) tetraacylation of lipid A with longer acyl chains (16–18 carbons); An unusual feature of the Francisella LPS core region is the presence of a single Kdo unit. Francisella initially synthesizes its LPS with two Kdo sugars and Kdo hydrolase is involved in removing the second, side-chain Kdo moiety. A probable scenario is the lack of an extra Kdo may alter the bacterial surface and result in decreased access of additional surface molecules to the host’s innate immune system Abstract(s) in PubMed C2_02416 VFG042590 100.0 6.89e-134 372.0 VF1150 VFC0001 stgA StgA Escherichia coli O78:K80:H9 chi7122 C2_02417 VFG042591 100.0 1.41e-175 482.0 VF1150 VFC0001 stgB StgB Escherichia coli O78:K80:H9 chi7122 C2_02418 VFG042592 100.0 0.0 1674.0 VF1150 VFC0001 stgC StgC Escherichia coli O78:K80:H9 chi7122 C2_02419 VFG042593 98.3 4.02e-255 692.0 VF1150 VFC0001 stgD StgD Escherichia coli O78:K80:H9 chi7122 C2_02461 VFG045327 43.1 3.45e-27 99.0 VF0167 VFC0282 LPG_RS11000 Hsp20 family protein Legionella pneumophila subsp. pneumophila str. Philadelphia 1 GspA Global stress gene Legionella pneumophila Stress survival 19-kDa GroEL-like; dispensable for bacterial survival and growth in macrophage infection Abstract(s) in PubMed C2_02483 VFG032173 46.6 4.01e-132 389.0 VF0264 VFC0272 hpt hexose phosphate transport protein Listeria ivanovii subsp. ivanovii PAM 55 Hpt Hexose phosphate transporter Listeria monocytogenes Nutritional/Metabolic factor "Belongs to the organophosphate:inorganic phosphate antiporter (OPA) family, of the major facilitator superfamily of permease.; Hpt is the first virulence factor to be identified as specifically involved in the replication phase of a facultative intracellular pathogen. It could be termed ""metabolic"" virulence factor and represent an example of the concept in the biology of host-pathogen interaction: adaptation to parasitic life often involves the mimicry of eukaryotic host functions by microbial virulence factors.; Expression of the Hpt permease is tightly cotrolled by the PrfA." Homolog of the microsomal glucose-6-phosphate transporter (G6PT), a key element of glucose homeostasis in eukaryotes. The mammalian G6PT is responsible for the uptake of G6P from the cytosol into the endoplasmic reticulum for its conversion into the central fueling metabolite, glucose. Hpt mimics the function of the mammalian G6PT to steal fueling metabolites from host cell cytosol for the benefit of the microbe. Abstract(s) in PubMed C2_02502 VFG009933 40.3 4.05e-164 491.0 VF0287 VFC0301 relA Probable GTP pyrophosphokinase RelA (ATP:GTP 3'-pyrophosphotransferase) (PPGPP synthetase I) ((P)PPGPP synthetase) (GTP diphosphokinase) Mycobacterium sp. MCS RelA Mycobacterium tuberculosis Regulation Associated with stationary phase adaptation and long-term survival Produce ppGpp (guanosine 5'-diphosphate 3'-diphosphate), an 'alarmone' that suppresses synthesis of stable RNA, induces degradative pathways and modulates expression of genes involved in DNA replication Abstract(s) in PubMed C2_02518 VFG000320 49.7 2.41e-54 168.0 VF0056 VFC0258 kdtB lipopolysaccharide core biosynthesis protein Helicobacter pylori 26695 LPS Helicobacter pylori Immune modulation Under-phosphorylation and under-acylation of lipid A compared with enterobacterial lipid A; the average length of the fatty acid chains in H. pylori lipid A is longer (16 to 18 carbons) than in E. coli (12 to 14 carbons) H. pylori LPS have much lower immunobiological activities than enterobacterial LPS, thus may prolong H. pylori infection for longer; mediates a lectin-like interaction with laminin, the binding may disrupt epithelial cell-basement membrane interactions contributing to the disruption of gastric mucosal integrity and the development of gastric leakiness associated with the bacterium Abstract(s) in PubMed C2_02519 VFG013312 51.2 8.900000000000001e-145 419.0 VF0044 VFC0258 kdtA 3-deoxy-d-manno-octulosonic-acid transferase Haemophilus influenzae PittGG LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_02521 VFG000139 51.1 1.81e-135 391.0 VF0085 VFC0258 waaG B-band O-antigen polymerase Pseudomonas aeruginosa PAO1 LPS Pseudomonas aeruginosa Immune modulation Two distinct forms of LPS: A-band and B-band. A-band is a homopolymer of -linked D-rhamnose, whereas B-band LPS is a heteropolymer Mediates biological effects including resistance to serum killing and phagocytosis; the binding to normal CFTR (cystic fibrosis transmembrane conductance regulator) and invasion of host cells may make a contribution to virulence in the human eye; internalization by binding to normal CFTR protein expressed by airway epithelial cells followed by desquamation of bacteria-laden epithelial cells, constitutes a host defense mechanism. If this mechanism fails to function properly, abnormally high bacterial carriage would promote the establishment of chronic bacterial infection Binding interaction occurs between the first extracellular loop of CFTR (predicted to be in amino acids 108-117 of the mature protein) and the complete outer portion of the core polysaccharide of the LPS Abstract(s) in PubMed C2_02522 VFG000140 55.9 4.41e-100 293.0 VF0085 VFC0258 waaP UDP-glucose:(heptosyl) LPS alpha 1,3-glucosyltransferase WaaG Pseudomonas aeruginosa PAO1 LPS Pseudomonas aeruginosa Immune modulation Two distinct forms of LPS: A-band and B-band. A-band is a homopolymer of -linked D-rhamnose, whereas B-band LPS is a heteropolymer Mediates biological effects including resistance to serum killing and phagocytosis; the binding to normal CFTR (cystic fibrosis transmembrane conductance regulator) and invasion of host cells may make a contribution to virulence in the human eye; internalization by binding to normal CFTR protein expressed by airway epithelial cells followed by desquamation of bacteria-laden epithelial cells, constitutes a host defense mechanism. If this mechanism fails to function properly, abnormally high bacterial carriage would promote the establishment of chronic bacterial infection Binding interaction occurs between the first extracellular loop of CFTR (predicted to be in amino acids 108-117 of the mature protein) and the complete outer portion of the core polysaccharide of the LPS Abstract(s) in PubMed C2_02523 VFG013261 41.0 7.89e-18 78.6 VF0044 VFC0258 lgtC glycosyltransferase Haemophilus influenzae 86-028NP LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_02531 VFG013280 56.3 1.3e-118 344.0 VF0044 VFC0258 opsX/rfaC heptosyltransferase I Haemophilus somnus 129PT LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_02532 VFG013400 63.5 1.55e-152 432.0 VF0044 VFC0258 rfaF ADP-heptose-LPS heptosyltransferase II Haemophilus influenzae Rd KW20 LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_02533 VFG000332 78.2 4.38e-180 499.0 VF0044 VFC0258 rfaD ADP-L-glycero-D-mannoheptose-6-epimerase Haemophilus influenzae Rd KW20 LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_02536 VFG050195 49.0 1.98e-25 104.0 VF0659 VFC0258 BCAH187_RS26500 glycosyltransferase family 2 protein Bacillus cereus AH187 C2_02544 VFG005975 43.8 3.33e-15 71.2 VF0144 VFC0258 STU_RS14610 serine acetyltransferase Streptococcus thermophilus LMG 18311 Capsule Streptococcus pneumoniae Immune modulation Ninety different capsule types have been identified. Each has a structurally distinct capsule, composed of repeating oligosaccharide units joined by glycosidic linkages Resistant to complement deposition and masks cell wall-associated complement from being recognized by the complement receptors on phagocytes Abstract(s) in PubMed C2_02549 VFG035950 100.0 0.0 2023.0 VF1125 VFC0001 upaG/ehaG trimeric autotransporter adhesin EhaG Escherichia coli O103:H2 str. 12009 C2_02567 VFG037721 40.8 5.46e-212 633.0 VF0504 VFC0271 adeG cation/multidrug efflux pump Acinetobacter baumannii ATCC 17978 AdeFGH efflux pump Acinetobacter baumannii Biofilm Belongs to resistance-nodulation-cell division (RND)-type efflux system; RND efflux systems, composed of an inner membrane protein (RND pump) linked by a periplasmic adaptor protein (PAP) to an outer membrane factor (OMF), can extrude a wide range of substrates often unrelated in structure; To date, three Acinetobacter drug efflux (Ade) RND systems, AdeABC, AdeFGH, and AdeIJK, have been characterized in A. baumannii Play a potential role in the synthesis and transport of autoinducer molecules during biofilm formation Abstract(s) in PubMed C2_02605 VFG014995 45.2 6.51e-85 261.0 VF0091 VFC0271 algW AlgW protein Pseudomonas mendocina ymp Alginate Mucoid exopolysaccharide Pseudomonas aeruginosa Biofilm Alginate production is frequently referred to as mucoidy because colonies producing alginate have a wet glistening (mucoid) appearance, which is very different from that of colonies not producing alginate; most of the alginate biosynthetic genes are clustered in the algD operon; Alginate production is highly regulated. Regulatory genes are located in two areas far removed from the biosynthetic genes, with one exception algC Alginate is a linear polymer of high molecular weight composed of the uronic acids -D-mannuronate and its C-5 epimer, -L-guluronate, which are linked by -1,4 glycosidic bonds; The early steps in the biosynthesis of alginate to form GDP mannuronic acid require the products of algA and algC to convert fructose-6-phosphate to GDP-mannose and then require the product of algD to convert this to the uronic acid form, GDP-mannuronate Allows the bacteria form biofilm; contributes to the persistence of the bacteria in the CF lung: act as an adhesin, preventing the bacteria from being expelled from the lung, and alginate slime layer makes it more difficult for phagocytes to ingest and kill the bacteria Abstract(s) in PubMed C2_02632 VFG042736 56.2 9.41e-155 449.0 VF0082 VFC0001 rpoN RNA polymerase factor sigma-54 Pseudomonas aeruginosa PAO1 Type IV pili Pseudomonas aeruginosa Adherence PilA, B, C, D, E, F, M, N, O, P, Q, T, U, V, W, X, Y1, Y2, Z, and fimT, U, V are involved in the biogenesis and mechanical function of pili, pilG, H, I, K, chpA, B, C, D, E, pilS, R, fimS, rpoN, algR, algU, and vfr are involved in transcriptional regulation and chemosensory pathways that control the expression or activity of the twitching motility of the pili Attaches to host cells, but not to mucin, causing a twitching motility that allows the bacteria to move along the cell surface; biofilm formation The C-terminal receptor-binding domain of pilin binds to asialoGM1 gangliosides on host cells. Generally, GM1 gangliosides contain a sialic acid moiety. P.aeruginosa produces a neuraminidase which removes sialic acid residues from the GM1 to form the asialoGM1, which is a better receptor for the pili; The asialoGM1 is present in increased abundance on the surface of cystic fibrosis respiratory epithelial cells Abstract(s) in PubMed C2_02637 VFG011729 46.1 8.87e-87 263.0 VF0323 VFC0258 kpsF KpsF/GutQ family sugar-phosphate isomerase Campylobacter jejuni subsp. jejuni 81-176 Capsule Campylobacter jejuni Immune modulation Major antigenic component of the classic Penner serotyping system; Variation in the capsule structure may cause by multiple mechanisms, such as exchange of capsular genes and entire clusters by horizontal transfer, gene duplication, deletion, fusion and the presence of homopolymeric G tracts in several cps genes The capsule consists of repeating oligosaccharide units attached to a dipalmitoyl-glycerophosphate lipid anchor; The CPS is extensively substituted with variable O-methylphosphoramidate, methyl, ethanolamine, and N-glycerol groups Play an important role in bacterial survival and persistence in the environment and evasion of host immune response; the presence of heptose residues in the capsule may be important for virulence. Heptose residues found in some cell surface-located glycoconjugates are required for adhesion Abstract(s) in PubMed C2_02658 VFG013514 73.3 9.190000000000001e-234 646.0 VF0755 VFC0258 mrsA/glmM phosphoglucosamine mutase Haemophilus influenzae 86-028NP C2_02664 VFG039487 51.0 5.210000000000001e-43 139.0 VF0696 VFC0086 rimP Coxiella Dot/Icm type IVB secretion system translocated effector Coxiella burnetii CbuG_Q212 T4SS secreted effectors Coxiella burnetii Effector delivery system CBUA0020; CBU_0012*; CBU_0113; CBU_0122; CBU_0183; CBU_0201; CBU_0270; CBU_0295; CBU_0344*; CBU_0372; CBU_0375*; CBU_0469; CBU_0513; CBU_0534; CBU_0590; CBU_0635; CBU_0637; CBU_0820*; CBU_1048*; CBU_1079; CBU_1107*; CBU_1150*; CBU_1198; CBU_1268; CBU_1349; CBU_1370; CBU_1409; CBU_1434; CBU_1493; CBU_1495*; CBU_1525*; CBU_1530; CBU_1566; CBU_1576; CBU_1594; CBU_1607; CBU_1614; CBU_1639; CBU_1665; CBU_1677; CBU_1685; CBU_1752; CBU_1754; CBU_1789; CBU_1790; CBU_1794; CBU_1818; CBU_1819; CBU_1863; CBU_2016; CBU_2028; CBU_2056; CBU_2059*; CBU_2076; AnkA; AnkB; AnkF; AnkG (Interacts with host protein p32 to block apoptosis. ); AnkH; AnkI; AnkM/cig58; AnkP; Cem1; Cem12; Cem13; Cem3; Cem4; Cem6; Cem9; CetCb1; CetCb2; CetCb3; CetCB4; CetCb5; CetCb6; CirA/coxCC1 (Phosphate transporter family protein. ); CirB; CirC/coxDFB1; CoxCC10/cig49; CoxCC11; CoxCC12; CoxCC14; CoxCC15; CoxCC3; CoxCC4; CoxCC5; CoxCC6; CoxCC7/cig44; CoxCC8; CoxDFB3; CoxDFB4 (Surface antigen. ); CoxDFB5/cig57; CoxDFB6; CoxFIC1; CoxH2/rimL (Acetyltransferase. ); CoxH3; CoxH4/cig61; CoxK1 (Protein kinase, putative. ); CoxK2; CoxTPR1 (Conserved domain protein. ); CoxU1; CoxU2; CpeA; CpeB; CpeC/coxU3 (Hypothetical protein plasmid QpH1. ); CpeD; CpeE; CpeF; CpeG; CpeH; CvpA; MceA; PhnB; CBUD_RS05145; CBUD_RS06720*; CBUD_RS08635; CBUD_RS11275; CBUD_RS12405; CBUG_RS02435; CBUK_RS06760 Abstract(s) in PubMed C2_02685 VFG011684 41.3 3.04e-41 138.0 VF0323 VFC0258 gmhA2 D-sedoheptulose 7-phosphate isomerase Campylobacter jejuni RM1221 Capsule Campylobacter jejuni Immune modulation Major antigenic component of the classic Penner serotyping system; Variation in the capsule structure may cause by multiple mechanisms, such as exchange of capsular genes and entire clusters by horizontal transfer, gene duplication, deletion, fusion and the presence of homopolymeric G tracts in several cps genes The capsule consists of repeating oligosaccharide units attached to a dipalmitoyl-glycerophosphate lipid anchor; The CPS is extensively substituted with variable O-methylphosphoramidate, methyl, ethanolamine, and N-glycerol groups Play an important role in bacterial survival and persistence in the environment and evasion of host immune response; the presence of heptose residues in the capsule may be important for virulence. Heptose residues found in some cell surface-located glycoconjugates are required for adhesion Abstract(s) in PubMed C2_02690 VFG021350 41.9 8.25e-207 608.0 VF0105 VFC0001 lpfC long polar fimbrial usher protein LpfC Salmonella enterica subsp. enterica serovar Agona str. SL483 Lpf Long polar fimbriae Salmonella enterica (serovar typhimurium) Adherence Chaperone-usher assembly pathway Mediate attachment to the Peyer's patches Abstract(s) in PubMed C2_02691 VFG000455 43.1 7.95e-50 162.0 VF0105 VFC0001 lpfB long polar fimbrial chaperone protein LpfB Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Lpf Long polar fimbriae Salmonella enterica (serovar typhimurium) Adherence Chaperone-usher assembly pathway Mediate attachment to the Peyer's patches Abstract(s) in PubMed C2_02716 VFG001381 62.3 4.5999999999999996e-177 501.0 VF0253 VFC0346 icl Isocitrate lyase Icl (isocitrase) (isocitratase) Mycobacterium tuberculosis H37Rv Isocitrate lyase Mycobacterium tuberculosis Others PDB code: 1F61 Required for persistent infection Isocitrate lyase is the initial enzyme in the glyoxylate shunt, a secondary metabolic pathway that allows bacteria to utilize fatty acids as carbon and energy sources when the availability of primary carbon sources is limiting; Isocitrate lyase, in combination with malate synthase, catalyzes the conversion of isocitrate to malate, a reaction that allows maintenance of the TCA cycle and synthesize carbohydrates from fatty acids Abstract(s) in PubMed C2_02719 VFG034777 98.8 4.1999999999999997e-290 790.0 VF1110 VFC0086 espL4 Type III secretion system effector EspL4 Escherichia coli O111:H- str. 11128 TTSS secreted effectors Escherichia coli (EHEC) Effector delivery system Cif (Deamidase. Induces cytopathic effects of actin stress fiber formation and cell cycle arrest. ); EspB (Pore formation, actin disruption, microvilli effacement, anti-phagocytosis. ); EspF (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspFu/tccP (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspG (TBC-like GTPase activating protein. Efficiently catalyzes GTP hydrolysis in Rab1 to disrupt of Rab1-mediated ER-to-Golgi trafficking. ); EspH (First bacterial effector acting directly on RhoGEFs, EspH directly binds to the DH-PH domain in RhoGEFs to disrupt RhoGEF-Rho signaling; critical for inhibiting macrophage phagocytosis. ); EspJ (Inhibit both IgG- and complement receptor-mediated phagocytosis. ); EspK; EspL1; EspL2 (Cysteine protease. Bounds F-actin-aggregating annexin 2 directly to increase annexin 2's ability to aggregate Tir-induced F-actin; block necroptosis and in flammation. ); EspL4; EspM1 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspM2 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspN; EspO1-1; EspO1-2; EspR1; EspR3; EspR4; EspT (GEF. Activates Rac1 and Cdc42 leading to formation of membrane ruffles and lamellipodia; induces membrane ruffles to facilitate bacterial invasion into non-phagocytic cells in a process involving Rac1 and Wave2. ); EspW; EspX1; EspX2; EspX4; EspX5; EspX6; EspX7/nleL (E3 ubiquitin ligase, HECT-like. Modulates pedestal formation. ); EspY1; EspY2; EspY3; EspY4; EspY5; Map (GEF. Mimics the host Dbl and catalyses the exchange of GDP for GTP in Cdc42, involved in effacement, SGLT1 inhibition, formation of filopodia and disruption of mitochondrial function. ); NleA/espI (Disruption of tight junctions by inhibition of host cell protein trafficking through COPII-dependent pathways. ); NleB1 (Blocks translocation of the p65 and to the host cell nucleus to inhibit NF-B pathway, but NleE and NleB act at different points in the NF-B signaling pathway. ); NleB2 (May also have anti-inflammatory activity. ); NleC (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate RelA (p65), thus blocking NF-B pathway. ); NleD (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate JNK and p38, thus blocking AP-1 pathway. ); NleE (PMN tran-epithelial migration; blocks translocation of the p65 to the host cell nucleus by preventing IB degradation to inhibit NF-B pathway. ); NleF; NleG-1; NleG2-2; NleG2-3; NleG2-4; NleG5-1; NleG5-2; NleG6-1; NleG6-2; NleG6-3; NleG7 (U-box type E3 ubiquitin ligases. ); NleG8-2; NleH1 (Ser/Thr protein kinase. Binds directly to a subunit of NF-B, the ribosomal protein S3 (RPS3), reducing the nuclear abundance of RPS3 to dampen host transcriptional outputs; interact with Bax inhibitor-1 to block apoptosis. ); NleH2 (Putative kinase. Attenuates NF-B pathway. ); SepZ/espZ (EspZ interacts with CD98 in host cell membranes to promote host cell survival, therefore provide the pathogen with valuable time to colonize efficiently prior to dissemination. ); TccP2; Tir (Mimics host immunoreceptor tyrosine-based inhibition motifs (ITIMs), also see helicobacter CagA. EHEC Tir lacks the Nck binding site. Conserved NPY (Asn-Pro-Tyr) motif recruits the adaptor protein IRTKS and/or IRSp53. IRTKS/IRSp53 link Tir and TccP/EspFu, which in turn activates N-WASP; Receptor for intimin; effacement; SGLT1 inhibition; recruits SHIP2 to control actin-pedestal morphology; maintains the integrity of the epithelium by keeping the destructive activity of EspG and EspG2 in check. ) Abstract(s) in PubMed C2_02730 VFG013531 77.6 0.0 880.0 VF0755 VFC0258 pgi glucose-6-phosphate isomerase Haemophilus influenzae 86-028NP C2_02734 VFG007643 46.7 7.339999999999999e-220 632.0 VF0624 VFC0258 wbfB YjbH domain-containing protein Vibrio fischeri ES114 C2_02741 VFG030694 47.7 1.19e-102 308.0 VF0842 VFC0272 sugC sn-glycerol-3-phosphate ABC transporter ATP-binding protein UgpC Mycobacterium gilvum Spyr1 C2_02746 VFG034866 87.1 1.76e-257 709.0 VF1110 VFC0086 espX4 Type III secretion system effector EspX4 Escherichia coli O157:H7 str. EDL933 TTSS secreted effectors Escherichia coli (EHEC) Effector delivery system Cif (Deamidase. Induces cytopathic effects of actin stress fiber formation and cell cycle arrest. ); EspB (Pore formation, actin disruption, microvilli effacement, anti-phagocytosis. ); EspF (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspFu/tccP (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspG (TBC-like GTPase activating protein. Efficiently catalyzes GTP hydrolysis in Rab1 to disrupt of Rab1-mediated ER-to-Golgi trafficking. ); EspH (First bacterial effector acting directly on RhoGEFs, EspH directly binds to the DH-PH domain in RhoGEFs to disrupt RhoGEF-Rho signaling; critical for inhibiting macrophage phagocytosis. ); EspJ (Inhibit both IgG- and complement receptor-mediated phagocytosis. ); EspK; EspL1; EspL2 (Cysteine protease. Bounds F-actin-aggregating annexin 2 directly to increase annexin 2's ability to aggregate Tir-induced F-actin; block necroptosis and in flammation. ); EspL4; EspM1 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspM2 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspN; EspO1-1; EspO1-2; EspR1; EspR3; EspR4; EspT (GEF. Activates Rac1 and Cdc42 leading to formation of membrane ruffles and lamellipodia; induces membrane ruffles to facilitate bacterial invasion into non-phagocytic cells in a process involving Rac1 and Wave2. ); EspW; EspX1; EspX2; EspX4; EspX5; EspX6; EspX7/nleL (E3 ubiquitin ligase, HECT-like. Modulates pedestal formation. ); EspY1; EspY2; EspY3; EspY4; EspY5; Map (GEF. Mimics the host Dbl and catalyses the exchange of GDP for GTP in Cdc42, involved in effacement, SGLT1 inhibition, formation of filopodia and disruption of mitochondrial function. ); NleA/espI (Disruption of tight junctions by inhibition of host cell protein trafficking through COPII-dependent pathways. ); NleB1 (Blocks translocation of the p65 and to the host cell nucleus to inhibit NF-B pathway, but NleE and NleB act at different points in the NF-B signaling pathway. ); NleB2 (May also have anti-inflammatory activity. ); NleC (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate RelA (p65), thus blocking NF-B pathway. ); NleD (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate JNK and p38, thus blocking AP-1 pathway. ); NleE (PMN tran-epithelial migration; blocks translocation of the p65 to the host cell nucleus by preventing IB degradation to inhibit NF-B pathway. ); NleF; NleG-1; NleG2-2; NleG2-3; NleG2-4; NleG5-1; NleG5-2; NleG6-1; NleG6-2; NleG6-3; NleG7 (U-box type E3 ubiquitin ligases. ); NleG8-2; NleH1 (Ser/Thr protein kinase. Binds directly to a subunit of NF-B, the ribosomal protein S3 (RPS3), reducing the nuclear abundance of RPS3 to dampen host transcriptional outputs; interact with Bax inhibitor-1 to block apoptosis. ); NleH2 (Putative kinase. Attenuates NF-B pathway. ); SepZ/espZ (EspZ interacts with CD98 in host cell membranes to promote host cell survival, therefore provide the pathogen with valuable time to colonize efficiently prior to dissemination. ); TccP2; Tir (Mimics host immunoreceptor tyrosine-based inhibition motifs (ITIMs), also see helicobacter CagA. EHEC Tir lacks the Nck binding site. Conserved NPY (Asn-Pro-Tyr) motif recruits the adaptor protein IRTKS and/or IRSp53. IRTKS/IRSp53 link Tir and TccP/EspFu, which in turn activates N-WASP; Receptor for intimin; effacement; SGLT1 inhibition; recruits SHIP2 to control actin-pedestal morphology; maintains the integrity of the epithelium by keeping the destructive activity of EspG and EspG2 in check. ) Abstract(s) in PubMed C2_02770 VFG000421 40.0 6.9e-17 73.6 VF0138 VFC0258 caf1R F1 operon positive regulatory protein Yersinia pestis CO92 F1 antigen Fraction 1 capsular antigen Yersinia pestis Immune modulation Virulence factors unique to Y. pestis, Forms fibrillar structures on the bacterial surface and appears to prevent phagocytosis Abstract(s) in PubMed C2_02774 VFG034873 88.4 3.8e-197 552.0 VF1110 VFC0086 espX5 Type III secretion system effector EspX5 Escherichia coli O157:H7 str. EDL933 TTSS secreted effectors Escherichia coli (EHEC) Effector delivery system Cif (Deamidase. Induces cytopathic effects of actin stress fiber formation and cell cycle arrest. ); EspB (Pore formation, actin disruption, microvilli effacement, anti-phagocytosis. ); EspF (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspFu/tccP (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspG (TBC-like GTPase activating protein. Efficiently catalyzes GTP hydrolysis in Rab1 to disrupt of Rab1-mediated ER-to-Golgi trafficking. ); EspH (First bacterial effector acting directly on RhoGEFs, EspH directly binds to the DH-PH domain in RhoGEFs to disrupt RhoGEF-Rho signaling; critical for inhibiting macrophage phagocytosis. ); EspJ (Inhibit both IgG- and complement receptor-mediated phagocytosis. ); EspK; EspL1; EspL2 (Cysteine protease. Bounds F-actin-aggregating annexin 2 directly to increase annexin 2's ability to aggregate Tir-induced F-actin; block necroptosis and in flammation. ); EspL4; EspM1 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspM2 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspN; EspO1-1; EspO1-2; EspR1; EspR3; EspR4; EspT (GEF. Activates Rac1 and Cdc42 leading to formation of membrane ruffles and lamellipodia; induces membrane ruffles to facilitate bacterial invasion into non-phagocytic cells in a process involving Rac1 and Wave2. ); EspW; EspX1; EspX2; EspX4; EspX5; EspX6; EspX7/nleL (E3 ubiquitin ligase, HECT-like. Modulates pedestal formation. ); EspY1; EspY2; EspY3; EspY4; EspY5; Map (GEF. Mimics the host Dbl and catalyses the exchange of GDP for GTP in Cdc42, involved in effacement, SGLT1 inhibition, formation of filopodia and disruption of mitochondrial function. ); NleA/espI (Disruption of tight junctions by inhibition of host cell protein trafficking through COPII-dependent pathways. ); NleB1 (Blocks translocation of the p65 and to the host cell nucleus to inhibit NF-B pathway, but NleE and NleB act at different points in the NF-B signaling pathway. ); NleB2 (May also have anti-inflammatory activity. ); NleC (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate RelA (p65), thus blocking NF-B pathway. ); NleD (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate JNK and p38, thus blocking AP-1 pathway. ); NleE (PMN tran-epithelial migration; blocks translocation of the p65 to the host cell nucleus by preventing IB degradation to inhibit NF-B pathway. ); NleF; NleG-1; NleG2-2; NleG2-3; NleG2-4; NleG5-1; NleG5-2; NleG6-1; NleG6-2; NleG6-3; NleG7 (U-box type E3 ubiquitin ligases. ); NleG8-2; NleH1 (Ser/Thr protein kinase. Binds directly to a subunit of NF-B, the ribosomal protein S3 (RPS3), reducing the nuclear abundance of RPS3 to dampen host transcriptional outputs; interact with Bax inhibitor-1 to block apoptosis. ); NleH2 (Putative kinase. Attenuates NF-B pathway. ); SepZ/espZ (EspZ interacts with CD98 in host cell membranes to promote host cell survival, therefore provide the pathogen with valuable time to colonize efficiently prior to dissemination. ); TccP2; Tir (Mimics host immunoreceptor tyrosine-based inhibition motifs (ITIMs), also see helicobacter CagA. EHEC Tir lacks the Nck binding site. Conserved NPY (Asn-Pro-Tyr) motif recruits the adaptor protein IRTKS and/or IRSp53. IRTKS/IRSp53 link Tir and TccP/EspFu, which in turn activates N-WASP; Receptor for intimin; effacement; SGLT1 inhibition; recruits SHIP2 to control actin-pedestal morphology; maintains the integrity of the epithelium by keeping the destructive activity of EspG and EspG2 in check. ) Abstract(s) in PubMed C2_02818 VFG036816 44.1 2.37e-148 437.0 VF0899 VFC0315 lptA lipooligosaccharide phosphoethanolamine transferase LptA Neisseria gonorrhoeae NCCP11945 C2_02847 VFG010484 75.0 4.66e-272 751.0 VF0159 VFC0001 htpB Hsp60, 60K heat shock protein HtpB Legionella pneumophila str. Paris Hsp60 Legionella pneumophila Adherence Mediate a complement-independent attachment to mammalian and amoebal host cells Specific receptors have not been identified Abstract(s) in PubMed C2_02879 VFG043534 47.3 2.24e-137 400.0 VF0694 VFC0001 ugpB sn-glycerol-3-phosphate ABC transporter substrate-binding protein UgpB Brucella melitensis bv. 1 str. 16M C2_02882 VFG030692 50.7 8.69e-113 333.0 VF0842 VFC0272 sugC sn-glycerol-3-phosphate ABC transporter ATP-binding protein UgpC Mycobacterium sp. JDM601 C2_02885 VFG047610 53.9 1.44e-186 537.0 VF0553 VFC0272 ggt gamma-glutamyltranspeptidase Francisella sp. TX077308 GGT -glutamyl transpeptidase Francisella tularensis Nutritional/Metabolic factor Cleavage of cysteine containing peptides (glutathione and -glutamyl-cysteine peptides) by GGT activity thus provides the essential source of cysteine required for intracellular multiplication Abstract(s) in PubMed C2_02889 VFG041226 68.1 1.69e-106 319.0 VF1264 VFC0086 hcp type VI secretion system tube protein Hcp Citrobacter rodentium ICC168 C2_02923 VFG047402 46.9 3.2e-231 664.0 VF0550 VFC0272 feoB Fe(2+) transporter permease subunit FeoB Francisella tularensis subsp. tularensis WY96-3418 FupA Fe utilization protein A Francisella tularensis Nutritional/Metabolic factor FupA and FslE are paralogs belonging to a family of proteins unique to Francisella Both FupA and FslE fold as - barrels in the outer membrane with amino-terminal periplasmic domains High-affinity iron transport Protein involved in ferrous iron acquisition Abstract(s) in PubMed C2_02924 VFG045722 53.8 6.24e-12 55.1 VF0160 VFC0272 feoA ferrous iron transporter A Legionella longbeachae NSW150 FeoAB Legionella pneumophila Nutritional/Metabolic factor A feoB mutant of L. pneumophila has a lowered Fe2+ uptake and is attenuated for intracellular growth The FeoB protein is a G protein with properties of GTPase activity kinetics and GTP/GDP binding that differ from those of the eukaryotic proteins. The GTPase activity of FeoB is necessary for Fe2+ transport Abstract(s) in PubMed C2_02943 VFG013119 40.3 3.5e-84 263.0 VF0753 VFC0001 comE/pilQ type IV pilus secretin PilQ Haemophilus influenzae 86-028NP C2_02948 VFG046604 65.3 1.93e-99 288.0 VF0543 VFC0258 rpe ribulose-phosphate 3-epimerase Francisella philomiragia subsp. philomiragia ATCC 25017 Capsule Francisella tularensis Immune modulation Group 4 capsule; high molecular weight (HMW) O-antigen capsule A polymer of the tetrasaccharide repeat, 4)-a-D-GalNAcAN-(1-.4)-a-D-GalNAcAN-(1-.3)-b-D-QuiNAc-(1-.2)-b-D-Qui4NFm-(1-, which is identical to F. tularensis O-antigen subunit; F. tularensis synthesizes an O-antigen capsule containing approximately 125 to 300 or more O-antigen repeating units Providing a stealth shield that prevents the host immune system from detecting this potent pathogen Abstract(s) in PubMed C2_02970 VFG041304 40.7 3.29e-22 88.6 VF0798 VFC0086 lirB Dot/Icm type IV secretion system effector LirB Legionella pneumophila subsp. pneumophila str. Philadelphia 1 Dot/Icm T4SS secreted effectors Legionella pneumophila Effector delivery system AnkB/legAU13/ceg27 (E3 Ubiquitin Ligase Activity, bounds Skp1, targets host protein parvin B. ); AnkC/legA12 (Ankyrin repeat. ); AnkD/legA15 (Ankyrin repeat. ); AnkF/legA14/ceg31 (Ankyrin repeat. ); AnkG/ankZ/legA7 (Ankyrin repeat. ); AnkH/legA3/ankW (Ankyrin repeat, NF-B inhibitor. ); AnkI/legAS4 (Ankyrin repeat. ); AnkJ/legA11 (Ankyrin repeat. ); AnkK/legA5 (Ankyrin repeat. ); AnkN/ankX/legA8 (Phosphocholination of Rab1 and Rab35 to regulate their activity; modulation of endosomal trafficking. ); AnkQ/legA10; AnkY/legA9 (Ankyrin repeat, STPK, Enhancer of autophagy. ); Ceg10; Ceg14/sidL (Inhibition of host protein synthesis leading to activation of the NF-B pathway. ); Ceg15; Ceg17; Ceg18; Ceg19 (Vesicle trafficking. ); Ceg23; Ceg25; Ceg28; Ceg29; Ceg3; Ceg30; Ceg32/sidI (Interacts with eEF1A to inhibit host protein synthesis. ); Ceg33; Ceg34; Ceg4; Ceg5; Ceg7; Ceg8; Ceg9 (Vesicle trafficking. ); CegC1 (Zinc metallophospholipase C. Zinc metallophospholipase C. ); CegC2 (Ninein domain. ); CegC3; CegC4; DrrA/sidM (Rab1-GEF and GDF (RabGDI displacement factor) activity responsible for Rab1 recruitment to LCV, C-terminal PI4P binding domain responsible for membrane binding; N-terminal AMPylation activity. ); LaiE (SidE paralog. ); LegA1; LegA2; LegA6; LegA7; LegC1; LegC3/ppeA (Vesicle trafficking. ); LegC4 (Coiled-coil. ); LegC6 (Coiled-coil. ); LegD1; LegD2; LegG2 (Ras GEF. ); LegK1 (Eukaryotic-like Ser/Thr kinase activity, directly activates NF-B pathway by phosphorylating the IB family of inhibitors. ); LegK2 (Ser/Thr kinase. ); LegK3 (STPK. ); LegL1 (Leucine-rich repeats. ); LegL2 (Leucine-rich repeats. ); LegL3 (Leucine-rich repeats. ); LegL5 (Leucine-rich repeats. ); LegL6 (Leucine-rich repeats. ); LegL7 (Leucine-rich repeats. ); LegLC4 (Leucine-rich repeats, coiled-coil. ); LegLC8 (Leucine-rich repeats, coiled-coil. ); LegN; LegP (Astacin protease. ); LegS1; LegS2 (Putative Sphingosine-1-phosphate lyase 1 (SP-lyase). ); LegT (Thaumatin domain. ); LegU1 (E3 Ubiquitin Ligase, targets host chaperone protein BAT3. ); LegY; Lem1; Lem10; Lem11; Lem12; Lem14; Lem15; Lem16; Lem17; Lem19; Lem2; Lem20; Lem21; Lem22; Lem23; Lem24; Lem25; Lem26; Lem27; Lem28; Lem29; Lem3 (Dephosphoryl-cholinase relieving the AnkX-mediated modification on Rab1. ); Lem4/smdA (PI4P-binding protein. ); Lem5; Lem6; Lem7; Lem8; Lem9; LepA (Nonlytic release from protozoa. ); LepB (Rab1 GAP, vesicle trafficking and bacterial egress. ); Lgt2/legC8 (Glucosyltransferase, inhibits host protein systhesis by glucosylating mammalian elongation factor eEF1A at serine-53. ); Lgt3/legC5 (Glucosyltransferase, inhibits host protein systhesis by glucosylating mammalian elongation factor eEF1A at serine-53. ); LidA (Promotion of Rab1 recruitment and tethering of ER derived vesicles to the LCV; stabilization of Rab guanosine nucleotide complex. ); LidL (EnhC paralogue. ); LirA; LirB (Peptidyl-prolyl cis-trans isomerase A (rotamase A). ); Lpg0045; Lpg0081; Lpg0294; Lpg0365; Lpg0518; Lpg0634; Lpg0963; Lpg1148; Lpg1158; Lpg1273; Lpg1689; Lpg1717; Lpg1751; Lpg2160 (Associates with BAT3 independently of LegU1; LegU1 and Lpg2160 may function redundantly or in concert to modulate BAT3 activity during the course of infection. ); Lpg2327; Lpg2407; Lpg2525 (F-box protein. ); Lpg2527; Lpg2744; LpnE (Putative Beta-lactamase. ); LubX/legU2 (E3 ubiquitin ligase, targets another effector protein SidH to proteasome-mediated protein degradation in the host cells; cell cycle modulation via Clk1. ); MavA; MavB; MavC; MavE; MavF; MavG; MavH; MavI; MavJ; MavL; MavM; MavN; MavV; PieA/lirC; PieB/lirD; PieC/lirE; PieD/lirF; PieE; PieF; PieG/legG1 (Regulator of chromosome condensation RCC. ); PpeB; PpgA (Regulator of chromosome condensation. ); RalF (Arf-GEF; Arf1 recuitment to LCV. ); RavE; RavF; RavG; RavH; RavI; RavJ; RavK; RavL; RavM; RavN; RavO; RavP; RavQ; RavR; RavS; RavT; RavW; RavX; RavY; RavZ (Cysteine protease. Inhibits host autophagy by cleaving and deconjugating LC3-PE. ); RvfA; SdbA (Contributes to sustained NF-B activation. ); SdbB (SidB paralog. ); SdbC (SidB paralog. ); SdcA (SidC paralog, anchors to PtdIns(4)P on LCVs. ); SdeA/laiA (Adherence and/or uptake. ); SdeB/laiB; SdeC/laiC; SdeD/laiF (SidE paralog. ); SdhA (Maintenance of LCV integrity preventing cell death and type I interferon induction. ); SdhB (Paralog of sidH, ANTH domain. ); SdjA; SetA (Vesicle trafficking. ); SidA; SidB (Rtx toxin, lipase. ); SidC (ER recuitment. ); SidD; SidE/laiD; SidF (Anti-apoptosis by targeting pro-death members of the Bcl2 protein family. ); SidG (Coiled-coil. ); SidH (A substrate of LubX E3 ubiquitin ligase. ); SidJ (ER recuitment. ); SidK (Interacting with VatA, a key component of the proton pump. Inhibition of LCV acidification. ); VipA (Actin nucleator contributing to modulate organelle trafficking. ); VipD (Phospholipase A1, removes PI(3)P from early endosomes. ); VipE; VipF (N-terminal acetyltransferase, GNAT family. ); VpdA/vipD2 (VipD paralog, Acyl transferase/acyl hydrolase/lysophospholipase. ); VpdB/vipD3 (VipD paralog, phospholipase. ); VpdC; WipA; WipB; YlfA/legC7 (Vesicle trafficking. ); YlfB/legC2 (Vesicle trafficking. ); CegC4; MesI; LPG_RS00040; LPG_RS00105; LPG_RS00150; LPG_RS00200; LPG_RS00235; LPG_RS00300; LPG_RS00665 (PI-3-phosphatase. ); LPG_RS00825; LPG_RS00870; LPG_RS00880; LPG_RS00925; LPG_RS01290; LPG_RS01305; LPG_RS01820; LPG_RS01880; LPG_RS02025; LPG_RS03550; LPG_RS03935; LPG_RS04800; LPG_RS05365; LPG_RS05490; LPG_RS05590; LPG_RS05660; LPG_RS05710; LPG_RS05830; LPG_RS07260; LPG_RS07280; LPG_RS07435; LPG_RS07905; LPG_RS08210; LPG_RS08285; LPG_RS08320; LPG_RS08345; LPG_RS08350; LPG_RS08370; LPG_RS08445; LPG_RS08450; LPG_RS08485; LPG_RS08595; LPG_RS08775; LPG_RS08895; LPG_RS09040; LPG_RS09470; LPG_RS09565; LPG_RS09650; LPG_RS09825; LPG_RS09915; LPG_RS09965; LPG_RS10290; LPG_RS10795; LPG_RS10800; LPG_RS11170; LPG_RS11255; LPG_RS11415; LPG_RS11860; LPG_RS11920; LPG_RS11940; LPG_RS11990; LPG_RS12190; LPG_RS12265; LPG_RS12310; LPG_RS12405; LPG_RS12815; LPG_RS12820; LPG_RS12830; LPG_RS12855; LPG_RS12885; LPG_RS12900; LPG_RS13265; LPG_RS13310; LPG_RS13590; LPG_RS13860; LPG_RS14265; LPG_RS14285; LPG_RS14345; LPG_RS14500; LPG_RS14525; LPG_RS14550; LPG_RS14555; LPG_RS14570; LPG_RS14710; LPG_RS14840; LPG_RS15050; LPG_RS15170 Abstract(s) in PubMed C2_02976 VFG042734 66.8 2.46e-94 274.0 VF0082 VFC0001 vfr cAMP-regulatory protein Pseudomonas aeruginosa PAO1 Type IV pili Pseudomonas aeruginosa Adherence PilA, B, C, D, E, F, M, N, O, P, Q, T, U, V, W, X, Y1, Y2, Z, and fimT, U, V are involved in the biogenesis and mechanical function of pili, pilG, H, I, K, chpA, B, C, D, E, pilS, R, fimS, rpoN, algR, algU, and vfr are involved in transcriptional regulation and chemosensory pathways that control the expression or activity of the twitching motility of the pili Attaches to host cells, but not to mucin, causing a twitching motility that allows the bacteria to move along the cell surface; biofilm formation The C-terminal receptor-binding domain of pilin binds to asialoGM1 gangliosides on host cells. Generally, GM1 gangliosides contain a sialic acid moiety. P.aeruginosa produces a neuraminidase which removes sialic acid residues from the GM1 to form the asialoGM1, which is a better receptor for the pili; The asialoGM1 is present in increased abundance on the surface of cystic fibrosis respiratory epithelial cells Abstract(s) in PubMed C2_02999 VFG030314 42.5 5.360000000000001e-47 164.0 VF0840 VFC0258 adhD Putative zinc-type alcohol dehydrogenase AdhD (aldehyde reductase) Mycobacterium tuberculosis CAS/NITR204 C2_03023 VFG050705 41.9 3.24e-66 221.0 VF1334 VFC0001 pilR sigma-54 dependent transcriptional regulator Acinetobacter baumannii D1279779 TFP Type IV pili Acinetobacter baumannii Adherence Essential for twitching motility and natural competence, and contribute to host cell adherence Abstract(s) in PubMed C2_03041 VFG044084 40.0 3.4e-06 47.8 VF0094 VFC0272 PA2383 transcriptional regulator Pseudomonas aeruginosa PAO1 Pyoverdine Pseudomonas aeruginosa Nutritional/Metabolic factor A greenish-yellow compound, a hydroxyquinolone chromophore to which an amino acid tail is attached, the tail can vary in length; the synthesis of pyoverdine requires a special factor, PvdS, which is in turn regulated by the Fur repressor; also called pseudobactin Effective at acquiring iron from transferrin and lactoferrin; cytotoxic due to its ability to stimulating the production of reactive oxygen species Pvd is a fluorescent dihydroxyquinoline derivative connected to a small peptide and contains hydroxamate and catecholate residues to chelate ferric ion, Fe (III). Pvd chelates Fe (III) in a 1:1 stoichiometry with high affinity (stability constant, 10**32); FpvA is the specific receptor for Fe(III)-pyoverdin Abstract(s) in PubMed C2_03043 VFG035984 99.9 0.0 2445.0 VF1127 VFC0001 ehaA autotransporter adhesin EhaA Escherichia coli O104:H4 str. 2009EL-2050 C2_03056 VFG034554 99.7 0.0 2694.0 VF1119 VFC0001 eaeH intimin-like adhesin FdeC Escherichia coli O103:H2 str. 12009 C2_03060 VFG034382 100.0 5.74e-128 356.0 VF0404 VFC0001 ykgK/ecpR regulator protein EcpR Escherichia coli O104:H4 str. 2009EL-2050 ECP E. coli common pilus Escherichia coli (EHEC) Adherence ECP, composed of a 21-kDa pilin subunit EspA, is a pilus-adherence factor that is crucial to the virulence of E. coli O157 in humans, and is also carried by commensal strains of E. coli.; It is suggested that pathogenic E. coli strains may use ECP to mimic commensal E. coli and provide themselves with an ecological advantage for host colonization and evasion of the immune system. Abstract(s) in PubMed C2_03061 VFG034419 100.0 1.8700000000000002e-129 361.0 VF0404 VFC0001 yagZ/ecpA E. coli common pilus structural subunit EcpA Escherichia coli E24377A ECP E. coli common pilus Escherichia coli (EHEC) Adherence ECP, composed of a 21-kDa pilin subunit EspA, is a pilus-adherence factor that is crucial to the virulence of E. coli O157 in humans, and is also carried by commensal strains of E. coli.; It is suggested that pathogenic E. coli strains may use ECP to mimic commensal E. coli and provide themselves with an ecological advantage for host colonization and evasion of the immune system. Abstract(s) in PubMed C2_03062 VFG018205 100.0 1.12e-157 435.0 VF0404 VFC0001 yagY/ecpB E. coli common pilus chaperone EcpB Escherichia coli str. K-12 substr. MG1655 ECP E. coli common pilus Escherichia coli (EHEC) Adherence ECP, composed of a 21-kDa pilin subunit EspA, is a pilus-adherence factor that is crucial to the virulence of E. coli O157 in humans, and is also carried by commensal strains of E. coli.; It is suggested that pathogenic E. coli strains may use ECP to mimic commensal E. coli and provide themselves with an ecological advantage for host colonization and evasion of the immune system. Abstract(s) in PubMed C2_03063 VFG034465 99.8 0.0 1637.0 VF0404 VFC0001 yagX/ecpC E. coli common pilus usher EcpC Escherichia coli O104:H4 str. 2009EL-2050 ECP E. coli common pilus Escherichia coli (EHEC) Adherence ECP, composed of a 21-kDa pilin subunit EspA, is a pilus-adherence factor that is crucial to the virulence of E. coli O157 in humans, and is also carried by commensal strains of E. coli.; It is suggested that pathogenic E. coli strains may use ECP to mimic commensal E. coli and provide themselves with an ecological advantage for host colonization and evasion of the immune system. Abstract(s) in PubMed C2_03064 VFG034492 100.0 0.0 1105.0 VF0404 VFC0001 yagW/ecpD polymerized tip adhesin of ECP fibers Escherichia coli O26:H11 str. 11368 ECP E. coli common pilus Escherichia coli (EHEC) Adherence ECP, composed of a 21-kDa pilin subunit EspA, is a pilus-adherence factor that is crucial to the virulence of E. coli O157 in humans, and is also carried by commensal strains of E. coli.; It is suggested that pathogenic E. coli strains may use ECP to mimic commensal E. coli and provide themselves with an ecological advantage for host colonization and evasion of the immune system. Abstract(s) in PubMed C2_03065 VFG034520 99.6 3.21e-173 475.0 VF0404 VFC0001 yagV/ecpE E. coli common pilus chaperone EcpE Escherichia coli O26:H11 str. 11368 ECP E. coli common pilus Escherichia coli (EHEC) Adherence ECP, composed of a 21-kDa pilin subunit EspA, is a pilus-adherence factor that is crucial to the virulence of E. coli O157 in humans, and is also carried by commensal strains of E. coli.; It is suggested that pathogenic E. coli strains may use ECP to mimic commensal E. coli and provide themselves with an ecological advantage for host colonization and evasion of the immune system. Abstract(s) in PubMed C2_03095 VFG043246 58.9 1.1399999999999998e-68 212.0 VF1028 VFC0346 lafU putative lateral flagellar export/assembly protein LafU Yersinia pestis CO92 C2_03096 VFG038861 54.7 4.13e-213 608.0 VF0474 VFC0204 lfhA lateral flagellar biosynthesis protein Aeromonas salmonicida subsp. salmonicida A449 Lateral flagella Aeromonas salmonicida Motility Inducible lateral peritrichous flagellar system is responsible for movement across solid surfaces or through viscous environments known as swarming motility; glycosylation of the lateral flagellin is essential for swarming motility over surfaces Abstract(s) in PubMed C2_03104 VFG013422 75.0 1.01e-100 288.0 VF0044 VFC0258 gmhA/lpcA phosphoheptose isomerase Haemophilus ducreyi 35000HP LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_03108 VFG035996 99.9 0.0 1928.0 VF1128 VFC0001 ehaB autotransporter outer membrane beta-barrel domain-containing protein Escherichia coli O103:H2 str. 12009 C2_03132 VFG031730 40.7 6.62e-50 162.0 VF0858 VFC0301 regX3 two-component sensory transduction protein RegX Mycobacterium smegmatis str. MC2 155 C2_03173 VFG000077 66.5 8.09e-91 264.0 VF0074 VFC0282 clpP ATP-dependent Clp protease proteolytic subunit Listeria monocytogenes EGD-e ClpP Listeria monocytogenes Stress survival 21.6 kDa protein belongs to a family of proteases highly conserved in prokaryotes and eukaryotes Serine protease involved in proteolysis and is required for growth under stress conditions Abstract(s) in PubMed C2_03178 VFG043478 42.9 7.72e-14 62.8 VF1230 VFC0001 PM_RS08640 ComEA family DNA-binding protein Pasteurella multocida subsp. multocida str. Pm70 C2_03194 VFG001306 41.9 1.07e-13 65.9 VF0003 VFC0258 cap8J type 8 capsular polysaccharide synthesis protein Cap8J Staphylococcus aureus subsp. aureus MW2 Capsule Staphylococcus aureus Immune modulation Produced by over 90% of Staphylococcus aureus strains. Two serotypes (5 and 8) predominate among clinical isolates of S. aureus from humans Prevent phagocytosis Abstract(s) in PubMed C2_03197 VFG049144 91.5 0.0 1831.0 VF0568 VFC0325 acrB acriflavine resistance protein B Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 AcrAB Klebsiella pneumoniae Antimicrobial activity/Competitive advantage May mediate resistance against host-derived antimicrobial peptides; associated with antibiotic resistance Abstract(s) in PubMed C2_03198 VFG049125 85.9 1.77e-237 651.0 VF0568 VFC0325 acrA acriflavine resistance protein A Klebsiella oxytoca E718 AcrAB Klebsiella pneumoniae Antimicrobial activity/Competitive advantage May mediate resistance against host-derived antimicrobial peptides; associated with antibiotic resistance Abstract(s) in PubMed C2_03210 VFG013617 50.6 5.48e-115 335.0 VF0758 VFC0272 hemH ferrochelatase Haemophilus somnus 129PT C2_03218 VFG016797 42.0 1.03e-12 59.7 VF0679 VFC0346 vapA1 HigA family addiction module antidote protein Bartonella henselae str. Houston-1 C2_03221 VFG043453 49.3 1.97e-08 53.9 VF1000 VFC0001 aae autolysin/adhesin Aae Staphylococcus epidermidis ATCC 12228 C2_03225 VFG041031 49.6 1.4200000000000002e-72 236.0 VF0944 VFC0086 PA2359 transcriptional regulator Pseudomonas aeruginosa PAO1 HSI-3 Pseudomonas aeruginosa Effector delivery system The expression of T6SSs in P. aeruginosa is regulated by the QS system. There are several QS systems in P. aeruginosa, two N-acyl-homoserine lactone based QS systems (las and rhl systems) and one quinolone PQS system (pqs). The expression of H1-T6SS is negatively regulated by both las and pqs QS systems, while the expression of H2- and H3-T6SS is positively regulated by las, rhl, and pqs TseF dependent on H3-T6SS directly interacts with PQS and is incorporated with outer membrane vesicles (OMVs) for iron acquisition Abstract(s) in PubMed C2_03255 VFG038907 67.0 2.57e-93 271.0 VF0647 VFC0235 B565_RS04085 hemolysin III Aeromonas veronii B565 C2_03311 VFG045607 48.3 9.93e-73 221.0 VF0798 VFC0086 LPG_RS14840 Dot/Icm type IV secretion system effector Legionella pneumophila subsp. pneumophila str. Philadelphia 1 Dot/Icm T4SS secreted effectors Legionella pneumophila Effector delivery system AnkB/legAU13/ceg27 (E3 Ubiquitin Ligase Activity, bounds Skp1, targets host protein parvin B. ); AnkC/legA12 (Ankyrin repeat. ); AnkD/legA15 (Ankyrin repeat. ); AnkF/legA14/ceg31 (Ankyrin repeat. ); AnkG/ankZ/legA7 (Ankyrin repeat. ); AnkH/legA3/ankW (Ankyrin repeat, NF-B inhibitor. ); AnkI/legAS4 (Ankyrin repeat. ); AnkJ/legA11 (Ankyrin repeat. ); AnkK/legA5 (Ankyrin repeat. ); AnkN/ankX/legA8 (Phosphocholination of Rab1 and Rab35 to regulate their activity; modulation of endosomal trafficking. ); AnkQ/legA10; AnkY/legA9 (Ankyrin repeat, STPK, Enhancer of autophagy. ); Ceg10; Ceg14/sidL (Inhibition of host protein synthesis leading to activation of the NF-B pathway. ); Ceg15; Ceg17; Ceg18; Ceg19 (Vesicle trafficking. ); Ceg23; Ceg25; Ceg28; Ceg29; Ceg3; Ceg30; Ceg32/sidI (Interacts with eEF1A to inhibit host protein synthesis. ); Ceg33; Ceg34; Ceg4; Ceg5; Ceg7; Ceg8; Ceg9 (Vesicle trafficking. ); CegC1 (Zinc metallophospholipase C. Zinc metallophospholipase C. ); CegC2 (Ninein domain. ); CegC3; CegC4; DrrA/sidM (Rab1-GEF and GDF (RabGDI displacement factor) activity responsible for Rab1 recruitment to LCV, C-terminal PI4P binding domain responsible for membrane binding; N-terminal AMPylation activity. ); LaiE (SidE paralog. ); LegA1; LegA2; LegA6; LegA7; LegC1; LegC3/ppeA (Vesicle trafficking. ); LegC4 (Coiled-coil. ); LegC6 (Coiled-coil. ); LegD1; LegD2; LegG2 (Ras GEF. ); LegK1 (Eukaryotic-like Ser/Thr kinase activity, directly activates NF-B pathway by phosphorylating the IB family of inhibitors. ); LegK2 (Ser/Thr kinase. ); LegK3 (STPK. ); LegL1 (Leucine-rich repeats. ); LegL2 (Leucine-rich repeats. ); LegL3 (Leucine-rich repeats. ); LegL5 (Leucine-rich repeats. ); LegL6 (Leucine-rich repeats. ); LegL7 (Leucine-rich repeats. ); LegLC4 (Leucine-rich repeats, coiled-coil. ); LegLC8 (Leucine-rich repeats, coiled-coil. ); LegN; LegP (Astacin protease. ); LegS1; LegS2 (Putative Sphingosine-1-phosphate lyase 1 (SP-lyase). ); LegT (Thaumatin domain. ); LegU1 (E3 Ubiquitin Ligase, targets host chaperone protein BAT3. ); LegY; Lem1; Lem10; Lem11; Lem12; Lem14; Lem15; Lem16; Lem17; Lem19; Lem2; Lem20; Lem21; Lem22; Lem23; Lem24; Lem25; Lem26; Lem27; Lem28; Lem29; Lem3 (Dephosphoryl-cholinase relieving the AnkX-mediated modification on Rab1. ); Lem4/smdA (PI4P-binding protein. ); Lem5; Lem6; Lem7; Lem8; Lem9; LepA (Nonlytic release from protozoa. ); LepB (Rab1 GAP, vesicle trafficking and bacterial egress. ); Lgt2/legC8 (Glucosyltransferase, inhibits host protein systhesis by glucosylating mammalian elongation factor eEF1A at serine-53. ); Lgt3/legC5 (Glucosyltransferase, inhibits host protein systhesis by glucosylating mammalian elongation factor eEF1A at serine-53. ); LidA (Promotion of Rab1 recruitment and tethering of ER derived vesicles to the LCV; stabilization of Rab guanosine nucleotide complex. ); LidL (EnhC paralogue. ); LirA; LirB (Peptidyl-prolyl cis-trans isomerase A (rotamase A). ); Lpg0045; Lpg0081; Lpg0294; Lpg0365; Lpg0518; Lpg0634; Lpg0963; Lpg1148; Lpg1158; Lpg1273; Lpg1689; Lpg1717; Lpg1751; Lpg2160 (Associates with BAT3 independently of LegU1; LegU1 and Lpg2160 may function redundantly or in concert to modulate BAT3 activity during the course of infection. ); Lpg2327; Lpg2407; Lpg2525 (F-box protein. ); Lpg2527; Lpg2744; LpnE (Putative Beta-lactamase. ); LubX/legU2 (E3 ubiquitin ligase, targets another effector protein SidH to proteasome-mediated protein degradation in the host cells; cell cycle modulation via Clk1. ); MavA; MavB; MavC; MavE; MavF; MavG; MavH; MavI; MavJ; MavL; MavM; MavN; MavV; PieA/lirC; PieB/lirD; PieC/lirE; PieD/lirF; PieE; PieF; PieG/legG1 (Regulator of chromosome condensation RCC. ); PpeB; PpgA (Regulator of chromosome condensation. ); RalF (Arf-GEF; Arf1 recuitment to LCV. ); RavE; RavF; RavG; RavH; RavI; RavJ; RavK; RavL; RavM; RavN; RavO; RavP; RavQ; RavR; RavS; RavT; RavW; RavX; RavY; RavZ (Cysteine protease. Inhibits host autophagy by cleaving and deconjugating LC3-PE. ); RvfA; SdbA (Contributes to sustained NF-B activation. ); SdbB (SidB paralog. ); SdbC (SidB paralog. ); SdcA (SidC paralog, anchors to PtdIns(4)P on LCVs. ); SdeA/laiA (Adherence and/or uptake. ); SdeB/laiB; SdeC/laiC; SdeD/laiF (SidE paralog. ); SdhA (Maintenance of LCV integrity preventing cell death and type I interferon induction. ); SdhB (Paralog of sidH, ANTH domain. ); SdjA; SetA (Vesicle trafficking. ); SidA; SidB (Rtx toxin, lipase. ); SidC (ER recuitment. ); SidD; SidE/laiD; SidF (Anti-apoptosis by targeting pro-death members of the Bcl2 protein family. ); SidG (Coiled-coil. ); SidH (A substrate of LubX E3 ubiquitin ligase. ); SidJ (ER recuitment. ); SidK (Interacting with VatA, a key component of the proton pump. Inhibition of LCV acidification. ); VipA (Actin nucleator contributing to modulate organelle trafficking. ); VipD (Phospholipase A1, removes PI(3)P from early endosomes. ); VipE; VipF (N-terminal acetyltransferase, GNAT family. ); VpdA/vipD2 (VipD paralog, Acyl transferase/acyl hydrolase/lysophospholipase. ); VpdB/vipD3 (VipD paralog, phospholipase. ); VpdC; WipA; WipB; YlfA/legC7 (Vesicle trafficking. ); YlfB/legC2 (Vesicle trafficking. ); CegC4; MesI; LPG_RS00040; LPG_RS00105; LPG_RS00150; LPG_RS00200; LPG_RS00235; LPG_RS00300; LPG_RS00665 (PI-3-phosphatase. ); LPG_RS00825; LPG_RS00870; LPG_RS00880; LPG_RS00925; LPG_RS01290; LPG_RS01305; LPG_RS01820; LPG_RS01880; LPG_RS02025; LPG_RS03550; LPG_RS03935; LPG_RS04800; LPG_RS05365; LPG_RS05490; LPG_RS05590; LPG_RS05660; LPG_RS05710; LPG_RS05830; LPG_RS07260; LPG_RS07280; LPG_RS07435; LPG_RS07905; LPG_RS08210; LPG_RS08285; LPG_RS08320; LPG_RS08345; LPG_RS08350; LPG_RS08370; LPG_RS08445; LPG_RS08450; LPG_RS08485; LPG_RS08595; LPG_RS08775; LPG_RS08895; LPG_RS09040; LPG_RS09470; LPG_RS09565; LPG_RS09650; LPG_RS09825; LPG_RS09915; LPG_RS09965; LPG_RS10290; LPG_RS10795; LPG_RS10800; LPG_RS11170; LPG_RS11255; LPG_RS11415; LPG_RS11860; LPG_RS11920; LPG_RS11940; LPG_RS11990; LPG_RS12190; LPG_RS12265; LPG_RS12310; LPG_RS12405; LPG_RS12815; LPG_RS12820; LPG_RS12830; LPG_RS12855; LPG_RS12885; LPG_RS12900; LPG_RS13265; LPG_RS13310; LPG_RS13590; LPG_RS13860; LPG_RS14265; LPG_RS14285; LPG_RS14345; LPG_RS14500; LPG_RS14525; LPG_RS14550; LPG_RS14555; LPG_RS14570; LPG_RS14710; LPG_RS14840; LPG_RS15050; LPG_RS15170 Abstract(s) in PubMed C2_03316 VFG009862 44.0 9.56e-58 182.0 VF0298 VFC0301 mprA response regulator transcription factor Mycobacterium ulcerans Agy99 MprAB Mycobacterial persistence regulator Mycobacterium tuberculosis Regulation MprB, sensor kinase, can undergo autophosphorylation. MprA, transcriptional factor, can accept phosphate from MprB or from small phosphodonors including acetyl phosphate Required for establishment and maintenance of persistent infection Abstract(s) in PubMed C2_03317 VFG034663 100.0 4.57e-317 858.0 VF0237 VFC0083 ibeB Cu(+)/Ag(+) efflux RND transporter outer membrane channel CusC Escherichia coli O103:H2 str. 12009 Ibes Invasion of brain endothelial cells Escherichia coli (NMEC) Invasion IbeA is unique to E. coli K1. The ibeB and ibeC are found to have K12 homologues p77211 and yijP respectively. IbeA and IbeB encode outer membrane proteins with three and two transmembrane domains, respectively; IbeC has a signal peptide-like sequence and five or six transmembrane segments at its N terminus Contributes to brain microvascular endothelial cells (BMECs) invasion via a ligand-receptor interaction Unknown; the roles of Ibe proteins in E. coli K1 invasion of BMECs were verified by deletion and complementation experiments Abstract(s) in PubMed C2_03329 VFG013004 99.0 1.32e-154 426.0 VF0984 VFC0272 entD enterobactin synthase multienzyme complex phosphopantetheinyltransferase Shigella flexneri 2a str. 301 C2_03330 VFG020175 99.7 0.0 1517.0 VF0984 VFC0272 fepA siderophore enterobactin receptor FepA Shigella boydii CDC 3083-94 C2_03331 VFG044159 96.3 6.269999999999998e-308 830.0 VF0228 VFC0272 fes enterobactin/ferric enterobactin esterase Escherichia coli CFT073 Enterobactin Escherichia coli (UPEC) Nutritional/Metabolic factor An extremely effective iron chelator, with a formation constant for the iron complex of 1049. Fe3+ is coordinated by six catechol oxygens to form a metal chelate with a net negative charge of three A 669-kDa catecholate (which contain catechol rings) that is synthesized by E. coli and S. typhimurium; Ferric enterobactin receptor FepA is a 724-residue integral outer membrane protein that transports ferric enterobactin into the periplasm; crystal structure of FepA: 1FEP Iron uptake: the siderophore enterobactin imported through the FepA receptor and the FepBCDG system Abstract(s) in PubMed C2_03332 VFG026493 43.5 7.84e-16 64.7 VF0299 VFC0272 mbtH putative protein MbtH Mycobacterium canettii CIPT 140070010 Mycobactin Mycobacterium tuberculosis Nutritional/Metabolic factor Mycobacteria produce two classes of siderophores, mycobactins and the exochelins. Pathogenic mycobacteria solely produce mycobactins, whereas saprophytic mycobacteria such as M. smegmatis and Mycobacterium neoarum produce both mycobactins and exochelins; Mycobactins are salicylate containing siderophores, and exochelins are peptidic molecules; Mycobactins are found in two forms that differ in the length of an alkyl substitution and hence in polarity and solubility. The less polar form remains cell associated (mycobactin), whereas the more polar one (carboxymycobactin) is secreted into the medium. Cell-association mycobactin participates in iron internalization and/or to serve as a temporary iron-holding molecule to prevent sudden influx of excess iron if the metal suddenly becomes available after a period of iron limitation Abstract(s) in PubMed C2_03333 VFG013002 98.8 0.0 2536.0 VF0984 VFC0272 entF enterobactin non-ribosomal peptide synthetase EntF Shigella sonnei Ss046 C2_03334 VFG000927 93.4 5.33e-245 669.0 VF0228 VFC0272 fepE LPS O-antigen length regulator Escherichia coli CFT073 Enterobactin Escherichia coli (UPEC) Nutritional/Metabolic factor An extremely effective iron chelator, with a formation constant for the iron complex of 1049. Fe3+ is coordinated by six catechol oxygens to form a metal chelate with a net negative charge of three A 669-kDa catecholate (which contain catechol rings) that is synthesized by E. coli and S. typhimurium; Ferric enterobactin receptor FepA is a 724-residue integral outer membrane protein that transports ferric enterobactin into the periplasm; crystal structure of FepA: 1FEP Iron uptake: the siderophore enterobactin imported through the FepA receptor and the FepBCDG system Abstract(s) in PubMed C2_03335 VFG013021 99.6 4.76e-197 538.0 VF0984 VFC0272 fepC iron-enterobactin ABC transporter ATP-binding protein Shigella dysenteriae Sd197 C2_03336 VFG013037 99.7 1.61e-220 603.0 VF0984 VFC0272 fepG iron-enterobactin ABC transporter permease Shigella boydii Sb227 C2_03337 VFG013029 99.7 4.920000000000001e-217 594.0 VF0984 VFC0272 fepD Fe(3+)-siderophore ABC transporter permease Shigella flexneri 2a str. 2457T C2_03338 VFG044165 99.5 5.12e-281 763.0 VF0228 VFC0272 entS enterobactin exporter, iron-regulated Escherichia coli CFT073 Enterobactin Escherichia coli (UPEC) Nutritional/Metabolic factor An extremely effective iron chelator, with a formation constant for the iron complex of 1049. Fe3+ is coordinated by six catechol oxygens to form a metal chelate with a net negative charge of three A 669-kDa catecholate (which contain catechol rings) that is synthesized by E. coli and S. typhimurium; Ferric enterobactin receptor FepA is a 724-residue integral outer membrane protein that transports ferric enterobactin into the periplasm; crystal structure of FepA: 1FEP Iron uptake: the siderophore enterobactin imported through the FepA receptor and the FepBCDG system Abstract(s) in PubMed C2_03339 VFG020176 99.4 1.2799999999999999e-220 602.0 VF0984 VFC0272 fepB Fe2+-enterobactin ABC transporter substrate-binding protein Shigella boydii CDC 3083-94 C2_03340 VFG012991 99.5 2.44e-280 759.0 VF0984 VFC0272 entC isochorismate synthase EntC Shigella dysenteriae Sd197 C2_03341 VFG012989 98.9 0.0 1058.0 VF0984 VFC0272 entE (2,3-dihydroxybenzoyl)adenylate synthase EntE Shigella boydii Sb227 C2_03342 VFG012980 99.6 6.86e-213 580.0 VF0984 VFC0272 entB 2,3-dihydro-2,3-dihydroxybenzoate synthetase Shigella flexneri 2a str. 301 C2_03343 VFG012977 100.0 1.6999999999999999e-174 479.0 VF0984 VFC0272 entA 2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase EntA Shigella boydii Sb227 C2_03370 VFG011228 45.6 2.84e-40 135.0 VF0684 VFC0258 pagP lipid IV(A) palmitoyltransferase PagP Bordetella avium 197N C2_03459 VFG031435 48.1 2.5600000000000003e-22 92.0 VF0850 VFC0282 ompA OmpA family protein Mycobacterium sp. JDM601 C2_03522 VFG047505 50.7 1.4200000000000002e-110 324.0 VF0552 VFC0272 bioB biotin synthase Francisella novicida U112 Biotin synthesis Francisella tularensis Nutritional/Metabolic factor Biotin is an important enzyme cofactor that acts as a covalently bound prosthetic group; Biotin plays critical roles in central metabolic processes involving carboxylation, decarboxylation and transcarboxylation; F. novicida has evolved two distinct biotin protein ligases BplA and BirA with specific roles. Only BplA is required for pathogenicity Critical for rapid phagosomal escape. Sequestration of biotin could restrict Francisella to the phagosome, blocking their escape and preventing them from reaching their replicative niche in the cytoplasm Abstract(s) in PubMed C2_03538 VFG013286 57.7 1.25e-137 394.0 VF0044 VFC0258 galE UDP-glucose 4-epimerase Haemophilus influenzae Rd KW20 LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_03556 VFG039075 40.4 3.34e-18 78.6 VF0499 VFC0083 ompA outer membrane protein OmpA Anaplasma marginale str. Florida OmpA Anaplasma phagocytophilum Invasion High degree of sequence conservation Binding domain lies within amino acids 59 to 74 Binds to 2,3-sialic acid of sialyl Lewis x, this receptor-ligand interaction is required for efficient cellular entry Abstract(s) in PubMed C2_03581 VFG021484 40.6 5.11e-49 161.0 VF0956 VFC0001 stdC fimbrial biogenesis chaperone StdC Salmonella enterica subsp. enterica serovar Agona str. SL483 C2_03600 VFG042771 40.0 4.24e-17 78.6 VF0213 VFC0001 cofS CofS Escherichia coli str. 260-1 Adhesive fimbriae Escherichia coli (ETEC) Adherence Adherence is mediated by proteinaceous surface structures that are referred to as colonization factors (CFs), colonization factor antigens (CFAs), coli surface antigens (CSAs), or putative colonization factors (PCFs); ETEC strains are host-specific. The CFs confer host specificity on the strain. In human-specific ETEC strains, 21 different CFs have been identified. Approximately 75% of human ETEC express either CFA/I, CFA/II or CFA/IV. Animal-specific ETEC strains produce a variety of CFs that are distinct from those produced by human-specific isolates, such as K88 and K99; ETEC strains typically possess multiple plasmids with a wide range of molecular masses. The genes encoding CFs generally are found on a plasmid that also encodes ST and/or LT ETEC CFs can be classified as fimbriae or fibrillae depending on their structure. The fimbrial CFs are rigid filamentous, rodlike structures, whereas the fibrillar CFs are thinner, more flexible, and have fewer subunits in each helical turn than do fimbrial CFs Adhesin, receptor is the oligosaccharide components of glycolipids and glycoproteins Abstract(s) in PubMed C2_03654 VFG040771 40.8 3.36e-21 85.9 VF0491 VFC0235 pld phospholipase D Rickettsia bellii OSU 85-389 Pld Rickettsia typhi Exotoxin Plays an important role in phagosomal escape Abstract(s) in PubMed C2_03664 VFG016192 54.6 4.32e-139 401.0 VF0082 VFC0001 pilU twitching motility protein PilU Pseudomonas syringae pv. tomato str. DC3000 Type IV pili Pseudomonas aeruginosa Adherence PilA, B, C, D, E, F, M, N, O, P, Q, T, U, V, W, X, Y1, Y2, Z, and fimT, U, V are involved in the biogenesis and mechanical function of pili, pilG, H, I, K, chpA, B, C, D, E, pilS, R, fimS, rpoN, algR, algU, and vfr are involved in transcriptional regulation and chemosensory pathways that control the expression or activity of the twitching motility of the pili Attaches to host cells, but not to mucin, causing a twitching motility that allows the bacteria to move along the cell surface; biofilm formation The C-terminal receptor-binding domain of pilin binds to asialoGM1 gangliosides on host cells. Generally, GM1 gangliosides contain a sialic acid moiety. P.aeruginosa produces a neuraminidase which removes sialic acid residues from the GM1 to form the asialoGM1, which is a better receptor for the pili; The asialoGM1 is present in increased abundance on the surface of cystic fibrosis respiratory epithelial cells Abstract(s) in PubMed C2_03674 VFG000823 44.9 1.7500000000000001e-29 105.0 VF0191 VFC0086 etgA T3SS-associated peptidoglycan lytic enzyme Escherichia coli O157:H7 str. EDL933 TTSS Type III secretion system Escherichia coli (EHEC) Effector delivery system Encoded on the pathogenicity island known as the locus of enterocyte effacement (LEE) Injects Tir and other effector molecules directly into the host cell. Effector molecules activate cell-signaling pathways, causing alterations in the host cell cytoskeleton and resulting in the depolymerization of actin and the loss of microvilli Abstract(s) in PubMed C2_03680 VFG002310 41.2 1.8500000000000002e-103 322.0 VF0401 VFC0001 pilN type IV pilus inner membrane platform protein PilN Yersinia enterocolitica subsp. enterocolitica 8081 Type IV pili Yersinia pseudotuberculosis Adherence Pil operon maybe acquired by horizontal gene transfer Contributes to the virulence of Y. pseudotuberculosis. Abstract(s) in PubMed C2_03702 VFG032880 41.0 2.52e-13 63.2 VF0449 VFC0315 prsA2 post translocation chaperone PrsA2 Listeria welshimeri serovar 6b str. SLCC5334 PrsA2 Listeria monocytogenes Post-translational modification A conserved post-translocation chaperone and a peptidyl prolyl cis-trans isomerase (PPIase) contributing to LLO folding and pore-forming ability and to the activity of the broad-range PC-PLC Required for virulence and contributes to the integrity of the L.monocytogenes cell wall as well as swimming motility and bacterial resistance to osmotic stress PrsA2 is a critical post-translocation secretion chaperone. It is a member of a family of membrane-associated lipoproteins that contribute to the folding and stability of secreted proteins as they cross the bacterial membrane Abstract(s) in PubMed C2_03709 VFG013509 55.9 5.810000000000001e-123 358.0 VF0044 VFC0258 wecA undecaprenyl-phosphate alpha-N-acetylglucosaminyltransferase Haemophilus influenzae 86-028NP LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_03710 VFG023778 69.9 3.36e-171 480.0 VF0392 VFC0258 wzzE ECA polysaccharide chain length modulation protein Yersinia enterocolitica subsp. palearctica 105.5R(r) O-antigen Yersinia enterocolitica Immune modulation "Clinical Y. enterocolitica isolates from humans predominantly belong to serotypes O:3, O:9, O:8 and O:5,27; Y. enterocolitica O antigen expression is temperature regulated." LPS O antigen mutants were severely impaired in their ability to colonize the Peyer's patches and did not colonize spleen and liver. The absence of O antigen in the outer membrane affects the expression of other Yersinia virulence factors. Abstract(s) in PubMed C2_03711 VFG007640 72.0 4.91e-196 545.0 VF0624 VFC0258 wbjD/wecB UDP-N-acetylglucosamine 2-epimerase (non-hydrolyzing) Vibrio vulnificus YJ016 C2_03712 VFG014138 67.1 2.96e-206 574.0 VF0085 VFC0258 wecC UDP-N-acetyl-D-mannosamine dehydrogenase Pseudomonas aeruginosa UCBPP-PA14 LPS Pseudomonas aeruginosa Immune modulation Two distinct forms of LPS: A-band and B-band. A-band is a homopolymer of -linked D-rhamnose, whereas B-band LPS is a heteropolymer Mediates biological effects including resistance to serum killing and phagocytosis; the binding to normal CFTR (cystic fibrosis transmembrane conductance regulator) and invasion of host cells may make a contribution to virulence in the human eye; internalization by binding to normal CFTR protein expressed by airway epithelial cells followed by desquamation of bacteria-laden epithelial cells, constitutes a host defense mechanism. If this mechanism fails to function properly, abnormally high bacterial carriage would promote the establishment of chronic bacterial infection Binding interaction occurs between the first extracellular loop of CFTR (predicted to be in amino acids 108-117 of the mature protein) and the complete outer portion of the core polysaccharide of the LPS Abstract(s) in PubMed C2_03713 VFG007659 79.8 1.98e-215 592.0 VF0624 VFC0258 rmlB dTDP-glucose 4,6-dehydratase Vibrio fischeri ES114 C2_03714 VFG048826 75.2 1.92e-158 442.0 VF0560 VFC0258 KPHS_35570 glucose-1-phosphate thymidylyltransferase Klebsiella pneumoniae subsp. pneumoniae HS11286 Capsule Klebsiella pneumoniae Immune modulation The Klebsiella polysaccharide capsule is produced through a Wzy-dependent process, for which the synthesis and export machinery are encoded in a single 10-30 kb region of the genome known as the K locus.; 78 distinct capsule phenotypes have been recognized by serological typing, but many isolates are serologically non-typable.; capsular serotypes vary substantially in the degree of serum resistance; K1, K2 and K5 are highly serum resistant and are associated with hypervirulent strains that differ from classical K. pneumoniae in that they commonly cause community-acquired disease. Assisting in evading the host immune system by protecting bacteria from opsonophagocytosis and serum killing Abstract(s) in PubMed C2_03716 VFG037926 41.8 3.71e-35 132.0 VF0465 VFC0258 ABBFA_RS17125 DegT/DnrJ/EryC1/StrS aminotransferase family protein Acinetobacter baumannii AB307-0294 Capsule Acinetobacter baumannii Immune modulation A. baumannii pan-genome was shown to include a highly diverse repertoire of gene sequences. In particular, capsule gene cluster is highly variable. The cluster at the K locus often contains either capsule export genes (wza, wzb, and wzc) or genes for simple sugar synthesis (galU, ugd, gpi, gne1, and pgm), which flank a central variable region that would be required for the synthesis of a specific monosaccharide. Plays an important role in protecting bacteria from the host innate immune response Abstract(s) in PubMed C2_03727 VFG001444 93.5 1.2300000000000002e-21 85.1 VF0238 VFC0083 aslA putative arylsulfatase Escherichia coli O18:K1:H7 str. RS218 AslA Escherichia coli (NMEC) Invasion Homology to aslA of E. coli K12; based on its protein sequence, AslA is predicted to be a member of the arylsulfatase family of enzymes that contains highly conserved sulfatase motifs, but E. coli AslA failed to exhibit in vitro arylsulfatase activity A 52-kDa protein with two transmembrane domains and an N-terminal signal sequence Contributes to brain microvascular endothelial cells (BMECs) invasion Unknown; the roles of AslA proteins in E. coli K1 invasion of BMECs were verified by deletion and complementation experiments Abstract(s) in PubMed C2_03729 VFG013206 43.1 7.81e-53 181.0 VF0758 VFC0272 hemX uroporphyrinogen-III C-methyltransferase Haemophilus somnus 2336 C2_03730 VFG013199 41.5 4.750000000000001e-56 179.0 VF0758 VFC0272 hemD uroporphyrinogen-III synthase Haemophilus somnus 2336 C2_03731 VFG013198 62.8 2.77e-130 374.0 VF0758 VFC0272 hemC hydroxymethylbilane synthase Haemophilus somnus 2336 C2_03778 VFG013201 46.3 2.8699999999999997e-54 169.0 VF0758 VFC0272 hemG menaquinone-dependent protoporphyrinogen IX dehydrogenase Haemophilus somnus 2336 C2_03782 VFG049114 73.8 6.88e-167 465.0 VF0572 VFC0272 allS DNA-binding transcriptional activator AllS Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Allantion utilization Klebsiella pneumoniae Nutritional/Metabolic factor An allantoin utilization operon has been associated with hypervirulent K. pneumoniae strains that cause pyogenic liver abscesses. Providing a nitrogen source to increase virulence in K. pneumoniae at certain sites of infection Allantoin is a metabolic intermediate of purine degradation by various organisms including microbes and has been identified as a source of nitrogen in various bacterial species and as both a nitrogen source and a carbon source in K. pneumoniae. Abstract(s) in PubMed C2_03783 VFG049116 74.4 8.21e-91 261.0 VF0572 VFC0272 allA ureidoglycolate hydrolase Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Allantion utilization Klebsiella pneumoniae Nutritional/Metabolic factor An allantoin utilization operon has been associated with hypervirulent K. pneumoniae strains that cause pyogenic liver abscesses. Providing a nitrogen source to increase virulence in K. pneumoniae at certain sites of infection Allantoin is a metabolic intermediate of purine degradation by various organisms including microbes and has been identified as a source of nitrogen in various bacterial species and as both a nitrogen source and a carbon source in K. pneumoniae. Abstract(s) in PubMed C2_03784 VFG049118 86.2 2.59e-167 463.0 VF0572 VFC0272 allR DNA-binding transcriptional repressor AllR Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Allantion utilization Klebsiella pneumoniae Nutritional/Metabolic factor An allantoin utilization operon has been associated with hypervirulent K. pneumoniae strains that cause pyogenic liver abscesses. Providing a nitrogen source to increase virulence in K. pneumoniae at certain sites of infection Allantoin is a metabolic intermediate of purine degradation by various organisms including microbes and has been identified as a source of nitrogen in various bacterial species and as both a nitrogen source and a carbon source in K. pneumoniae. Abstract(s) in PubMed C2_03789 VFG049120 91.4 2.86e-315 853.0 VF0572 VFC0272 allB allantoinase Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Allantion utilization Klebsiella pneumoniae Nutritional/Metabolic factor An allantoin utilization operon has been associated with hypervirulent K. pneumoniae strains that cause pyogenic liver abscesses. Providing a nitrogen source to increase virulence in K. pneumoniae at certain sites of infection Allantoin is a metabolic intermediate of purine degradation by various organisms including microbes and has been identified as a source of nitrogen in various bacterial species and as both a nitrogen source and a carbon source in K. pneumoniae. Abstract(s) in PubMed C2_03793 VFG049122 81.2 1.4499999999999998e-250 686.0 VF0572 VFC0272 allC allantoate amidohydrolase Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Allantion utilization Klebsiella pneumoniae Nutritional/Metabolic factor An allantoin utilization operon has been associated with hypervirulent K. pneumoniae strains that cause pyogenic liver abscesses. Providing a nitrogen source to increase virulence in K. pneumoniae at certain sites of infection Allantoin is a metabolic intermediate of purine degradation by various organisms including microbes and has been identified as a source of nitrogen in various bacterial species and as both a nitrogen source and a carbon source in K. pneumoniae. Abstract(s) in PubMed C2_03794 VFG049124 83.1 5.2e-215 590.0 VF0572 VFC0272 allD ureidoglycolate dehydrogenase Klebsiella pneumoniae subsp. pneumoniae NTUH-K2044 Allantion utilization Klebsiella pneumoniae Nutritional/Metabolic factor An allantoin utilization operon has been associated with hypervirulent K. pneumoniae strains that cause pyogenic liver abscesses. Providing a nitrogen source to increase virulence in K. pneumoniae at certain sites of infection Allantoin is a metabolic intermediate of purine degradation by various organisms including microbes and has been identified as a source of nitrogen in various bacterial species and as both a nitrogen source and a carbon source in K. pneumoniae. Abstract(s) in PubMed C2_03801 VFG013326 49.6 2.62e-77 233.0 VF0044 VFC0258 lpxH UDP-2,3-diacylglucosamine pyrophosphohydrolase Haemophilus somnus 129PT LOS Haemophilus influenzae Immune modulation Lic1A (phosphorylcholine (ChoP) kinase) 5'-CAAT-3' within the 5'-end of its coding sequence; lic2A, also referred to as lexA, variation in the number of 5'-CAAT-3' repeats has been shown to correlate directly with phase variation of the Gal-(1-4)-Gal LPS structure; But lgtC (glycosyltransferase), another phase-variable gene, ultimately dictates whether this structure is synthesized. lic3A encode a sialyl transferase which directs the substitution of LPS with sialic acid. Comprising Lipid A, an inner core of one molecule 3-deoxy-D-manno-oct-2-ulopyranosonic acid (Kdo) and three molecules of heptose, and an outer core composed of a heteropolymer of the neutral sugars glucose and galactose. Substitution of the out core with phosphorylcholine or sialic acid results in the heterogeneity of LPS; Lack O-antigen Major immunogen; LOS phosphorylcholine (ChoP) may influence invasion via interaction with PAF receptor and stimulates of inflammatory signals; LPS phase variation is characterized by the spontaneous loss and gain of oligosaccharide structures present in the outer core. the phase variable expression of LPS biosynthesis genes promotes evasion of antigen-specific host immune defences and allow colonization of different host microenvironments Lic1(lic1A-lic1D) responsible for the addition of phosphorylcholine to LPS. lic1A mediates phase variation (tetranucleotide repeat region); phase-variable gene lic3A encodes an -2,3-sialyltransferase that is responsible for the addition of Neu5Ac to terminal lactose in the LPS, LPS sialylation has been shown to be important for resistance to the killing effectors of normal human serum Abstract(s) in PubMed C2_03807 VFG042679 66.3 3.36e-75 223.0 VF1211 VFC0001 fimA gene major fimbrial subunit Citrobacter freundii str. 3009 C2_03808 VFG042681 67.3 5.11e-105 302.0 VF1211 VFC0001 fimC gene fimbrial chaperone protein Citrobacter freundii str. 3009 C2_03809 VFG042682 71.6 0.0 1312.0 VF1211 VFC0001 fimD gene outer membrane usher protein Citrobacter freundii str. 3009 C2_03810 VFG021168 70.4 4.630000000000001e-167 468.0 VF0102 VFC0001 fimH type I fimbriae minor fimbrial subunit FimH, adhesin Salmonella enterica subsp. enterica serovar Enteritidis str. P125109 Type 1 fimbriae Salmonella enterica (serovar typhimurium) Adherence Chaperone-usher assembly pathway The adhesin FimH mediates T3SS1-independent uptake in murine DCs. Abstract(s) in PubMed C2_03811 VFG042684 63.1 1.16e-66 200.0 VF1211 VFC0001 fimF gene major fimbrial subunit Citrobacter freundii str. 3009 C2_03812 VFG000449 71.4 9.18e-103 295.0 VF0102 VFC0001 fimZ DNA-binding response regulator Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Type 1 fimbriae Salmonella enterica (serovar typhimurium) Adherence Chaperone-usher assembly pathway The adhesin FimH mediates T3SS1-independent uptake in murine DCs. Abstract(s) in PubMed C2_03832 VFG035333 56.4 2.6399999999999998e-40 149.0 VF1120 VFC0086 EC55989_RS17050 GIY-YIG nuclease family protein Escherichia coli 55989 C2_03841 VFG042756 43.2 4.56e-19 84.0 VF0213 VFC0001 lngS LngS Escherichia coli O8:H9 str. E9034A Adhesive fimbriae Escherichia coli (ETEC) Adherence Adherence is mediated by proteinaceous surface structures that are referred to as colonization factors (CFs), colonization factor antigens (CFAs), coli surface antigens (CSAs), or putative colonization factors (PCFs); ETEC strains are host-specific. The CFs confer host specificity on the strain. In human-specific ETEC strains, 21 different CFs have been identified. Approximately 75% of human ETEC express either CFA/I, CFA/II or CFA/IV. Animal-specific ETEC strains produce a variety of CFs that are distinct from those produced by human-specific isolates, such as K88 and K99; ETEC strains typically possess multiple plasmids with a wide range of molecular masses. The genes encoding CFs generally are found on a plasmid that also encodes ST and/or LT ETEC CFs can be classified as fimbriae or fibrillae depending on their structure. The fimbrial CFs are rigid filamentous, rodlike structures, whereas the fibrillar CFs are thinner, more flexible, and have fewer subunits in each helical turn than do fimbrial CFs Adhesin, receptor is the oligosaccharide components of glycolipids and glycoproteins Abstract(s) in PubMed C2_03867 VFG049194 95.0 0.0 1551.0 VF0783 VFC0086 clpV ATP-dependent chaperone ClpB Klebsiella pneumoniae JM45 C2_03877 VFG049933 41.0 1.11e-22 100.0 VF0660 VFC0271 papR DUF4084 domain-containing protein Bacillus cereus E33L C2_03878 VFG049233 50.0 3.07e-14 68.9 VF0784 VFC0086 ompA OmpA family protein Klebsiella pneumoniae subsp. rhinoscleromatis SB3432 C2_03947 VFG043568 64.9 4.94e-165 466.0 VF0969 VFC0001 nmpC phosphoporin PhoE Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 C2_03982 VFG005360 60.9 1.54e-134 385.0 VF1042 VFC0001 plr/gapA type I glyceraldehyde-3-phosphate dehydrogenase Streptococcus mutans UA159 C2_03984 VFG035328 65.5 7.050000000000001e-21 78.6 VF1120 VFC0086 EC55989_RS17055 hypothetical protein Escherichia coli 55989 C2_03986 VFG043365 45.9 3.32e-11 65.9 VF0051 VFC0204 tlpC membrane-bound chemoreceptor Helicobacter pylori 26695 Flagella Helicobacter pylori Motility H. pylori typically produce 4-6 unipolar flagella, which are encased in a membranous sheath and capped by terminal bulbs Comprised of three main components (filament, hook and basal body). The flagellar filament is composed primarily of repeating subunits of two polypeptides: FlaA (the major component) and FlaB (a minor component). The flagellar hook is comprised primarily of FlgE. The basal body is a multiprotein structure that serves as the proton motive force-driven motor that propels rotation. Confers motility, allows the bacteria to penetrate and colonize the gastric mucus layer. The lumenal pH of the fasting human stomach is <2, but with the gastric mucus there is a pH gradient that ranges from pH 2 at the luminal surface to nearly neutral pH at the epithelial cell surface, so entry into the gastric mucus layer is important for H. pylori to escape extremely low pH Abstract(s) in PubMed C2_04016 VFG002308 44.6 1.18e-17 83.2 VF0401 VFC0001 pilL type IV pilus biosynthesis protein PilL Yersinia enterocolitica subsp. enterocolitica 8081 Type IV pili Yersinia pseudotuberculosis Adherence Pil operon maybe acquired by horizontal gene transfer Contributes to the virulence of Y. pseudotuberculosis. Abstract(s) in PubMed C2_04026 VFG011590 40.4 2.9600000000000004e-43 154.0 VF0365 VFC0086 virB10 type IV secretion system channel protein VirB10 Brucella ovis ATCC 25840 VirB type IV secretion system Brucella melitensis Effector delivery system Phagosome acidification is required for intracellular expression of the VirB type IV secretion system; the LuxR family regulator VjbR regulated the virB operon directly by bounding a fragment of the virB promoter containing an 18 bp palindromic motif The Brucella VirB type IV secretion apparatus is not required for early survival stages, like LPS or cyclic -1,2-glucan are, but rather for late Brucella containing vacuole (BCV) maturation events corresponding to sustained interaction and fusion with the endoplasmic reticulum (ER). Brucella initiates interactions with Sar1/COPII-dependent ERES (ER exit sites), the early secretory pathway. Unlike Legionella, that intercepts COPI-dependent vesicular trafficking from the ER for the biogenesis of its ER-derived replicative organelle; The acidified Brucella containing vacuole (BCV) interacts with late endosome/lysosomes, acquiring markers such as LAMP-1, CD63 and Rab7. Subsequently, wild-type Brucella is able to exclude these late endosomal/lysosomal markers from its vacuole and acquire markers of the endoplasmic reticulum. The replicative organelle contains not only the ER marker calreticulin, but also two proteins, Rab2 and GAPDH, that regulate membrane traffic between the ER and Vesicular Tubular Compartments (VTC), a compartment in the secretory pathway between ER and Golgi in which proteins are sorted either to an anterograde pathway to the Golgi, or for recycling to the ER. These components of the BCV are critical for the ability of Brucella to replicate intracellularly; VceA and VceC, also regulated by VjbR, are novel effectors, both require intact C termini for translocation through the VirB system Abstract(s) in PubMed C2_04033 VFG017841 45.9 2.09e-118 358.0 VF0401 VFC0001 pilQ type IV pilus biogenesis protein PilQ Yersinia pseudotuberculosis IP 31758 Type IV pili Yersinia pseudotuberculosis Adherence Pil operon maybe acquired by horizontal gene transfer Contributes to the virulence of Y. pseudotuberculosis. Abstract(s) in PubMed C2_04036 VFG042890 54.3 8.68e-48 152.0 VF0966 VFC0001 STY_RS21730 lytic transglycosylase domain-containing protein Salmonella enterica subsp. enterica serovar Typhi str. CT18 C2_04038 VFG017853 41.5 2.92e-78 248.0 VF0401 VFC0001 pilV type IV pilus biogenesis protein PilV Yersinia pseudotuberculosis IP 31758 Type IV pili Yersinia pseudotuberculosis Adherence Pil operon maybe acquired by horizontal gene transfer Contributes to the virulence of Y. pseudotuberculosis. Abstract(s) in PubMed C2_04077 VFG042718 99.3 6.129999999999998e-221 602.0 VF1153 VFC0001 ydeQ fimbrial protein Escherichia coli O157:H7 str. EDL933 C2_04078 VFG033339 99.4 4.82e-116 325.0 VF0221 VFC0001 fimG FimG protein precursor Escherichia coli O44:H18 042 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_04079 VFG033311 99.4 7.89e-124 345.0 VF0221 VFC0001 fimF FimF protein precursor Escherichia coli O44:H18 042 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_04080 VFG033280 99.3 0.0 1748.0 VF0221 VFC0001 fimD Outer membrane usher protein fimD precursor Escherichia coli O104:H4 str. 2009EL-2050 Type 1 fimbriae Escherichia coli (UPEC) Adherence Mannose-sensitive (MSHA) fimbriae, the ability to hemagglutinate erythrocytes was blocked by the presence of mannose; the genes responsible for type I fimbriae are found in almost all subgroups of E.coli, not just in UPEC strains, but the fimbriae function as a virulence factor in the pathogenesis of E.coli UTI; Expression of type I fimbriae undergoes phase variation controlled at the transcriptional level by invertible element. The 70 promoter for FimA is located within this 314bp invertible DNA element flanked on both ends by inverted DNA repeats of 9bp in length. Leucine-responsive protein (LRP), integration host factor (IHF), and the histone-like protein (H-NS) affect the switching of the invertible element by binding to DNA sequences around and within the invertible element region, thus assisting or blocking the switching actions of the FimB and FimE recombinases FimC-FimH chaperone adhesin complex: 1QUN Makes an important contribution to colonization of the bladder FimH is the adhesin protein binding to mannose-containing glycoprotein receptors, known as uroplakins, which are located on the luminal surface of the bladder epithelial cells. This binding is followed by invasion of uroepithelia cells Abstract(s) in PubMed C2_04081 VFG042714 99.2 4.71e-166 457.0 VF1153 VFC0001 Z_RS10335 fimbria/pilus periplasmic chaperone Escherichia coli O157:H7 str. EDL933 C2_04082 VFG042713 100.0 1.49e-122 343.0 VF1153 VFC0001 fimA type 1 fimbrial major subunit FimA Escherichia coli O157:H7 str. EDL933 C2_04106 VFG042570 40.6 5.59e-18 77.4 lda VFC0001 AAX78184 LdaA Escherichia coli C2_04155 VFG026443 46.3 4.6200000000000004e-29 108.0 VF0289 VFC0272 mgtC Possible Mg2+ transport P-type ATPase C MgtC Mycobacterium abscessus subsp. bolletii 50594 MgtC Mycobacterium tuberculosis Nutritional/Metabolic factor Homology to MgtC of Salmonella enterica, which is essential for the survival of S.enterica within macrophages Magnesium acquisition Abstract(s) in PubMed C2_04188 VFG034823 99.8 7.58e-266 726.0 VF1110 VFC0086 espR1 Type III secretion system effector espR1 Escherichia coli O111:H- str. 11128 TTSS secreted effectors Escherichia coli (EHEC) Effector delivery system Cif (Deamidase. Induces cytopathic effects of actin stress fiber formation and cell cycle arrest. ); EspB (Pore formation, actin disruption, microvilli effacement, anti-phagocytosis. ); EspF (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspFu/tccP (Inducing degradation of the aniapoptic protein AbcF2, tight junction disruption, microvilli effacement and elongation, mitochondrial dysfunction, N-WASP activation, SGLT-1 inactivation, pedestal maturation, inhibition of NHE3 activity, membrane remodelling; targets and disrupts the nucleolus late in infection, which is temporally controlled by host mitochondria. ); EspG (TBC-like GTPase activating protein. Efficiently catalyzes GTP hydrolysis in Rab1 to disrupt of Rab1-mediated ER-to-Golgi trafficking. ); EspH (First bacterial effector acting directly on RhoGEFs, EspH directly binds to the DH-PH domain in RhoGEFs to disrupt RhoGEF-Rho signaling; critical for inhibiting macrophage phagocytosis. ); EspJ (Inhibit both IgG- and complement receptor-mediated phagocytosis. ); EspK; EspL1; EspL2 (Cysteine protease. Bounds F-actin-aggregating annexin 2 directly to increase annexin 2's ability to aggregate Tir-induced F-actin; block necroptosis and in flammation. ); EspL4; EspM1 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspM2 (GEF. Activates the RhoA signaling pathway and induce the formation of stress fibres; inhibit pedestal formation and induce tight junction mislocalization. ); EspN; EspO1-1; EspO1-2; EspR1; EspR3; EspR4; EspT (GEF. Activates Rac1 and Cdc42 leading to formation of membrane ruffles and lamellipodia; induces membrane ruffles to facilitate bacterial invasion into non-phagocytic cells in a process involving Rac1 and Wave2. ); EspW; EspX1; EspX2; EspX4; EspX5; EspX6; EspX7/nleL (E3 ubiquitin ligase, HECT-like. Modulates pedestal formation. ); EspY1; EspY2; EspY3; EspY4; EspY5; Map (GEF. Mimics the host Dbl and catalyses the exchange of GDP for GTP in Cdc42, involved in effacement, SGLT1 inhibition, formation of filopodia and disruption of mitochondrial function. ); NleA/espI (Disruption of tight junctions by inhibition of host cell protein trafficking through COPII-dependent pathways. ); NleB1 (Blocks translocation of the p65 and to the host cell nucleus to inhibit NF-B pathway, but NleE and NleB act at different points in the NF-B signaling pathway. ); NleB2 (May also have anti-inflammatory activity. ); NleC (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate RelA (p65), thus blocking NF-B pathway. ); NleD (Metalloprotease. Zn-dependent endopeptidases that specifically clip and inactivate JNK and p38, thus blocking AP-1 pathway. ); NleE (PMN tran-epithelial migration; blocks translocation of the p65 to the host cell nucleus by preventing IB degradation to inhibit NF-B pathway. ); NleF; NleG-1; NleG2-2; NleG2-3; NleG2-4; NleG5-1; NleG5-2; NleG6-1; NleG6-2; NleG6-3; NleG7 (U-box type E3 ubiquitin ligases. ); NleG8-2; NleH1 (Ser/Thr protein kinase. Binds directly to a subunit of NF-B, the ribosomal protein S3 (RPS3), reducing the nuclear abundance of RPS3 to dampen host transcriptional outputs; interact with Bax inhibitor-1 to block apoptosis. ); NleH2 (Putative kinase. Attenuates NF-B pathway. ); SepZ/espZ (EspZ interacts with CD98 in host cell membranes to promote host cell survival, therefore provide the pathogen with valuable time to colonize efficiently prior to dissemination. ); TccP2; Tir (Mimics host immunoreceptor tyrosine-based inhibition motifs (ITIMs), also see helicobacter CagA. EHEC Tir lacks the Nck binding site. Conserved NPY (Asn-Pro-Tyr) motif recruits the adaptor protein IRTKS and/or IRSp53. IRTKS/IRSp53 link Tir and TccP/EspFu, which in turn activates N-WASP; Receptor for intimin; effacement; SGLT1 inhibition; recruits SHIP2 to control actin-pedestal morphology; maintains the integrity of the epithelium by keeping the destructive activity of EspG and EspG2 in check. ) Abstract(s) in PubMed C2_04190 VFG001391 46.9 0.0 1164.0 VF0302 VFC0272 narG nitrate reductase subunit alpha Mycobacterium tuberculosis H37Rv Nitrate reductase Mycobacterium tuberculosis Nutritional/Metabolic factor NarX function as a respiratory fused nitrate reductase (three different domains present in this protein encode the difference subunits of nitrate reductase: the N-terminal domain showing similarity to narG, the central domain showing homology with narJ and the C-terminus showing homology to narI); NarGHJI is a membrane-bound nitrate reductase complex; NarK2, a putative nitrite-extrusion protein Nitrate respiration helps the bacteria to survive in O2-depleted areas of inflammatory or necrotic tissue Abstract(s) in PubMed C2_04191 VFG024081 57.8 2.2200000000000003e-213 601.0 VF0302 VFC0272 narH nitrate reductase subunit beta Mycobacterium indicus pranii MTCC 9506 Nitrate reductase Mycobacterium tuberculosis Nutritional/Metabolic factor NarX function as a respiratory fused nitrate reductase (three different domains present in this protein encode the difference subunits of nitrate reductase: the N-terminal domain showing similarity to narG, the central domain showing homology with narJ and the C-terminus showing homology to narI); NarGHJI is a membrane-bound nitrate reductase complex; NarK2, a putative nitrite-extrusion protein Nitrate respiration helps the bacteria to survive in O2-depleted areas of inflammatory or necrotic tissue Abstract(s) in PubMed C2_04219 VFG009407 50.2 5.100000000000001e-168 481.0 VF0816 VFC0272 glnA1 type I glutamate--ammonia ligase Mycobacterium gilvum PYR-GCK C2_04221 VFG042915 42.3 3.7e-93 291.0 VF1212 VFC0001 DNO_RS02105 sigma-54 dependent transcriptional regulator Dichelobacter nodosus VCS1703A C2_04223 VFG013205 69.2 3.49e-239 660.0 VF0758 VFC0272 hemN oxygen-independent coproporphyrinogen III oxidase Haemophilus somnus 2336 C2_04238 VFG041913 41.0 4.790000000000001e-65 215.0 VF0909 VFC0086 PSPTO_RS07240 transglycosylase SLT domain-containing protein Pseudomonas syringae pv. tomato str. DC3000 C2_04247 VFG049898 100.0 1.11e-113 318.0 VF0579 VFC0086 hcp1/tssD1 type VI secretion system protein, Hcp family Shigella sonnei Ss046 T6SS Type VI secretion system Shigella sonnei Effector delivery system Plays a role in interbacterial competition and host colonization T6SS encoded by chromosome in S. sonnei gives S. sonnei an advantage in a niche-specific enviroment over E. coli, S. flexneri and other closely related species. T6SS predominate S. sonnei colonization in host and help it during interbacterial competition. Abstract(s) in PubMed C2_04248 VFG035469 99.1 0.0 870.0 VF1122 VFC0086 aec31 type VI secretion system ImpA and VasL domain-containing protein Escherichia coli O103:H2 str. 12009 C2_04249 VFG035501 98.6 0.0 2243.0 VF1122 VFC0086 aec30 type VI secretion system membrane subunit TssM Escherichia coli E24377A C2_04250 VFG035526 100.0 9.62e-130 372.0 VF1122 VFC0086 aec29 type VI secretion system protein TssA Escherichia coli UMNK88 C2_04251 VFG035543 100.0 4.72e-176 483.0 VF1122 VFC0086 aec28 type VI secretion system-associated protein TagO Escherichia coli O111:H- str. 11128 C2_04252 VFG035569 99.2 0.0 1721.0 VF1122 VFC0086 aec27/clpV type VI secretion system ATPase TssH Escherichia coli O111:H- str. 11128 C2_04253 VFG035596 100.0 6.759999999999999e-188 514.0 VF1122 VFC0086 aec26 type IVB secretion system protein IcmH/DotU Escherichia coli O26:H11 str. 11368 C2_04254 VFG035621 99.8 0.0 886.0 VF1122 VFC0086 aec25 type VI secretion system baseplate subunit TssK Escherichia coli O111:H- str. 11128 C2_04255 VFG035645 100.0 4.58e-122 341.0 VF1122 VFC0086 aec24 type VI secretion system lipoprotein TssJ Escherichia coli O103:H2 str. 12009 C2_04256 VFG035671 100.0 4.31e-310 837.0 VF1122 VFC0086 aec23 type VI secretion system-associated FHA domain protein TagH Escherichia coli O103:H2 str. 12009 C2_04257 VFG035696 100.0 4.81e-269 728.0 VF1122 VFC0086 aec22 type VI secretion system baseplate subunit TssG Escherichia coli O103:H2 str. 12009 C2_04258 VFG035710 99.7 0.0 1251.0 VF1176 VFC0086 tssF type VI secretion system baseplate subunit TssF Escherichia coli O157:H7 str. EDL933 C2_04259 VFG035740 100.0 1.6e-95 271.0 VF1122 VFC0086 aec19 type VI secretion system baseplate subunit TssE Escherichia coli O55:H7 str. CB9615 C2_04260 VFG035769 100.0 0.0 986.0 VF1122 VFC0086 aec18 type VI secretion system contractile sheath large subunit Escherichia coli O111:H- str. 11128 C2_04261 VFG041049 100.0 3.16e-50 151.0 VF1176 VFC0086 Z_RS01215 hypothetical protein Escherichia coli O157:H7 str. EDL933 C2_04262 VFG049914 100.0 2.48e-113 318.0 VF0579 VFC0086 tssB Type VI secretion system protein TssB Shigella sonnei Ss046 T6SS Type VI secretion system Shigella sonnei Effector delivery system Plays a role in interbacterial competition and host colonization T6SS encoded by chromosome in S. sonnei gives S. sonnei an advantage in a niche-specific enviroment over E. coli, S. flexneri and other closely related species. T6SS predominate S. sonnei colonization in host and help it during interbacterial competition. Abstract(s) in PubMed C2_04263 VFG035808 100.0 4.61e-130 361.0 VF1176 VFC0086 aec16 Hcp family type VI secretion system effector Escherichia coli O157:H7 str. EDL933 C2_04264 VFG041051 98.9 0.0 1160.0 VF1176 VFC0086 Z_RS01240 type VI secretion system tip protein VgrG Escherichia coli O157:H7 str. EDL933 C2_04275 VFG034718 99.7 0.0 1168.0 VF0237 VFC0083 ibeC phosphoethanolamine transferase CptA Escherichia coli E24377A Ibes Invasion of brain endothelial cells Escherichia coli (NMEC) Invasion IbeA is unique to E. coli K1. The ibeB and ibeC are found to have K12 homologues p77211 and yijP respectively. IbeA and IbeB encode outer membrane proteins with three and two transmembrane domains, respectively; IbeC has a signal peptide-like sequence and five or six transmembrane segments at its N terminus Contributes to brain microvascular endothelial cells (BMECs) invasion via a ligand-receptor interaction Unknown; the roles of Ibe proteins in E. coli K1 invasion of BMECs were verified by deletion and complementation experiments Abstract(s) in PubMed C2_04283 VFG044083 40.6 2.13e-10 60.5 VF0094 VFC0272 ptxR transcriptional regulator PtxR Pseudomonas aeruginosa PAO1 Pyoverdine Pseudomonas aeruginosa Nutritional/Metabolic factor A greenish-yellow compound, a hydroxyquinolone chromophore to which an amino acid tail is attached, the tail can vary in length; the synthesis of pyoverdine requires a special factor, PvdS, which is in turn regulated by the Fur repressor; also called pseudobactin Effective at acquiring iron from transferrin and lactoferrin; cytotoxic due to its ability to stimulating the production of reactive oxygen species Pvd is a fluorescent dihydroxyquinoline derivative connected to a small peptide and contains hydroxamate and catecholate residues to chelate ferric ion, Fe (III). Pvd chelates Fe (III) in a 1:1 stoichiometry with high affinity (stability constant, 10**32); FpvA is the specific receptor for Fe(III)-pyoverdin Abstract(s) in PubMed C2_04306 VFG013612 79.4 2.6999999999999997e-208 574.0 VF0758 VFC0272 hemE uroporphyrinogen decarboxylase Haemophilus somnus 129PT C2_04309 VFG043551 41.6 9.84e-18 73.6 VF0867 VFC0001 ML_RS08565 HU family DNA-binding protein Mycobacterium leprae TN C2_04314 VFG019760 45.3 4.07e-117 350.0 VF0082 VFC0001 pilR two-component response regulator PilR Pseudomonas fluorescens SBW25 Type IV pili Pseudomonas aeruginosa Adherence PilA, B, C, D, E, F, M, N, O, P, Q, T, U, V, W, X, Y1, Y2, Z, and fimT, U, V are involved in the biogenesis and mechanical function of pili, pilG, H, I, K, chpA, B, C, D, E, pilS, R, fimS, rpoN, algR, algU, and vfr are involved in transcriptional regulation and chemosensory pathways that control the expression or activity of the twitching motility of the pili Attaches to host cells, but not to mucin, causing a twitching motility that allows the bacteria to move along the cell surface; biofilm formation The C-terminal receptor-binding domain of pilin binds to asialoGM1 gangliosides on host cells. Generally, GM1 gangliosides contain a sialic acid moiety. P.aeruginosa produces a neuraminidase which removes sialic acid residues from the GM1 to form the asialoGM1, which is a better receptor for the pili; The asialoGM1 is present in increased abundance on the surface of cystic fibrosis respiratory epithelial cells Abstract(s) in PubMed C2_04331 VFG000478 99.3 6.05e-108 303.0 VF0113 VFC0301 fur ferric iron uptake transcriptional regulator Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Fur Ferric uptake regulator Salmonella enterica (serovar typhimurium) Regulation Repress the expression of iron-regulated genes; also required for acid-induced activation of atr genes Abstract(s) in PubMed C2_04341 VFG045340 42.5 3.4099999999999995e-24 93.2 VF0695 VFC0086 ricA type IV secretion system effector RicA, Rab2 interacting conserved protein A Brucella melitensis bv. 1 str. 16M T4SS secreted effectors Brucella melitensis Effector delivery system "BPE005 (Might have an effect on cAMP-dependent signaling pathways in the host cell blocking the binding between cAMP and PKA. ); BPE043; BPE123; BPE275; BspA; BspB (Promotes rBCV biogenesis and intracellular proliferation. ); BspC; BspE; BspF (Contributes to bacterial growth within the replication-permissive rBCVs. ); BspL (Regulates the late stages of the Brucella intracellular cycle. ); RicA (Modulates rBCV biogenesis. ); SepA (Endosome-like Brucella-containing vacuole (eBCV) trafficking. ); VceA; VceC (Activating ER stress and further manipulating UPR to inhibit GTC apoptosis. )" Abstract(s) in PubMed C2_04384 VFG013806 44.0 1.3e-34 122.0 VF0082 VFC0001 xcpA/pilD type 4 prepilin peptidase PilD Pseudomonas mendocina ymp Type IV pili Pseudomonas aeruginosa Adherence PilA, B, C, D, E, F, M, N, O, P, Q, T, U, V, W, X, Y1, Y2, Z, and fimT, U, V are involved in the biogenesis and mechanical function of pili, pilG, H, I, K, chpA, B, C, D, E, pilS, R, fimS, rpoN, algR, algU, and vfr are involved in transcriptional regulation and chemosensory pathways that control the expression or activity of the twitching motility of the pili Attaches to host cells, but not to mucin, causing a twitching motility that allows the bacteria to move along the cell surface; biofilm formation The C-terminal receptor-binding domain of pilin binds to asialoGM1 gangliosides on host cells. Generally, GM1 gangliosides contain a sialic acid moiety. P.aeruginosa produces a neuraminidase which removes sialic acid residues from the GM1 to form the asialoGM1, which is a better receptor for the pili; The asialoGM1 is present in increased abundance on the surface of cystic fibrosis respiratory epithelial cells Abstract(s) in PubMed C2_04389 VFG009706 42.9 4.8e-47 153.0 VF0304 VFC0282 sodA superoxide dismutase Mycobacterium sp. JLS SodA Mycobacterium tuberculosis Stress survival Iron-dependent enzyme, important for survival of intracellular pathogens during infection Abstract(s) in PubMed C2_04420 VFG005041 46.1 8.83e-15 68.2 VF0003 VFC0258 SAUSA300_RS00840 CatB-related O-acetyltransferase Staphylococcus aureus subsp. aureus USA300_FPR3757 Capsule Staphylococcus aureus Immune modulation Produced by over 90% of Staphylococcus aureus strains. Two serotypes (5 and 8) predominate among clinical isolates of S. aureus from humans Prevent phagocytosis Abstract(s) in PubMed C2_04468 VFG033838 88.3 0.0 1356.0 VF1114 VFC0271 agn43 autotransporter adhesin Ag43 Escherichia coli O26:H11 str. 11368 C2_04485 VFG031407 44.9 1.89e-150 460.0 VF0849 VFC0272 ctpV copper-translocating P-type ATPase Mycobacterium canettii CIPT 140070010 C2_04499 VFG036043 94.2 0.0 1893.0 VF1133 VFC0001 aatA autotransporter outer membrane beta-barrel domain-containing protein Escherichia coli APEC O1 C2_04505 VFG036017 94.6 0.0 1448.0 VF1129 VFC0271 cah Ag43/Cah family autotransporter adhesin Escherichia coli O103:H2 str. 12009 C2_04517 VFG003671 41.7 1.31e-22 94.0 SPI-1 encode VFC0086 hilD transcriptional regulator HilD Salmonella enterica subsp. enterica serovar Typhi str. CT18 C2_04518 VFG012928 58.0 3.71e-133 380.0 SopA VFC0251 icsP/sopA outer membrane protease of the OmpP family, involved in cleavage of surface exposed IcsA Shigella boydii Sb227 C2_04519 VFG018562 41.2 1.08e-19 85.9 SPI-1 encode VFC0086 hilC invasion transcriptional regulator HilC Salmonella enterica subsp. arizonae serovar 62:z4,z23:-- str. RSK2980 C2_04524 VFG013075 40.8 1.14e-16 77.0 VF0979 VFC0301 virF transcriptional activator VirF Shigella flexneri 2a str. 301 C2_04539 VFG026887 60.5 5.82e-306 853.0 VF0303 VFC0282 katG catalase/peroxidase HPI Mycobacterium smegmatis JS623 KatG Mycobacterium tuberculosis Stress survival Catalase:peroxidase degrades H2O2 and organic peroxides, the major role is to catabolize the peroxides generated by phagocyte NADPH oxidase Abstract(s) in PubMed C2_04559 VFG011816 47.1 6.649999999999999e-45 146.0 VF0326 VFC0258 gmhB D-glycero-beta-D-manno-heptose 1,7-bisphosphate 7-phosphatase Campylobacter fetus subsp. fetus 82-40 LOS Lipooligosaccharide Campylobacter jejuni Immune modulation LOS diversity is important for the ability to colonize a wide variety of hosts and intestinal niches; the ability to generate variation at high frequency, the molecular mimicry evident in LOS structure support a role in the avoidance of host defences; the similarity of LOS structures to host gangliosides and the subsequent ability to generate crossreacting antibodies forms the pathological basis for the association of preceding C. jejuni infection with Guillain-Barre syndrome Abstract(s) in PubMed C2_04562 VFG045346 67.5 1.09e-128 365.0 VF0513 VFC0001 IlpA immunogenic lipoprotein A Vibrio vulnificus YJ016 IlpA Immunogenic lipoprotein A Vibrio vulnificus Adherence Dual functions as an adhesin and an immunostimulant A lipoprotein that stimulates production of proinflammatory cytokines via TLR2 in human monocytes; involved in bacterial adherence to host cells Abstract(s) in PubMed C2_04567 VFG013197 42.5 1.65e-72 227.0 VF0758 VFC0272 hemB porphobilinogen synthase Haemophilus somnus 2336 C2_04570 VFG001206 40.6 5e-41 144.0 VF0272 VFC0272 fbpC iron(III) ABC transporter, ATP-binding protein Neisseria meningitidis MC58 FbpABC Neisseria meningitidis Nutritional/Metabolic factor Encodes a periplasmic-binding protein-dependent iron transport system necessary for the utilization of iron bound to transferrin or iron chelates, FbpA is the periplasmic Fe3+ binding protein Abstract(s) in PubMed C2_04587 VFG049917 74.7 7.38e-121 380.0 VF0579 VFC0086 rhs/PAAR Type VI secretion system protein, PAAR family Shigella sonnei Ss046 T6SS Type VI secretion system Shigella sonnei Effector delivery system Plays a role in interbacterial competition and host colonization T6SS encoded by chromosome in S. sonnei gives S. sonnei an advantage in a niche-specific enviroment over E. coli, S. flexneri and other closely related species. T6SS predominate S. sonnei colonization in host and help it during interbacterial competition. Abstract(s) in PubMed