qseqid VFDB_internal_id pident evalue bitscore VFID VFCID gene protein_name Organism VF_Name VF_FullName Bacteria VFcategory Characteristics Structure Function Mechanism Reference Z1_00012 VFG044365 49.1 2.89e-241 687.0 VF1242 VFC0272 DDA3937_RS14700 TonB-dependent siderophore receptor Dickeya dadantii 3937 Z1_00026 VFG013421 78.1 4.05e-107 305.0 VF0044 VFC0258 gmhA/lpcA phosphoheptose isomerase 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 Z1_00034 VFG045607 49.6 2.46e-73 223.0 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 Z1_00038 VFG042917 44.2 1.16e-89 272.0 VF1212 VFC0001 DNO_RS03295 type IV pilus twitching motility protein PilT Dichelobacter nodosus VCS1703A Z1_00042 VFG013268 55.4 2.49e-72 217.0 VF0044 VFC0258 orfM deoxyribonucleotide triphosphate pyrophosphatase 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 Z1_00043 VFG013626 68.7 1.67e-196 546.0 VF0758 VFC0272 hemN radical SAM family heme chaperone HemW Haemophilus influenzae 86-028NP Z1_00063 VFG000531 43.6 3.1e-14 70.9 SPI-1 encode VFC0086 hilC AraC family transcriptional regulator Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Z1_00076 VFG045670 40.0 1.21e-09 58.5 VF0362 VFC0271 bopD sugar-binding transcriptional regulator, LacI family Enterococcus faecium Aus0004 BopD Enterococcus faecalis Biofilm Homologous to a sugar-binding transcriptional regulator involved in biofilm production; The actual role is unknown, but the association of enhanced biofilm formation in the presence of glucose and the possible involvement of a sugar-binding transcriptional regulator suggest a linkage to increased biofilm production in E. faecalis in the presence of specific carbohydrates Abstract(s) in PubMed Z1_00086 VFG043807 99.8 0.0 918.0 VF1332 VFC0235 PMI_RS01355 serralysin family metalloprotease Proteus mirabilis HI4320 Z1_00087 VFG044153 53.9 2.21e-192 552.0 VF0940 VFC0272 PFL_RS27280 type I secretion system permease/ATPase Pseudomonas fluorescens Pf-5 Z1_00088 VFG044152 40.1 1.48e-95 294.0 VF0940 VFC0272 PFL_RS27275 HlyD family type I secretion periplasmic adaptor subunit Pseudomonas fluorescens Pf-5 Z1_00094 VFG042629 100.0 3.36e-76 219.0 MR/P VFC0001 mrpJ transcriptional regulator MrpJ Proteus mirabilis HI4320 Z1_00095 VFG042628 99.6 1.42e-200 548.0 MR/P VFC0001 mrpH MR/P fimbria adhesin subunit MrpH Proteus mirabilis HI4320 Z1_00096 VFG042627 100.0 2.33e-128 357.0 MR/P VFC0001 PMI_RS01305 type 1 fimbrial protein Proteus mirabilis HI4320 Z1_00097 VFG042626 100.0 2.4e-104 295.0 MR/P VFC0001 PMI_RS01300 fimbrial protein Proteus mirabilis HI4320 Z1_00098 VFG042625 100.0 3.7400000000000003e-129 359.0 MR/P VFC0001 PMI_RS01295 fimbrial protein Proteus mirabilis HI4320 Z1_00099 VFG042624 100.0 9.17e-181 496.0 MR/P VFC0001 mrpD MR/P fimbria assembly chaperone MrpD Proteus mirabilis HI4320 Z1_00100 VFG042623 100.0 0.0 1751.0 MR/P VFC0001 mrpC MR/P fimbria usher protein MrpC Proteus mirabilis HI4320 Z1_00101 VFG042622 100.0 1.42e-130 363.0 MR/P VFC0001 mrpB MR/P fimbria assembly terminator MrpB Proteus mirabilis HI4320 Z1_00102 VFG042621 100.0 2.26e-118 332.0 MR/P VFC0001 mrpA MR/P fimbria major subunit MrpA Proteus mirabilis HI4320 Z1_00103 VFG042620 100.0 8.109999999999999e-141 389.0 MR/P VFC0001 mrpI phase variation DNA invertase MrpI Proteus mirabilis HI4320 Z1_00107 VFG042637 59.1 5.81e-55 171.0 VF1232 VFC0001 mrfG MrfG Photorhabdus luminescens str. K122 Z1_00108 VFG021581 40.0 5.53e-21 84.7 VF0958 VFC0001 stfE fimbrial protein Salmonella enterica subsp. enterica serovar Enteritidis str. P125109 Z1_00109 VFG038417 49.8 1.34e-77 234.0 VF0486 VFC0001 fimD fimbrial chaperone protein Aeromonas hydrophila ML09-119 Type I pili Aeromonas hydrophila Adherence Short-rigid pili; chaperone-usher pathway assembled pili Involved in the initial stages of colonisation Abstract(s) in PubMed Z1_00125 VFG044290 98.6 1.14e-107 302.0 VF1252 VFC0272 PMI_RS01160 ParB N-terminal domain-containing protein Proteus mirabilis HI4320 Z1_00126 VFG044289 99.5 2.7199999999999998e-278 753.0 VF1252 VFC0272 PMI_RS01155 ABC transporter substrate-binding protein Proteus mirabilis HI4320 Z1_00127 VFG044288 98.8 4.89e-277 752.0 VF1252 VFC0272 PMI_RS01150 MFS transporter Proteus mirabilis HI4320 Z1_00128 VFG044287 98.7 4.630000000000001e-291 786.0 VF1252 VFC0272 PMI_RS01145 NAD/NADP-dependent octopine/nopaline dehydrogenase family protein Proteus mirabilis HI4320 Z1_00129 VFG044286 99.7 3.24e-244 663.0 VF1252 VFC0272 PMI_RS01140 cysteine synthase family protein Proteus mirabilis HI4320 Z1_00130 VFG044285 98.9 0.0 945.0 VF1252 VFC0272 PMI_RS01135 Y4yA family PLP-dependent enzyme Proteus mirabilis HI4320 Z1_00131 VFG044284 99.6 0.0 1380.0 VF1252 VFC0272 PMI_RS01130 TonB-dependent siderophore receptor Proteus mirabilis HI4320 Z1_00132 VFG044283 99.2 0.0 1283.0 VF1252 VFC0272 PMI_RS01125 IucA/IucC family siderophore biosynthesis protein Proteus mirabilis HI4320 Z1_00133 VFG044282 99.6 7.63e-202 551.0 VF1252 VFC0272 PMI_RS01120 CoA ester lyase Proteus mirabilis HI4320 Z1_00134 VFG044281 98.1 3.8300000000000004e-179 493.0 VF1252 VFC0272 PMI_RS01115 ABC transporter ATP-binding protein Proteus mirabilis HI4320 Z1_00135 VFG044280 99.2 1.08e-240 656.0 VF1252 VFC0272 PMI_RS01110 iron ABC transporter permease Proteus mirabilis HI4320 Z1_00146 VFG041913 44.3 3.31e-60 204.0 VF0909 VFC0086 PSPTO_RS07240 transglycosylase SLT domain-containing protein Pseudomonas syringae pv. tomato str. DC3000 Z1_00149 VFG005580 59.6 3.45e-168 479.0 VF1060 VFC0251 eno phosphopyruvate hydratase Streptococcus pneumoniae TIGR4 Z1_00152 VFG001887 43.0 7.759999999999999e-219 631.0 VF0260 VFC0301 relA GTP diphosphokinase Legionella pneumophila subsp. pneumophila str. Philadelphia 1 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 Z1_00158 VFG013203 70.1 1.54e-229 634.0 VF0758 VFC0272 hemL glutamate-1-semialdehyde 2,1-aminomutase Haemophilus somnus 2336 Z1_00167 VFG009302 49.1 5.65e-67 211.0 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 Z1_00168 VFG008117 52.6 1.84e-37 124.0 VF0319 VFC0272 panD aspartate 1-decarboxylase Mycobacterium liflandii 128FXT 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 Z1_00181 VFG041225 43.6 5.05e-29 109.0 VF1264 VFC0086 hcp type VI secretion system tube protein Hcp Citrobacter rodentium ICC168 Z1_00226 VFG049129 62.7 1.46e-153 439.0 VF0568 VFC0325 acrA acriflavine resistance protein A Klebsiella pneumoniae subsp. pneumoniae HS11286 AcrAB Klebsiella pneumoniae Antimicrobial activity/Competitive advantage May mediate resistance against host-derived antimicrobial peptides; associated with antibiotic resistance Abstract(s) in PubMed Z1_00227 VFG049146 75.9 0.0 1535.0 VF0568 VFC0325 acrB acriflavine resistance protein B Klebsiella variicola At-22 AcrAB Klebsiella pneumoniae Antimicrobial activity/Competitive advantage May mediate resistance against host-derived antimicrobial peptides; associated with antibiotic resistance Abstract(s) in PubMed Z1_00239 VFG043478 44.8 1.15e-08 49.3 VF1230 VFC0001 PM_RS08640 ComEA family DNA-binding protein Pasteurella multocida subsp. multocida str. Pm70 Z1_00240 VFG032882 41.5 3.95e-10 61.2 VF0449 VFC0315 prsA2 post translocation chaperone PrsA2 Listeria monocytogenes HCC23 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 Z1_00244 VFG000077 64.4 3.62e-87 255.0 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 Z1_00284 VFG009680 40.8 2.36e-34 120.0 VF0306 VFC0282 ahpC peroxiredoxin Mycobacterium smegmatis str. MC2 155 AhpC Mycobacterium tuberculosis Stress survival Alkyl hydroperoxide reductase involved in protecting mycobacteria from the oxidative and nitrosative responses of macrophages Abstract(s) in PubMed Z1_00285 VFG047605 49.9 1.7399999999999997e-170 497.0 VF0553 VFC0272 ggt gamma-glutamyltranspeptidase Francisella cf. novicida Fx1 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 Z1_00298 VFG009865 40.4 5.33e-52 167.0 VF0298 VFC0301 mprA response regulator transcription factor Mycobacterium vanbaalenii PYR-1 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 Z1_00330 VFG047710 57.5 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 Z1_00331 VFG047726 47.6 2.66e-119 351.0 VF0558 VFC0272 carA carbamoyl phosphate synthase small subunit Francisella tularensis subsp. tularensis SCHU S4 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 Z1_00339 VFG044083 40.0 9.86e-09 55.5 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 Z1_00341 VFG015291 48.5 3.03e-10 60.8 VF0911 VFC0086 hopI1 DnaJ domain-containing protein Pseudomonas syringae pv. syringae B728a Z1_00342 VFG043573 61.6 1.46e-237 672.0 VF0713 VFC0001 dnaK chaperone protein DnaK Chlamydia trachomatis D/UW-3/CX Z1_00353 VFG042570 41.3 1.65e-19 86.7 lda VFC0001 AAX78184 LdaA Escherichia coli Z1_00381 VFG006496 64.3 1.6999999999999998e-92 268.0 VF0050 VFC0282 ureG urease accessory protein (ureG) Helicobacter hepaticus ATCC 51449 Urease Helicobacter pylori Stress survival ~550kDa nickel metalloenzyme comprised of two distinct subunits-UreA and UreB, the UreEFGH proteins are required for activation of urease by incorporating nickel ions into the urease apoenzyme, UreI functions as an acid-dependent urea channel; PDB code: 1E9Z An important colonization factor, contributes to acid resistance, epithelial cell damage, chemotactic behavior, and nitrogen metabolism A Ni2+-containing enzyme, catalyzes the hydrolysis of urea to ammonium and carbon dioxide. Urea channels (UreI) present in the inner membrane are opened at pH<6.5, allowing delivery of urea to urease. The ammonia produced diffuses into, and thus buffers the periplasm. Abstract(s) in PubMed Z1_00384 VFG006476 62.7 4.31e-261 725.0 VF0050 VFC0282 ureB urease beta subunit UreB, urea amidohydrolase Helicobacter hepaticus ATCC 51449 Urease Helicobacter pylori Stress survival ~550kDa nickel metalloenzyme comprised of two distinct subunits-UreA and UreB, the UreEFGH proteins are required for activation of urease by incorporating nickel ions into the urease apoenzyme, UreI functions as an acid-dependent urea channel; PDB code: 1E9Z An important colonization factor, contributes to acid resistance, epithelial cell damage, chemotactic behavior, and nitrogen metabolism A Ni2+-containing enzyme, catalyzes the hydrolysis of urea to ammonium and carbon dioxide. Urea channels (UreI) present in the inner membrane are opened at pH<6.5, allowing delivery of urea to urease. The ammonia produced diffuses into, and thus buffers the periplasm. Abstract(s) in PubMed Z1_00386 VFG006471 61.0 1.04e-35 120.0 VF0050 VFC0282 ureA urease alpha subunit UreA Helicobacter hepaticus ATCC 51449 Urease Helicobacter pylori Stress survival ~550kDa nickel metalloenzyme comprised of two distinct subunits-UreA and UreB, the UreEFGH proteins are required for activation of urease by incorporating nickel ions into the urease apoenzyme, UreI functions as an acid-dependent urea channel; PDB code: 1E9Z An important colonization factor, contributes to acid resistance, epithelial cell damage, chemotactic behavior, and nitrogen metabolism A Ni2+-containing enzyme, catalyzes the hydrolysis of urea to ammonium and carbon dioxide. Urea channels (UreI) present in the inner membrane are opened at pH<6.5, allowing delivery of urea to urease. The ammonia produced diffuses into, and thus buffers the periplasm. Abstract(s) in PubMed Z1_00403 VFG015769 40.6 6.93e-81 258.0 VF0091 VFC0271 mucD serine protease MucD precursor Pseudomonas putida W619 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 Z1_00404 VFG014988 42.3 2.85e-85 263.0 VF0091 VFC0271 algW AlgW protein 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 Z1_00416 VFG011729 46.9 1.14e-83 255.0 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 Z1_00421 VFG042736 56.0 6.22e-177 506.0 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 Z1_00453 VFG041964 44.8 3.57e-06 47.4 VF1301 VFC0086 XCC_RS00270 avirulence protein Xanthomonas campestris pv. campestris str. ATCC 33913 Z1_00454 VFG043534 49.5 9.850000000000001e-143 414.0 VF0694 VFC0001 ugpB sn-glycerol-3-phosphate ABC transporter substrate-binding protein UgpB Brucella melitensis bv. 1 str. 16M Z1_00457 VFG030679 47.2 3.17e-108 322.0 VF0842 VFC0272 sugC sn-glycerol-3-phosphate ABC transporter ATP-binding protein UgpC Mycobacterium smegmatis str. MC2 155 Z1_00481 VFG015921 46.7 7.24e-06 48.5 VF0920 VFC0325 hcnB cyanide-forming glycine dehydrogenase subunit HcnB Pseudomonas aeruginosa PA7 Z1_00493 VFG043319 46.2 2.71e-82 264.0 VF0157 VFC0204 fleQ transcriptional regulator FleQ 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 Z1_00501 VFG024083 57.7 6.29e-204 577.0 VF0302 VFC0272 narH nitrate reductase subunit beta Mycobacterium intracellulare MOTT-02 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 Z1_00502 VFG009597 49.3 0.0 1221.0 VF0302 VFC0272 narG nitrate reductase subunit alpha Mycobacterium vanbaalenii PYR-1 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 Z1_00520 VFG013201 50.3 2.35e-59 182.0 VF0758 VFC0272 hemG menaquinone-dependent protoporphyrinogen IX dehydrogenase Haemophilus somnus 2336 Z1_00589 VFG015903 43.7 3.72e-82 252.0 VF0917 VFC0235 argK ornithine carbamoyltransferase Pseudomonas syringae pv. phaseolicola 1448A Z1_00591 VFG047700 43.4 1.05e-70 221.0 VF0558 VFC0272 pyrB aspartate carbamoyltransferase Francisella sp. TX077308 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 Z1_00605 VFG033369 47.4 2.19e-84 256.0 VF0221 VFC0001 fimH FimH protein precursor Escherichia coli O78:H11:K80 str. H10407 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 Z1_00606 VFG012313 52.1 9.800000000000001e-59 180.0 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 Z1_00607 VFG048281 51.5 3.460000000000001e-56 174.0 VF0566 VFC0001 fimF type 1 fimbrial minor component Klebsiella oxytoca KCTC 1686 Type I fimbriae Klebsiella pneumoniae Adherence Type I fimbriae are expressed in 90% of both clinical and environmental K. pneumoniae isolates as well as almost all members of the Enterobacteriaceae.; Type I fimbriae are filamentous, membrane-bound, adhesive structures composed primarily of FimA subunits, with the FimH subunit on the tip. Adhering to human mucosal or epithelial surfaces Abstract(s) in PubMed Z1_00608 VFG046058 55.6 6.43e-286 805.0 VF0221 VFC0001 fimD Outer membrane usher protein fimD precursor Escherichia coli VR50 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 Z1_00609 VFG012337 46.2 1.2e-07 46.2 VF0222 VFC0001 sfaF S fimbriae outer membrane usher SfaF Escherichia coli UTI89 S fimbriae Escherichia coli (UPEC) Adherence Encoded by sfa operon composed of nine genes Composed of a major subunit SfaA and three minor subunits SfaG, SfaH and SfaS. The SfaS subunit has been localized to S pilus tips and can mediate bacterial interactions with sialic acid residues on receptors S fimbriae binds to receptors containing sialic acid sugar moieties, the sialic acid residues are presented on UP3, one of four integral membrane uroplakin proteins Abstract(s) in PubMed Z1_00610 VFG048260 59.9 1.02e-87 258.0 VF0566 VFC0001 fimC periplasmic chaperone Klebsiella oxytoca E718 Type I fimbriae Klebsiella pneumoniae Adherence Type I fimbriae are expressed in 90% of both clinical and environmental K. pneumoniae isolates as well as almost all members of the Enterobacteriaceae.; Type I fimbriae are filamentous, membrane-bound, adhesive structures composed primarily of FimA subunits, with the FimH subunit on the tip. Adhering to human mucosal or epithelial surfaces Abstract(s) in PubMed Z1_00611 VFG048240 57.2 5.37e-61 187.0 VF0566 VFC0001 fimA type 1 major fimbrial subunit precursor Klebsiella oxytoca E718 Type I fimbriae Klebsiella pneumoniae Adherence Type I fimbriae are expressed in 90% of both clinical and environmental K. pneumoniae isolates as well as almost all members of the Enterobacteriaceae.; Type I fimbriae are filamentous, membrane-bound, adhesive structures composed primarily of FimA subunits, with the FimH subunit on the tip. Adhering to human mucosal or epithelial surfaces Abstract(s) in PubMed Z1_00631 VFG039491 47.2 5.49e-40 131.0 VF0696 VFC0086 CBU_1434 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 Z1_00635 VFG013515 74.1 1.76e-238 658.0 VF0755 VFC0258 mrsA/glmM phosphoglucosamine mutase Haemophilus influenzae PittEE Z1_00660 VFG037101 41.3 1.24e-34 128.0 VF0456 VFC0282 msrA/B(pilB ) trifunctional thioredoxin/methionine sulfoxide reductase A/B protein Neisseria gonorrhoeae FA 1090 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 Z1_00661 VFG038900 60.3 5.47e-182 515.0 VF0646 VFC0235 hlyA Hemolysin A Aeromonas hydrophila subsp. hydrophila ATCC 7966 Z1_00665 VFG010532 43.9 1.79e-47 155.0 VF0153 VFC0315 mip macrophage infectivity potentiator Mip Legionella pneumophila str. Lens 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 Z1_00719 VFG013198 64.4 2.77e-133 381.0 VF0758 VFC0272 hemC hydroxymethylbilane synthase Haemophilus somnus 2336 Z1_00720 VFG013611 45.1 1.72e-61 193.0 VF0758 VFC0272 hemD uroporphyrinogen-III synthase Haemophilus somnus 129PT Z1_00721 VFG013632 40.9 3.93e-64 211.0 VF0758 VFC0272 hemX uroporphyrinogen-III C-methyltransferase Haemophilus influenzae 86-028NP Z1_00734 VFG007661 74.8 8.240000000000002e-160 446.0 VF0624 VFC0258 rmlA glucose-1-phosphate thymidylyltransferase RfbA Vibrio fischeri ES114 Z1_00735 VFG007659 80.1 4.8799999999999996e-216 594.0 VF0624 VFC0258 rmlB dTDP-glucose 4,6-dehydratase Vibrio fischeri ES114 Z1_00736 VFG007635 68.9 6.520000000000001e-208 578.0 VF0624 VFC0258 wecC UDP-N-acetyl-D-mannosamine dehydrogenase Vibrio vulnificus CMCP6 Z1_00737 VFG007640 71.2 9.4e-194 539.0 VF0624 VFC0258 wbjD/wecB UDP-N-acetylglucosamine 2-epimerase (non-hydrolyzing) Vibrio vulnificus YJ016 Z1_00738 VFG023778 65.6 3.78e-157 444.0 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 Z1_00739 VFG013510 52.9 1.81e-119 349.0 VF0044 VFC0258 wecA undecaprenyl-phosphate alpha-N-acetylglucosaminyltransferase 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 Z1_00764 VFG045340 46.1 1.88e-24 94.0 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 Z1_00806 VFG046459 82.4 2.4100000000000007e-245 671.0 VF0460 VFC0001 tufA elongation factor Tu Francisella philomiragia subsp. philomiragia ATCC 25017 EF-Tu Francisella tularensis Adherence Surface-expressed elongation factor-Tu (EF-Tu) mediates attachment by interacting with host cell nucleolin Abstract(s) in PubMed Z1_00840 VFG016393 43.6 1.01e-25 105.0 VF0659 VFC0258 BCE_RS28105 glycosyltransferase family 2 protein Bacillus cereus ATCC 10987 Z1_00867 VFG007688 41.0 2.36e-12 67.4 VF0624 VFC0258 cpsF glycosyltransferase Vibrio parahaemolyticus RIMD 2210633 Z1_00872 VFG047095 44.7 1.86e-96 291.0 VF0542 VFC0258 wbtI DegT/DnrJ/EryC1/StrS family aminotransferase Francisella tularensis subsp. tularensis SCHU S4 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 Z1_00873 VFG018672 40.5 1.64e-19 89.0 VF0144 VFC0258 SGO_RS05030 glycosyltransferase family 2 protein Streptococcus gordonii str. Challis substr. CH1 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 Z1_00882 VFG019126 42.2 2.87e-25 102.0 VF0144 VFC0258 SPCG_RS01850 glycosyltransferase Streptococcus pneumoniae CGSP14 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 Z1_00884 VFG038088 53.2 1.33e-90 269.0 VF0465 VFC0258 M3Q_RS01495 glycosyltransferase Acinetobacter baumannii TYTH-1 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 Z1_00885 VFG019018 62.4 7.28e-146 413.0 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 Z1_00886 VFG048973 79.4 4.07e-227 624.0 VF0560 VFC0258 ugd UDP-glucose 6-dehydrogenase 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 Z1_00890 VFG005975 44.8 6.57e-17 75.9 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 Z1_00899 VFG013409 78.4 6.42e-178 493.0 VF0044 VFC0258 rfaD ADP-L-glycero-D-mannoheptose-6-epimerase 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 Z1_00900 VFG013400 60.6 1.45e-141 404.0 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 Z1_00901 VFG013152 58.0 2.61e-118 343.0 VF0044 VFC0258 opsX/rfaC heptosyltransferase I 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 Z1_00907 VFG013310 52.7 1.46e-148 428.0 VF0044 VFC0258 kdtA 3-deoxy-d-manno-octulosonic-acid transferase 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 Z1_00908 VFG013315 49.4 1.51e-78 237.0 VF0044 VFC0258 lgtF beta-1,4-glucosyltransferase 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 Z1_00909 VFG000320 42.7 7.63e-44 142.0 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 Z1_00991 VFG013144 40.1 2.04e-68 219.0 VF0753 VFC0001 comE/pilQ type IV pilus secretin PilQ Haemophilus somnus 2336 Z1_00996 VFG046612 65.8 7.53e-99 286.0 VF0543 VFC0258 rpe ribulose-phosphate 3-epimerase Francisella cf. tularensis subsp. novicida 3523 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 Z1_01000 VFG009705 40.6 2.6e-41 139.0 VF0304 VFC0282 sodA superoxide dismutase Mycobacterium smegmatis str. MC2 155 SodA Mycobacterium tuberculosis Stress survival Iron-dependent enzyme, important for survival of intracellular pathogens during infection Abstract(s) in PubMed Z1_01031 VFG047265 51.3 1.6399999999999998e-152 441.0 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 Z1_01033 VFG013192 44.6 6.86e-68 214.0 VF0268 VFC0272 hitC iron(III) ABC transporter, ATP-binding protein Haemophilus somnus 2336 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 Z1_01043 VFG004554 40.0 9.32e-07 47.4 VF0014 VFC0271 icaR ica operon transcriptional regulator IcaR Staphylococcus aureus RF122 Intercellular adhesion proteins Staphylococcus aureus Biofilm IcaA, icaB, icaC, icaD synthesize a polysaccharide, poly-n-succinyl--1,6 glucosamine (PNSG) during infection PNSG is critical to biofilm elaboration, allowing bacteria to adhere to one another, and may also promote adherence to other molecules, such as ECM components Abstract(s) in PubMed Z1_01063 VFG050173 45.7 2.59e-76 235.0 HA VFC0258 hasC UTP--glucose-1-phosphate uridylyltransferase Bacillus anthracis str. Ames Ancestor Z1_01132 VFG034418 52.0 3.34e-50 161.0 VF0404 VFC0001 yagZ/ecpA E. coli common pilus structural subunit EcpA Escherichia coli O17:K52:H18 str. UMN026 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 Z1_01133 VFG034435 42.3 2.31e-59 186.0 VF0404 VFC0001 yagY/ecpB E. coli common pilus chaperone EcpB Escherichia coli O103:H2 str. 12009 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 Z1_01138 VFG048740 46.6 1.17e-09 50.1 VF0569 VFC0086 KPHS_23120 PaaR repeat-containing protein Klebsiella pneumoniae subsp. pneumoniae HS11286 T6SS Klebsiella pneumoniae Effector delivery system Type VI bacterial lipase/phospholipase effectors (Tle) has been sub-divided into Tle1–Tle5. The Tle1–Tle4 families exhibit the GXSXG motif, while Tle5 present a dual HXKXXXXD motif Antibacterial activity The type VI membrane-targeting phospholipase effector Tle1 and Tli1 immunity proteins play a role in intraspecies antagonism Abstract(s) in PubMed Z1_01142 VFG041173 40.1 2.24e-112 355.0 VF0975 VFC0086 SG_RS05305 type VI secretion system tip protein VgrG Salmonella enterica subsp. enterica serovar Gallinarum str. 287/91 Z1_01143 VFG051500 60.6 2.03e-76 225.0 VF0943 VFC0086 hcpA Hcp family type VI secretion system effector Pseudomonas entomophila L48 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 Z1_01161 VFG023976 40.6 2e-14 70.1 VF0289 VFC0272 mgtC Possible Mg2+ transport P-type ATPase C MgtC Mycobacterium intracellulare ATCC 13950 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 Z1_01171 VFG044219 57.7 3.19e-92 271.0 VF0584 VFC0272 GBAA_RS25985 siderophore ABC transporter ATP-binding protein Bacillus anthracis str. Ames Ancestor Petrobactin Bacillus anthracis Nutritional/Metabolic factor Catechol-based siderophore;the biosynthetic pathway for petrobactin (the asb operon), the petrobactin-iron complex receptor (FhuA), import permeases (FpuB/FatC/FatD), ATPases (FpuC/FatE), and the petrobactin exporter (ApeX) Required for virulence in murine models of inhalational anthrax;Protects against oxidative stress and improve sporulation Abstract(s) in PubMed Z1_01173 VFG044221 41.4 1.2e-76 238.0 VF0584 VFC0272 GBAA_RS25995 iron chelate uptake ABC transporter family permease subunit Bacillus anthracis str. Ames Ancestor Petrobactin Bacillus anthracis Nutritional/Metabolic factor Catechol-based siderophore;the biosynthetic pathway for petrobactin (the asb operon), the petrobactin-iron complex receptor (FhuA), import permeases (FpuB/FatC/FatD), ATPases (FpuC/FatE), and the petrobactin exporter (ApeX) Required for virulence in murine models of inhalational anthrax;Protects against oxidative stress and improve sporulation Abstract(s) in PubMed Z1_01210 VFG047394 46.9 1.73e-237 681.0 VF0550 VFC0272 feoB Fe(2+) transporter permease subunit FeoB Francisella novicida U112 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 Z1_01211 VFG045722 55.8 2.28e-10 51.2 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 Z1_01240 VFG038216 40.9 5.549999999999998e-54 173.0 VF0463 VFC0301 bfmR biofilm-controlling response regulator Acinetobacter baumannii 1656-2 Z1_01246 VFG013205 68.7 1.05e-233 647.0 VF0758 VFC0272 hemN oxygen-independent coproporphyrinogen III oxidase Haemophilus somnus 2336 Z1_01247 VFG042915 42.5 1.58e-96 300.0 VF1212 VFC0001 DNO_RS02105 sigma-54 dependent transcriptional regulator Dichelobacter nodosus VCS1703A Z1_01249 VFG009407 48.7 2.04e-162 467.0 VF0816 VFC0272 glnA1 type I glutamate--ammonia ligase Mycobacterium gilvum PYR-GCK Z1_01308 VFG041304 41.1 9.12e-22 87.4 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 Z1_01311 VFG042734 65.8 2.12e-95 276.0 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 Z1_01319 VFG035450 49.7 3.64e-54 168.0 VF1122 VFC0086 aec32 Hcp family type VI secretion system effector Escherichia coli O44:H18 042 Z1_01322 VFG050680 60.0 3.64e-14 75.5 VF1334 VFC0001 pilJ methyl-accepting chemotaxis protein Acinetobacter baumannii TCDC-AB0715 TFP Type IV pili Acinetobacter baumannii Adherence Essential for twitching motility and natural competence, and contribute to host cell adherence Abstract(s) in PubMed Z1_01323 VFG015638 63.3 4.51e-14 75.1 VF0082 VFC0001 pilJ twitching motility protein PilJ Pseudomonas putida GB-1 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 Z1_01339 VFG046474 82.2 2.4100000000000007e-245 671.0 VF0460 VFC0001 tufA elongation factor Tu Francisella noatunensis subsp. orientalis str. Toba 04 EF-Tu Francisella tularensis Adherence Surface-expressed elongation factor-Tu (EF-Tu) mediates attachment by interacting with host cell nucleolin Abstract(s) in PubMed Z1_01352 VFG044378 41.7 2.9299999999999997e-55 181.0 VF0937 VFC0272 qbsC QbsC Pseudomonas fluorescens ATCC 17400 Z1_01357 VFG013200 78.0 8.290000000000001e-206 568.0 VF0758 VFC0272 hemE uroporphyrinogen decarboxylase Haemophilus somnus 2336 Z1_01360 VFG043551 42.7 1.38e-17 73.2 VF0867 VFC0001 ML_RS08565 HU family DNA-binding protein Mycobacterium leprae TN Z1_01373 VFG001381 61.3 4.13e-178 504.0 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 Z1_01377 VFG049118 43.4 4.38e-66 207.0 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 Z1_01382 VFG013531 77.4 0.0 873.0 VF0755 VFC0258 pgi glucose-6-phosphate isomerase Haemophilus influenzae 86-028NP Z1_01390 VFG013727 40.7 7.93e-07 51.6 VF0740 VFC0272 ciuD ABC transporter ATP-binding protein Corynebacterium diphtheriae NCTC 13129 Z1_01406 VFG045910 45.5 3.43e-261 748.0 ELF VFC0001 elfC fimbrial biogenesis usher protein Escherichia coli O7:K1 str. IAI39 Z1_01435 VFG020377 43.8 1.61e-44 150.0 SPI-1 encode VFC0086 prgK type III secretion system inner MS ring protein PrgK Salmonella enterica subsp. enterica serovar Agona str. SL483 Z1_01436 VFG025179 41.3 5.03e-09 48.9 VF0428 VFC0086 bsaK Type III secretion system protein BsaK Burkholderia mallei ATCC 23344 Bsa T3SS Burkholderia pseudomallei Effector delivery system Mxi-SpaA like T3SS, shares homology to Salmonella SPI-1 and Shigella T3SSs; Two additional T3SSs are discovered in B. Pseudomallei. T3SS1 is only present in B. pseudomallei and not in Burkholderia mallei or Burkholderia thailandensis, whereas T3SS2 and T3SS3 (Bsa) are present in all three species. T3SS1 and T3SS2 are closely related to the T3SS of the plant pathogens R. solanacearum and Xanthomonas spp. T3SS1 and T3SS2 are required during B. pseudomallei infection of tomato plants but not for infection of hamsters. Delivering effector proteins into host cells to manipulate host cell functions Three effectors: BopE, homolog of SopE and SopE2 of Salmonella, functions as GTPase involving bacterial invasion. BopA, homolog of IcsB of Shigella, suppresses autophagy. BopC, function unkown. Abstract(s) in PubMed Z1_01437 VFG012643 47.9 5.48e-14 60.8 VF0118 VFC0086 mxiH type III secretion system needle filament protein MxiH Shigella dysenteriae Sd197 TTSS Type III secretion system Shigella flexneri Effector delivery system Encoded on the large virulence plasimid; The activity of type III secretion systems is tightly regulated. It is activated upon contact with the cellular surface; Abbreviations: Ipg for invasion plasmid gene; Spa for surface presentation of invasion plasmid antigens; Mxi for membrane excretion of Ipa Composed of an external needle, a transmembrane domain and a cytoplasmic bulb, together termed the 'needle complex' Mxi-Spa system secretes approximately 20 proteins with the four Ipas A, B,C,D and IpgD being the most abundant; Recent findings indicate that TTSS in Shigella is responsible not only for protein secretion, but that it is also involved in the control mechanisms of transcription of other target genes located on the virulence plasmid, virA and ipaH9.8, these proteins were not constitutively synthesized and stored in the bacterial cytoplasm; their expression was markedly increased after initial activation of the secretion system, virA is not required for entry;Upon contact of the tip of the needle with the plasma membrane, the injectisome secretes its protein substrates into host cells. Some of these substrates act as translocators or effectors whose functions are key to the invasion of the cytosol and the cell-to-cell spread characterizing the lifestyle of Shigella spp. Abstract(s) in PubMed Z1_01440 VFG020107 40.2 1.19e-119 365.0 VF0118 VFC0086 mxiD type III secretion system secretin MxiD Shigella boydii CDC 3083-94 TTSS Type III secretion system Shigella flexneri Effector delivery system Encoded on the large virulence plasimid; The activity of type III secretion systems is tightly regulated. It is activated upon contact with the cellular surface; Abbreviations: Ipg for invasion plasmid gene; Spa for surface presentation of invasion plasmid antigens; Mxi for membrane excretion of Ipa Composed of an external needle, a transmembrane domain and a cytoplasmic bulb, together termed the 'needle complex' Mxi-Spa system secretes approximately 20 proteins with the four Ipas A, B,C,D and IpgD being the most abundant; Recent findings indicate that TTSS in Shigella is responsible not only for protein secretion, but that it is also involved in the control mechanisms of transcription of other target genes located on the virulence plasmid, virA and ipaH9.8, these proteins were not constitutively synthesized and stored in the bacterial cytoplasm; their expression was markedly increased after initial activation of the secretion system, virA is not required for entry;Upon contact of the tip of the needle with the plasma membrane, the injectisome secretes its protein substrates into host cells. Some of these substrates act as translocators or effectors whose functions are key to the invasion of the cytosol and the cell-to-cell spread characterizing the lifestyle of Shigella spp. Abstract(s) in PubMed Z1_01442 VFG003525 53.1 7.84e-227 648.0 VF1025 VFC0086 ysaV EscV/YscV/HrcV family type III secretion system export apparatus protein Yersinia enterocolitica subsp. enterocolitica 8081 Ysa TTSS Yersinia secretion apparatus (Ysa) Yersinia enterocolitica Effector delivery system Ysa system is encoded on the chromosome of highly virulent Y. enterocolitica biovar 1B strains Plays a role in colonization of the gut and the subsequent systemic phase of the disease Responsible for secreting at least 15 Ysps (Yersinia secreted proteins; also been shown to export some of the Yops Abstract(s) in PubMed Z1_01444 VFG003523 52.8 7.25e-155 444.0 VF1025 VFC0086 ysaN type III secretion system ATPase SctN Yersinia enterocolitica subsp. enterocolitica 8081 Ysa TTSS Yersinia secretion apparatus (Ysa) Yersinia enterocolitica Effector delivery system Ysa system is encoded on the chromosome of highly virulent Y. enterocolitica biovar 1B strains Plays a role in colonization of the gut and the subsequent systemic phase of the disease Responsible for secreting at least 15 Ysps (Yersinia secreted proteins; also been shown to export some of the Yops Abstract(s) in PubMed Z1_01448 VFG025091 57.7 1.71e-81 242.0 VF0428 VFC0086 spaP surface presentation of antigens protein SpaP Burkholderia thailandensis E264 Bsa T3SS Burkholderia pseudomallei Effector delivery system Mxi-SpaA like T3SS, shares homology to Salmonella SPI-1 and Shigella T3SSs; Two additional T3SSs are discovered in B. Pseudomallei. T3SS1 is only present in B. pseudomallei and not in Burkholderia mallei or Burkholderia thailandensis, whereas T3SS2 and T3SS3 (Bsa) are present in all three species. T3SS1 and T3SS2 are closely related to the T3SS of the plant pathogens R. solanacearum and Xanthomonas spp. T3SS1 and T3SS2 are required during B. pseudomallei infection of tomato plants but not for infection of hamsters. Delivering effector proteins into host cells to manipulate host cell functions Three effectors: BopE, homolog of SopE and SopE2 of Salmonella, functions as GTPase involving bacterial invasion. BopA, homolog of IcsB of Shigella, suppresses autophagy. BopC, function unkown. Abstract(s) in PubMed Z1_01449 VFG002454 63.8 1.38e-30 102.0 VF0428 VFC0086 bsaX Type III secretion system protein BsaX Burkholderia pseudomallei K96243 Bsa T3SS Burkholderia pseudomallei Effector delivery system Mxi-SpaA like T3SS, shares homology to Salmonella SPI-1 and Shigella T3SSs; Two additional T3SSs are discovered in B. Pseudomallei. T3SS1 is only present in B. pseudomallei and not in Burkholderia mallei or Burkholderia thailandensis, whereas T3SS2 and T3SS3 (Bsa) are present in all three species. T3SS1 and T3SS2 are closely related to the T3SS of the plant pathogens R. solanacearum and Xanthomonas spp. T3SS1 and T3SS2 are required during B. pseudomallei infection of tomato plants but not for infection of hamsters. Delivering effector proteins into host cells to manipulate host cell functions Three effectors: BopE, homolog of SopE and SopE2 of Salmonella, functions as GTPase involving bacterial invasion. BopA, homolog of IcsB of Shigella, suppresses autophagy. BopC, function unkown. Abstract(s) in PubMed Z1_01450 VFG003517 45.5 3.89e-54 175.0 VF1025 VFC0086 ysaT type III secretion system export apparatus subunit SctT Yersinia enterocolitica subsp. enterocolitica 8081 Ysa TTSS Yersinia secretion apparatus (Ysa) Yersinia enterocolitica Effector delivery system Ysa system is encoded on the chromosome of highly virulent Y. enterocolitica biovar 1B strains Plays a role in colonization of the gut and the subsequent systemic phase of the disease Responsible for secreting at least 15 Ysps (Yersinia secreted proteins; also been shown to export some of the Yops Abstract(s) in PubMed Z1_01451 VFG041463 42.8 2.24e-91 278.0 VF1271 VFC0086 EAMY_RS21105 EscU/YscU/HrcU family type III secretion system export apparatus switch protein Erwinia amylovora CFBP1430 Z1_01452 VFG000988 53.1 1.2899999999999997e-54 169.0 VF0118 VFC0086 ipgC type III secretion system chaperone for IpaB and IpaC Shigella flexneri 2a str. 301 TTSS Type III secretion system Shigella flexneri Effector delivery system Encoded on the large virulence plasimid; The activity of type III secretion systems is tightly regulated. It is activated upon contact with the cellular surface; Abbreviations: Ipg for invasion plasmid gene; Spa for surface presentation of invasion plasmid antigens; Mxi for membrane excretion of Ipa Composed of an external needle, a transmembrane domain and a cytoplasmic bulb, together termed the 'needle complex' Mxi-Spa system secretes approximately 20 proteins with the four Ipas A, B,C,D and IpgD being the most abundant; Recent findings indicate that TTSS in Shigella is responsible not only for protein secretion, but that it is also involved in the control mechanisms of transcription of other target genes located on the virulence plasmid, virA and ipaH9.8, these proteins were not constitutively synthesized and stored in the bacterial cytoplasm; their expression was markedly increased after initial activation of the secretion system, virA is not required for entry;Upon contact of the tip of the needle with the plasma membrane, the injectisome secretes its protein substrates into host cells. Some of these substrates act as translocators or effectors whose functions are key to the invasion of the cytosol and the cell-to-cell spread characterizing the lifestyle of Shigella spp. Abstract(s) in PubMed Z1_01475 VFG043577 44.6 9.94e-55 181.0 VF0619 VFC0001 gbpA N-acetylglucosamine-binding protein GbpA Vibrio cholerae O1 biovar El Tor str. N16961 GbpA N-Acetylglucosamine (GlcNAc)-binding protein A Vibrio cholerae Adherence Mucin contains extensively different types of carbohydrates, the residue, N-acetyl-D-glucosamine (GlcNAc), is one of the most abundant sugars in the carbohydrate side chains A four-domain structure of which domains 1 and 4 interact with chitin and domain 1 is also crucial for mucin binding and intestinal colonization. Domains 2 and 3 anchor to the V. cholerae surfaces A mucin-binding protein essential for intestinal colonization Abstract(s) in PubMed Z1_01500 VFG010484 74.9 1.33e-271 750.0 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 Z1_01700 VFG026971 60.3 5.38e-91 286.0 VF0257 VFC0301 sigA/rpoV RNA polymerase sigma factor Mycobacterium tuberculosis CAS/NITR204 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 Z1_01714 VFG013435 70.4 2.92e-238 660.0 VF0044 VFC0258 rfaE ADP-heptose synthase 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 Z1_01720 VFG044140 61.2 7.97e-178 506.0 VF1029 VFC0272 tolC outer membrane channel protein TolC Yersinia pestis CO92 Z1_01728 VFG042333 99.5 0.0 2178.0 Pta VFC0086 pta autotransporter Pta Proteus mirabilis HI4320 Z1_01790 VFG045688 45.4 1.62e-69 214.0 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 Z1_01791 VFG002189 42.1 3.3300000000000003e-31 117.0 VF0361 VFC0258 cpsB/cdsA phosphatidate cytidylyltransferase Enterococcus faecalis V583 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 Z1_01792 VFG015009 43.9 1.18e-120 359.0 VF0091 VFC0271 mucP metalloprotease protease Pseudomonas fluorescens Pf-5 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 Z1_01795 VFG013165 57.2 2.840000000000001e-103 306.0 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 Z1_01796 VFG011400 46.3 4.7599999999999987e-42 137.0 VF0367 VFC0258 fabZ (3R)-hydroxymyristoyl ACP dehydratase Brucella melitensis biovar Abortus 2308 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 Z1_01797 VFG013393 61.0 3.71e-91 270.0 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 Z1_01798 VFG013386 63.0 2.32e-163 463.0 VF0044 VFC0258 lpxB lipid-A-disaccharide synthase 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 Z1_01809 VFG045346 63.5 3.44e-125 357.0 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 Z1_01812 VFG002552 49.0 5.03e-51 162.0 VF0436 VFC0258 wcbN D-glycero-d-manno-heptose 1,7-bisphosphate phosphatase Burkholderia pseudomallei K96243 Capsule I Type I O-polysaccharide Burkholderia pseudomallei Immune modulation A key virulence determinant and that loss of capsule production results in severe attenuation in animal models of disease Plays a role in reducing B. pseudomallei phagocytosis by host cells by preventing complement factor C3b deposition on the surface of the bacterium Abstract(s) in PubMed Z1_01831 VFG015885 51.5 6.57e-61 188.0 VF0917 VFC0235 cysC1 adenylyl-sulfate kinase Pseudomonas syringae pv. phaseolicola 1448A Z1_01839 VFG000477 79.9 4.81e-178 495.0 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 Z1_01846 VFG042651 52.3 2.51e-45 147.0 VF1151 VFC0001 pixA PixA protein Escherichia coli str. X2194 Z1_01848 VFG042585 58.5 0.0 1016.0 VF1149 VFC0001 HKK20_RS00075 PapC/FimD family outer membrane usher protein Escherichia coli O157:H- str. 3072/96 Z1_01849 VFG042654 65.9 9.8e-112 320.0 VF1151 VFC0001 pixD PixD protein Escherichia coli str. X2194 Z1_01852 VFG000889 40.7 2.29e-34 119.0 VF0220 VFC0001 papF P pilus minor subunit PapF Escherichia coli CFT073 P fimbriae Escherichia coli (UPEC) Adherence Mannose-resistant (MRHA); Pap pili expression is tightly regulated in response to several environmental and nutritional factors, also controlled by a methylation-dependent phase variation mechanims; The pap operon is a useful example of pilus assembly since it contains many conserved features:; PapD, a conserved chaperone molecule with an Ig-like domain, is necessary to transport several pilus subunits from the cytoplasmic membrane to the outer membrane; PapD-subunit complexes are targeted to the PapC outer membrane usher, which forms a pore through which the the pili are translocated across the OM; The major subunit is PapA, which is assembled into a 6.8-nm thick helical rod that is anchored in the OM by PapH; At the distal end of the pilus rod is a 2-nm linear tip fibrillum composed of a PapE, which is adapted to the PapA rod by PapK. PapG is joined to the PapE tip fibrillum by the adapter protein PapF PapG adhesin receptor binding domain-unbound form: 1J8S; binary complex of the PapG receptor-binding domain bound To Gbo4 receptor PapG mediates binding to the -D-galactopyranosyl-(1-4)--D-galactopyranoside (Gal(1,4)Gal) moiety present in a globoseries of glycolipids found on host cells lining the upper urinary tract and erythrocytes; three adhesin variants of PapG-G-I, G-II, G-III recognize three different but related Gal(1,4)Gal receptors; PapG-mediated interactions with its Gal(1,4)Gal-containing glycolipid receptor can activate specific responses in the bacteria and in the epithelial cell that promote virulence: activating the UPEC iron-acquisition system and triggering the intracellular release from receptor glycolipids of ceramide, an important second messenger that can activate cytokine production, through the activation of serine/threonine protein kinases and phosphatase Abstract(s) in PubMed Z1_01856 VFG021661 42.7 5.65e-46 152.0 VF0961 VFC0001 stiB fimbrial biogenesis chaperone StiB Salmonella enterica subsp. enterica serovar Paratyphi C strain RKS4594 Z1_01857 VFG021660 43.0 2.86e-231 671.0 VF0961 VFC0001 stiC fimbrial outer membrane usher protein Salmonella enterica subsp. enterica serovar Schwarzengrund str. CVM19633 Z1_01872 VFG049114 56.2 2.44e-121 350.0 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 Z1_01885 VFG013617 49.1 8.4e-110 322.0 VF0758 VFC0272 hemH ferrochelatase Haemophilus somnus 129PT Z1_01886 VFG003407 41.7 1.38e-77 243.0 VF0392 VFC0258 fepE LPS O-antigen length regulator 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 Z1_01895 VFG031402 42.3 2.5000000000000002e-146 454.0 VF0849 VFC0272 ctpV copper-translocating P-type ATPase Mycobacterium indicus pranii MTCC 9506 Z1_01908 VFG013326 50.2 2.8e-79 238.0 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 Z1_01997 VFG012939 84.6 6.460000000000001e-192 528.0 VF0124 VFC0258 gtrB bactoprenol glucosyl transferase Shigella flexneri 5 str. 8401 LPS Shigella flexneri Immune modulation Composed of the O-antigen, core polysaccharides and lipid A; the genes involved in the biosynthesis of the basic O-antigen are located in the rfb/rfc loci; O-antigen modification is associated with temperate bacteriophages. Four different serotype-converting phages have been found: SfII, Sf6, SfV and SfX, which are involved in conversion of a serotype Y stain to serotypes 2a, 3b, 5a and X, respectively Required for resistance to host defense and for the intracellular spread, but not for bacterial invasion Abstract(s) in PubMed Z1_02028 VFG042332 99.2 1.49e-149 417.0 VF1293 VFC0086 aipA trimeric autotransporter adhesin AipA Proteus mirabilis HI4320 Z1_02062 VFG026391 46.9 4.03e-55 173.0 VF0814 VFC0272 leuD 3-isopropylmalate dehydratase small subunit Mycobacterium smegmatis JS623 Z1_02084 VFG013417 73.7 3.76e-170 473.0 VF0044 VFC0258 lpxC UDP-3-O-(R-3-hydroxymyristoyl)-N-acetylglucosamine deacetylase 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 Z1_02088 VFG042331 99.4 0.0 2911.0 VF1292 VFC0086 hpmA calcium-independent hemolysin HpmA Proteus mirabilis HI4320 Z1_02089 VFG042330 99.3 0.0 1107.0 VF1292 VFC0086 hpmB hemolysin secretion/activation protein HpmB Proteus mirabilis HI4320 Z1_02095 VFG045987 48.9 1.06e-109 328.0 HCP VFC0001 hcpB type II secretion system protein GspE Escherichia coli O104:H4 str. 2009EL-2050 Z1_02096 VFG045955 47.8 1.76e-36 122.0 HCP VFC0001 hcpA prepilin peptidase-dependent pilin Escherichia coli CFT073 Z1_02102 VFG000983 44.2 0.0 1992.0 VF0265 VFC0235 rtxA RTX toxin RtxA Vibrio cholerae O1 biovar El Tor str. N16961 MARTX Multifunctional autoprocessing RTX toxin Vibrio cholerae Exotoxin MARTX toxins are large exotoxins of 350-560 kDa produced by many species of Vibrio; RTX toxin is not associated with the hemolytic or cytolytic activities typical of other RTX toxins; the V. cholerae RTX gene cluster show significant similarity to members of the RTX family, such as hemolysin of E. coli and Cya adenylate cyclase in B. pertussis; The RTX toxin encoding gene rtxA is located adjacent to the ctx genes MARTXVc is composed of extensive 18- to 20-aa glycinerich repeats, an InsP6-inducible autoprocessing cysteine protease, and three effector domains: actin cross-linking domain, -hydrolase domain and Rho inactivation domain; N-and C-terminal repeat regions are thought to mediate host cell binding and translocation Inducing cytopathic activities in host cells including actin depolymerization, Rho inactivation, caspase 3/7-dependent apoptosis, and induction of reactive oxygen species; important for evasion of phagocytes The actin cross-linking domain (ACDVc) causes cell rounding by covalently crosslinking monomeric G-actin to form actin oligomers. It is related to the glutamine synthetase family of enzymes and irreversibly connects G-actin monomers via isopeptide bonds between residues Lys-50 and Glu-270 in the presence of ATP and Mg2+/Mn2+; Rho inactivation domain (RIDVc) induces a 90% decrease in cellular levels of active GTP-bound RhoA (RhoA-GTP) as well as reduced activation of related GTPases Cdc42 and Rac, the net results of the loss of active RhoA GTPases is depolymerization of the actin cytoskeleton Abstract(s) in PubMed Z1_02103 VFG038912 47.7 1.93e-09 55.5 VF0482 VFC0235 rtxA multifunctional autoprocessing repeats-in-toxins (MARTX) toxin Aeromonas hydrophila subsp. hydrophila ATCC 7966 RtxA The repeat in toxin Aeromonas hydrophila Exotoxin A member of a protein family that is produced by a wide range of Gram-negative bacteria, such as Vibrio cholerae, V. vulnificus, V. anguillarum, Actinobacillus actinomycetemcomitans, Actinobacillus pleuropneumoniae,etc.; the rtx operon consists of six genes (rtxACHBDE) in which rtxA encodes an exotoxin, rtxC codes for an RtxA activator, rtxH encodes a conserved hypothetical protein and rtxBDE genes code for an ABC transporter; important characteristics of this toxin include:; I) it requires post-translational modification, i.e., acylation to become biologically active; II) has a COOH-terminal calcium-binding domain with tandem glycine/aspartic acid-rich repeats; III) it has a high molecular mass of usually 100 to>400 kDa; IV) it is delivered to the extracellular milieu through the T1SS Inducing host cell rounding and apoptosis Actin cross-linking domain of RtxA catalyzed the covalent cross-linking of the host cellular actin, thus disrupted the actin cytoskeleton of host cells Abstract(s) in PubMed Z1_02104 VFG038915 69.6 9.93e-18 70.1 VF0482 VFC0235 rtxH conserved hypothetical protein in rtx gene loci Aeromonas hydrophila subsp. hydrophila ATCC 7966 RtxA The repeat in toxin Aeromonas hydrophila Exotoxin A member of a protein family that is produced by a wide range of Gram-negative bacteria, such as Vibrio cholerae, V. vulnificus, V. anguillarum, Actinobacillus actinomycetemcomitans, Actinobacillus pleuropneumoniae,etc.; the rtx operon consists of six genes (rtxACHBDE) in which rtxA encodes an exotoxin, rtxC codes for an RtxA activator, rtxH encodes a conserved hypothetical protein and rtxBDE genes code for an ABC transporter; important characteristics of this toxin include:; I) it requires post-translational modification, i.e., acylation to become biologically active; II) has a COOH-terminal calcium-binding domain with tandem glycine/aspartic acid-rich repeats; III) it has a high molecular mass of usually 100 to>400 kDa; IV) it is delivered to the extracellular milieu through the T1SS Inducing host cell rounding and apoptosis Actin cross-linking domain of RtxA catalyzed the covalent cross-linking of the host cellular actin, thus disrupted the actin cytoskeleton of host cells Abstract(s) in PubMed Z1_02115 VFG038918 49.1 5.98e-218 627.0 VF0482 VFC0235 rtxE RTX toxin transporter, ATPase protein Aeromonas hydrophila subsp. hydrophila ATCC 7966 RtxA The repeat in toxin Aeromonas hydrophila Exotoxin A member of a protein family that is produced by a wide range of Gram-negative bacteria, such as Vibrio cholerae, V. vulnificus, V. anguillarum, Actinobacillus actinomycetemcomitans, Actinobacillus pleuropneumoniae,etc.; the rtx operon consists of six genes (rtxACHBDE) in which rtxA encodes an exotoxin, rtxC codes for an RtxA activator, rtxH encodes a conserved hypothetical protein and rtxBDE genes code for an ABC transporter; important characteristics of this toxin include:; I) it requires post-translational modification, i.e., acylation to become biologically active; II) has a COOH-terminal calcium-binding domain with tandem glycine/aspartic acid-rich repeats; III) it has a high molecular mass of usually 100 to>400 kDa; IV) it is delivered to the extracellular milieu through the T1SS Inducing host cell rounding and apoptosis Actin cross-linking domain of RtxA catalyzed the covalent cross-linking of the host cellular actin, thus disrupted the actin cytoskeleton of host cells Abstract(s) in PubMed Z1_02116 VFG007029 47.9 2.63e-121 361.0 VF0265 VFC0235 rtxD RTX toxin transporter RtxD Vibrio vulnificus CMCP6 MARTX Multifunctional autoprocessing RTX toxin Vibrio cholerae Exotoxin MARTX toxins are large exotoxins of 350-560 kDa produced by many species of Vibrio; RTX toxin is not associated with the hemolytic or cytolytic activities typical of other RTX toxins; the V. cholerae RTX gene cluster show significant similarity to members of the RTX family, such as hemolysin of E. coli and Cya adenylate cyclase in B. pertussis; The RTX toxin encoding gene rtxA is located adjacent to the ctx genes MARTXVc is composed of extensive 18- to 20-aa glycinerich repeats, an InsP6-inducible autoprocessing cysteine protease, and three effector domains: actin cross-linking domain, -hydrolase domain and Rho inactivation domain; N-and C-terminal repeat regions are thought to mediate host cell binding and translocation Inducing cytopathic activities in host cells including actin depolymerization, Rho inactivation, caspase 3/7-dependent apoptosis, and induction of reactive oxygen species; important for evasion of phagocytes The actin cross-linking domain (ACDVc) causes cell rounding by covalently crosslinking monomeric G-actin to form actin oligomers. It is related to the glutamine synthetase family of enzymes and irreversibly connects G-actin monomers via isopeptide bonds between residues Lys-50 and Glu-270 in the presence of ATP and Mg2+/Mn2+; Rho inactivation domain (RIDVc) induces a 90% decrease in cellular levels of active GTP-bound RhoA (RhoA-GTP) as well as reduced activation of related GTPases Cdc42 and Rac, the net results of the loss of active RhoA GTPases is depolymerization of the actin cytoskeleton Abstract(s) in PubMed Z1_02117 VFG007023 47.8 6.84e-210 605.0 VF0265 VFC0235 rtxB RTX toxin transporter RtxB Vibrio cholerae O1 biovar El Tor str. N16961 MARTX Multifunctional autoprocessing RTX toxin Vibrio cholerae Exotoxin MARTX toxins are large exotoxins of 350-560 kDa produced by many species of Vibrio; RTX toxin is not associated with the hemolytic or cytolytic activities typical of other RTX toxins; the V. cholerae RTX gene cluster show significant similarity to members of the RTX family, such as hemolysin of E. coli and Cya adenylate cyclase in B. pertussis; The RTX toxin encoding gene rtxA is located adjacent to the ctx genes MARTXVc is composed of extensive 18- to 20-aa glycinerich repeats, an InsP6-inducible autoprocessing cysteine protease, and three effector domains: actin cross-linking domain, -hydrolase domain and Rho inactivation domain; N-and C-terminal repeat regions are thought to mediate host cell binding and translocation Inducing cytopathic activities in host cells including actin depolymerization, Rho inactivation, caspase 3/7-dependent apoptosis, and induction of reactive oxygen species; important for evasion of phagocytes The actin cross-linking domain (ACDVc) causes cell rounding by covalently crosslinking monomeric G-actin to form actin oligomers. It is related to the glutamine synthetase family of enzymes and irreversibly connects G-actin monomers via isopeptide bonds between residues Lys-50 and Glu-270 in the presence of ATP and Mg2+/Mn2+; Rho inactivation domain (RIDVc) induces a 90% decrease in cellular levels of active GTP-bound RhoA (RhoA-GTP) as well as reduced activation of related GTPases Cdc42 and Rac, the net results of the loss of active RhoA GTPases is depolymerization of the actin cytoskeleton Abstract(s) in PubMed Z1_02144 VFG004237 74.1 5.68e-86 250.0 VF0954 VFC0001 stbA type 1 fimbrial protein Salmonella enterica subsp. enterica serovar Typhi str. Ty2 Z1_02145 VFG021457 64.4 4.2e-115 330.0 VF0954 VFC0001 stbB fimbrial biogenesis chaperone StbB Salmonella enterica subsp. enterica serovar Dublin str. CT_02021853 Z1_02146 VFG018332 68.7 0.0 1206.0 VF0954 VFC0001 stbC fimbrial outer membrane usher protein Salmonella enterica subsp. enterica serovar Paratyphi B str. SPB7 Z1_02147 VFG021441 69.4 5.07e-214 596.0 VF0954 VFC0001 stbD fimbrial usher protein StbD Salmonella enterica subsp. enterica serovar Gallinarum str. 287/91 Z1_02148 VFG021435 56.6 1.98e-91 269.0 VF0954 VFC0001 stbE fimbrial biogenesis chaperone StbE Salmonella enterica subsp. enterica serovar Schwarzengrund str. CVM19633 Z1_02155 VFG038332 51.2 4.85e-86 257.0 VF0479 VFC0086 exsA Type III secretion system transcriptional regulator Aeromonas salmonicida subsp. salmonicida A449 T3SS Aeromonas salmonicida Effector delivery system Similar to the Yersinia T3SS "A needle-like structure, often described as an ""injectisome"" that can inject effectors directly into the cytoplasm of target cells; five effectors have been described: AexT, AexU, AopP, AopH and AopO; AexT and AexU are bifunctional toxins that contain a GTPase activating domain, allowing the interruption of host cell-signalling pathways and an ADP-ribosylating domain that can disrupt the host cytoskeleton, leading to the induction of apoptosis; AopP (NF-B inhibitor), AopH (tyrosine phosphatase) and AopO (serine/threonine kinase), all are able to interrupt host cell signalling pathways and induce toxicity" Abstract(s) in PubMed Z1_02166 VFG013287 61.3 4.36e-150 425.0 VF0044 VFC0258 galE UDP-glucose 4-epimerase 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 Z1_02172 VFG012633 56.8 6.899999999999999e-281 785.0 VF1117 VFC0272 ireA TonB-dependent siderophore receptor IreA Escherichia coli CFT073 Z1_02215 VFG037129 41.9 1.32e-82 268.0 VF0457 VFC0282 recN DNA repair protein RecN Neisseria meningitidis M04-240196 RecN Neisseria meningitidis Stress survival Recombinational repair protein that protects against ROS and non-oxidative killing by neutrophils Abstract(s) in PubMed Z1_02222 VFG000121 65.6 1.4e-86 253.0 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 Z1_02235 VFG042614 99.5 1.35e-127 355.0 VF1236 VFC0001 PMI_RS09285 type 1 fimbrial protein Proteus mirabilis HI4320 Z1_02236 VFG042613 99.7 4.97e-265 717.0 VF1236 VFC0001 PMI_RS09280 fimbrial protein Proteus mirabilis HI4320 Z1_02237 VFG042612 100.0 1.93e-183 503.0 VF1236 VFC0001 PMI_RS09275 molecular chaperone Proteus mirabilis HI4320 Z1_02238 VFG042611 99.9 0.0 1668.0 VF1236 VFC0001 PMI_RS09270 fimbria/pilus outer membrane usher protein Proteus mirabilis HI4320 Z1_02239 VFG042610 99.5 8.04e-121 338.0 VF1236 VFC0001 PMI_RS09265 fimbrial protein Proteus mirabilis HI4320 Z1_02244 VFG043345 44.9 6.359999999999998e-113 338.0 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 Z1_02267 VFG031464 46.6 2.44e-35 119.0 VF0851 VFC0258 ndk nucleoside-diphosphate kinase Mycobacterium gilvum PYR-GCK Z1_02382 VFG037029 69.0 8.48e-245 678.0 VF0454 VFC0282 katA catalase Neisseria gonorrhoeae FA 1090 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 Z1_02393 VFG049010 90.5 6.280000000000001e-132 369.0 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 Z1_02434 VFG037973 45.9 1.1e-09 54.7 VF0465 VFC0258 A1S_0057 capsular polysaccharide synthesis enzyme Acinetobacter baumannii ATCC 17978 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 Z1_02441 VFG013438 55.9 4.24e-118 342.0 VF0044 VFC0258 htrB lipid A biosynthesis lauroyl acyltransferase 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 Z1_02442 VFG001746 44.2 1.25e-06 45.1 chromosomally encoded VFC0086 YPO_RS02280 two component system response regulator Yersinia pestis CO92 Z1_02459 VFG004044 62.4 2.58e-89 263.0 VF0106 VFC0272 mgtC Mg2+ transport protein Salmonella enterica subsp. enterica serovar Typhi str. CT18 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 Z1_02460 VFG002359 81.0 1.92e-59 178.0 VF0394 VFC0204 flhD flagellar transcriptional activator FlhD 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 Z1_02461 VFG002687 82.8 3.6600000000000004e-110 312.0 VF0394 VFC0204 flhC flagellar biosynthesis transcription activator FlhC Yersinia pestis CO92 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 Z1_02462 VFG043213 72.3 2.75e-142 402.0 VF0394 VFC0204 motA flagellar motor protein MotA 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 Z1_02463 VFG043212 63.9 3.36e-116 342.0 VF0394 VFC0204 motB flagellar motor protein MotB 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 Z1_02464 VFG043211 64.9 4.31e-293 818.0 VF0394 VFC0204 cheA chemotaxis protein CheA 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 Z1_02465 VFG043210 81.0 5.959999999999998e-82 239.0 VF0394 VFC0204 cheW purine-binding chemotaxis protein CheW 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 Z1_02466 VFG043209 57.7 1.92e-139 415.0 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 Z1_02467 VFG014047 43.8 9.96e-19 89.7 VF0082 VFC0001 pilJ twitching motility protein PilJ Pseudomonas syringae pv. phaseolicola 1448A 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 Z1_02468 VFG043208 62.2 3.98e-125 358.0 VF0394 VFC0204 cheR chemotaxis methyltransferase CheR 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 Z1_02469 VFG043038 76.6 6.85e-188 522.0 VF0967 VFC0204 cheB chemotaxis response regulator protein-glutamate methylesterase Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Z1_02470 VFG043206 83.7 1.34e-72 212.0 VF0394 VFC0204 cheY chemotaxis regulatory protein CheY 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 Z1_02471 VFG043205 73.6 7.89e-100 288.0 VF0394 VFC0204 cheZ chemotaxis regulator CheZ 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 Z1_02472 VFG017341 63.5 6.92e-165 466.0 VF0394 VFC0204 flhB flagellar biosynthetic protein FlhB Yersinia pseudotuberculosis IP 31758 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 Z1_02473 VFG023690 77.9 0.0 1026.0 VF0394 VFC0204 flhA flagellar biosynthesis protein FlhA Yersinia enterocolitica subsp. palearctica 105.5R(r) 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 Z1_02474 VFG042317 40.6 1.21e-09 60.5 VF1261 VFC0086 CV_RS09355 hemagglutinin repeat-containing protein Chromobacterium violaceum ATCC 12472 Z1_02475 VFG002354 43.2 7.83e-35 118.0 VF0394 VFC0204 flgN flagella synthesis protein FlgN 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 Z1_02476 VFG023684 50.5 3.49e-24 87.8 VF0394 VFC0204 flgM negative regulator of flagellin synthesis Yersinia enterocolitica subsp. palearctica 105.5R(r) 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 Z1_02478 VFG002351 65.0 1.06e-59 180.0 VF0394 VFC0204 flgB flagellar basal-body rod protein FlgB 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 Z1_02479 VFG002679 77.6 3.73e-70 206.0 VF0394 VFC0204 flgC flagellar basal-body rod protein FlgC Yersinia pestis CO92 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 Z1_02481 VFG002677 53.0 9.92e-142 410.0 VF0394 VFC0204 flgE flagellar hook protein FlgE Yersinia pestis CO92 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 Z1_02482 VFG023672 62.9 1.51e-107 310.0 VF0394 VFC0204 flgF flagellar basal-body rod protein FlgF Yersinia enterocolitica subsp. palearctica 105.5R(r) 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 Z1_02483 VFG003433 83.5 9.65e-155 431.0 VF0394 VFC0204 flgG flagellar basal-body rod protein FlgG Yersinia pseudotuberculosis IP 32953 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 Z1_02484 VFG002345 75.4 5.6e-120 341.0 VF0394 VFC0204 flgH flagellar L-ring protein precursor FlgH 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 Z1_02485 VFG043029 76.3 7.04e-187 521.0 VF0967 VFC0204 flgI flagellar biosynthesis protein FlgA Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Z1_02486 VFG002343 54.8 3.29e-106 313.0 VF0394 VFC0204 flgJ -N-acetylglucosaminidase 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 Z1_02487 VFG002671 50.7 2.9e-186 534.0 VF0394 VFC0204 flgK flagellar hook-associated protein 1 FlgK Yersinia pestis CO92 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 Z1_02488 VFG002670 46.5 3.69e-90 271.0 VF0394 VFC0204 flgL flagellar hook-associated protein 3 FlgL Yersinia pestis CO92 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 Z1_02490 VFG002669 62.7 2.72e-105 305.0 VF0394 VFC0204 fliR flagellar biosynthetic protein FliR Yersinia pestis CO92 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 Z1_02491 VFG002339 77.5 1.1099999999999999e-41 131.0 VF0394 VFC0204 fliQ flagellar biosynthetic protein FliQ 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 Z1_02492 VFG002338 78.3 6e-127 360.0 VF0394 VFC0204 fliP flagellar biosynthetic protein FliP 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 Z1_02493 VFG043065 53.4 3.79e-26 95.5 VF0967 VFC0204 fliO flagellar biosynthesis protein Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Z1_02494 VFG043064 67.9 6.48e-56 171.0 VF0967 VFC0204 fliN flagellar motor switch protein FliN Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Z1_02495 VFG002335 78.7 1.42e-193 535.0 VF0394 VFC0204 fliM flagellar motor switch protein FliM 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 Z1_02496 VFG023647 53.4 2.02e-48 153.0 VF0394 VFC0204 fliL flagellar basal body protein FliL Yersinia enterocolitica subsp. palearctica 105.5R(r) 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 Z1_02497 VFG002333 47.5 1.6e-27 114.0 VF0394 VFC0204 fliK flagellar hook-length control protein FliK 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 Z1_02498 VFG002332 62.1 3.96e-53 164.0 VF0394 VFC0204 fliJ flagellar protein FliJ 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 Z1_02499 VFG002331 79.9 2.38e-253 696.0 VF0394 VFC0204 fliI flagellum-specific ATP synthase FliI 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 Z1_02500 VFG023639 60.3 1.01e-57 183.0 VF0394 VFC0204 fliH flagellar assembly protein H Yersinia enterocolitica subsp. palearctica 105.5R(r) 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 Z1_02501 VFG002329 81.7 1.1899999999999998e-188 522.0 VF0394 VFC0204 fliG flagellar motor switch protein G 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 Z1_02502 VFG023635 59.4 2.92e-224 632.0 VF0394 VFC0204 fliF flagellar M-ring protein FliF Yersinia enterocolitica subsp. palearctica 105.5R(r) 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 Z1_02503 VFG002327 58.4 5.180000000000001e-35 115.0 VF0394 VFC0204 fliE flagellar hook-basal body complex protein FliE 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 Z1_02508 VFG002326 43.0 9.63e-23 85.5 VF0394 VFC0204 fliT flagellar protein FliT 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 Z1_02509 VFG043053 58.7 8.089999999999999e-46 145.0 VF0967 VFC0204 fliS flagellar export chaperone FliS Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Z1_02510 VFG002653 48.7 5.020000000000001e-124 369.0 VF0394 VFC0204 fliD flagellar capping protein FliD Yersinia pestis CO92 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 Z1_02511 VFG011232 53.9 4.92e-95 288.0 VF0685 VFC0204 flaA flagellin FliC Bordetella avium 197N Z1_02513 VFG002319 83.5 6.39e-134 376.0 VF0394 VFC0204 fliA flagellar biosynthesis sigma factor 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 Z1_02514 VFG002318 67.3 1.06e-76 226.0 VF0394 VFC0204 fliZ alternative sigma factor regulatory protein 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 Z1_02541 VFG011225 40.9 1.7e-34 120.0 VF0684 VFC0258 pagP lipid IV(A) palmitoyltransferase PagP Bordetella pertussis Tohama I Z1_02561 VFG047574 43.7 6.92e-88 268.0 VF0559 VFC0272 purM phosphoribosylaminoimidazole synthetase Francisella sp. TX077308 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 Z1_02587 VFG044099 42.9 2.25e-63 201.0 VF0941 VFC0272 PA4705 hypothetical protein Pseudomonas aeruginosa PAO1 Z1_02588 VFG044141 43.5 2.66e-26 103.0 VF1029 VFC0272 YPO_RS20725 energy transducer TonB Yersinia pestis CO92 Z1_02614 VFG036556 40.9 3.19e-35 127.0 VF0272 VFC0272 fbpC iron(III) ABC transporter, ATP-binding protein Neisseria meningitidis M01-240355 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 Z1_02656 VFG019078 50.0 3.9800000000000004e-109 321.0 VF1042 VFC0001 plr/gapA type I glyceraldehyde-3-phosphate dehydrogenase Streptococcus pneumoniae CGSP14 Z1_02671 VFG013348 70.0 1.46e-147 416.0 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 Z1_02672 VFG049099 68.3 2.12e-172 481.0 VF0561 VFC0258 KOX_RS24955 NAD-dependent epimerase Klebsiella oxytoca KCTC 1686 LPS Klebsiella pneumoniae Immune modulation In K. pneumoniae there are nine main O-serotypes. Three of these, O1, O2, and O3, are responsible for almost 80% of all Klebsiella infections.; Compared with other Enterobacteriaceae, such as Escherichia coli 161 defined O serotypes and Shigella flexneri at least 47 O serotypes, Klebsiella has a surprisingly low number of reported O serotypes which promises a more viable alternative for vaccine development compared with K-antigen-based vaccines; The O-antigen biosynthesis enzymes are encoded on the rfb locus. Resistant to serum complement; also play a role in protecting bacteria from antimicrobial peptides, including polymyxin antibiotics Abstract(s) in PubMed Z1_02675 VFG006717 49.3 4.47e-276 788.0 VF0444 VFC0001 lap Listeria adhesion protein Lap Listeria monocytogenes EGD-e 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 Z1_02690 VFG016532 47.3 1.78e-38 139.0 VF0881 VFC0258 oppF oligopeptide ABC transporter permease Mycoplasma mycoides subsp. mycoides SC str. PG1 Z1_02692 VFG000443 51.6 8.31e-51 161.0 VF0102 VFC0001 fimA type-1 fimbrial protein subunit A 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 Z1_02694 VFG042681 49.8 1.96e-78 235.0 VF1211 VFC0001 fimC gene fimbrial chaperone protein Citrobacter freundii str. 3009 Z1_02695 VFG042682 45.0 2.43e-253 729.0 VF1211 VFC0001 fimD gene outer membrane usher protein Citrobacter freundii str. 3009 Z1_02696 VFG042683 49.3 6.11e-38 137.0 VF1211 VFC0001 fimH gene fimbrial adhesin subunit Citrobacter freundii str. 3009 Z1_02706 VFG013197 42.8 7.6e-71 223.0 VF0758 VFC0272 hemB porphobilinogen synthase Haemophilus somnus 2336 Z1_02731 VFG044295 99.6 2.85e-190 521.0 VF1253 VFC0272 PMI_RS06920 heme ABC transporter ATP-binding protein Proteus mirabilis HI4320 Z1_02732 VFG044294 100.0 3.99e-221 604.0 VF1253 VFC0272 PMI_RS06915 iron ABC transporter permease Proteus mirabilis HI4320 Z1_02733 VFG044293 99.6 5.26e-185 508.0 VF1253 VFC0272 PMI_RS06910 hemin ABC transporter substrate-binding protein Proteus mirabilis HI4320 Z1_02734 VFG044292 99.4 1.39e-251 683.0 VF1253 VFC0272 PMI_RS06905 hemin-degrading factor Proteus mirabilis HI4320 Z1_02735 VFG044291 99.7 0.0 1360.0 VF1253 VFC0272 PMI_RS06900 TonB-dependent hemoglobin/transferrin/lactoferrin family receptor Proteus mirabilis HI4320 Z1_02737 VFG044241 50.9 5.49e-11 52.8 VF1031 VFC0272 YE_RS01740 hemin uptake protein HemP Yersinia enterocolitica subsp. enterocolitica 8081 Z1_02738 VFG044185 55.3 8.29e-121 352.0 VF0626 VFC0272 BJE04_RS21750 3-deoxy-7-phosphoheptulonate synthase Vibrio vulnificus YJ016 Z1_02766 VFG001867 66.5 7.38e-98 281.0 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 Z1_02788 VFG001214 40.4 7.07e-65 211.0 VF0082 VFC0001 pilR two-component response regulator PilR 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 Z1_02796 VFG043148 42.8 1.6199999999999996e-68 226.0 VF0625 VFC0271 VP_RS22515 sigma-54 dependent transcriptional regulator Vibrio parahaemolyticus RIMD 2210633 Z1_02807 VFG023567 45.9 3.06e-47 152.0 VF0132 VFC0083 ail attachment invasion locus protein Yersinia enterocolitica subsp. palearctica 105.5R(r) Ail Attachment-invasion locus Yersinia pestis Invasion Ail is expressed in pathogenic Y.enterocolitica strains and Y.pseudotuberculosis, but generally the Y.pestis inv gene is inactivated by an insertion sequence, in strain CO92 it is intact; belongs to Ail/OmpX/PagC/Lom family, a family of outermembrane proteins (OMPs), including Ail, S. typhimurium Rck,PagC,or E. coli OmpX. Particular members of the family are responsible for conferring resistance to complement-mediated killing, survival in macrophages, and adhesion and invasion of host cells A small, monomeric, surface-associated protein localized in the OM; eight transmembrane -sheets and four cell surface-exposed loops, and the 3rd extracellular loop is important for Ail-mediated binding to host cells; PDB code :3QRA Promoting attachment to and subsequent invasion of eukaryotic cells, but a less powerful adhesion than Inv; promotes Yop delivery into the primary target of T3SS--the phagocytic cells, as well as into epithelial cells; promotes resistance to complement killing Binds negative regulator sof alternative (factor H),and classical and lectin [C4b-binding protein (C4BP)] complement pathways thus preventing complement attack; binds a 40kDA laminin fragment called LG4-5 (Laminin G-like domains 4 and 5) and 120 kDA fragment of fibronectin, 9FNIII module neighboring the RGD site present in 10FNIII region. Abstract(s) in PubMed Z1_02823 VFG026700 40.8 5.4499999999999995e-68 227.0 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 Z1_02833 VFG000463 52.9 8.410000000000001e-56 173.0 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 Z1_02941 VFG031747 40.1 1.36e-48 159.0 VF0858 VFC0301 regX3 two-component sensory transduction protein RegX Mycobacterium indicus pranii MTCC 9506 Z1_02988 VFG043367 53.8 1.88e-15 79.0 VF0051 VFC0204 tlpB membrane-bound chemoreceptor sensing pH and autoinducer-2 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 Z1_03013 VFG013087 58.6 5.24e-137 390.0 VF0981 VFC0346 msbB2 lauroyl-Kdo(2)-lipid IV(A) myristoyltransferase Shigella boydii Sb227 Z1_03021 VFG035866 51.2 1.71e-27 118.0 VF1122 VFC0086 UTI89_RS01245 DUF4150 domain-containing protein Escherichia coli UTI89 Z1_03024 VFG038365 89.5 3.11e-119 333.0 VF0480 VFC0086 hcp1 HcpA-like protein Aeromonas hydrophila subsp. hydrophila ATCC 7966 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03028 VFG039536 60.5 3.84e-99 289.0 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 Z1_03053 VFG013466 80.6 9.99e-169 468.0 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 Z1_03057 VFG013196 51.4 1.35e-136 398.0 VF0758 VFC0272 hemA glutamyl-tRNA reductase Haemophilus somnus 2336 Z1_03070 VFG042564 49.5 7.33e-69 210.0 VF0213 VFC0001 fedD FedD protein Escherichia coli 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 Z1_03083 VFG050291 42.2 4.57e-12 63.5 VF0603 VFC0001 DIP_RS19245 C40 family peptidase Corynebacterium diphtheriae NCTC 13129 DIP1621 Corynebacterium diphtheriae Adherence Surface-associated protein belongs to NlpC/P60 family Play a role in adhesion to epithelial cells Abstract(s) in PubMed Z1_03089 VFG046726 40.9 1.22e-07 52.4 VF0543 VFC0258 FPHI_RS07665 glycosyltransferase family 2 protein 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 Z1_03090 VFG011157 41.2 1.43e-98 298.0 VF0033 VFC0258 bplF lipopolysaccharide biosynthesis protein Bordetella bronchiseptica RB50 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 Z1_03100 VFG042718 50.2 2.2199999999999998e-101 299.0 VF1153 VFC0001 ydeQ fimbrial protein Escherichia coli O157:H7 str. EDL933 Z1_03101 VFG018546 41.0 1.25e-09 57.0 SPI-1 encode VFC0086 hilD transcriptional regulator HilD Salmonella enterica subsp. arizonae serovar 62:z4,z23:-- str. RSK2980 Z1_03106 VFG034194 61.7 2.89e-133 380.0 VF1116 VFC0272 sitA iron/manganese ABC transporter substrate-binding protein SitA Escherichia coli O44:H18 042 Z1_03107 VFG034214 61.6 1.31e-113 328.0 VF1116 VFC0272 sitB iron/manganese ABC transporter ATP-binding protein SitB Escherichia coli O45:K1:H7 str. S88 Z1_03108 VFG012585 67.5 1.31e-127 365.0 VF1116 VFC0272 sitC iron/manganese ABC transporter permease subunit SitC Escherichia coli APEC O1 Z1_03109 VFG012586 50.7 3.48e-86 259.0 VF1116 VFC0272 sitD iron/manganese ABC transporter permease subunit SitD Escherichia coli CFT073 Z1_03166 VFG042354 65.4 3.59e-24 102.0 Haemophilus adhesin A VFC0001 HIBPF_RS09175 YadA-like family protein Haemophilus influenzae F3031 Z1_03224 VFG004061 69.5 2.02e-115 328.0 VF0111 VFC0301 phoP two-component system response regulator PhoP Salmonella enterica subsp. enterica serovar Typhi str. CT18 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 Z1_03225 VFG018397 54.4 7.14e-180 513.0 VF0111 VFC0301 phoQ two-component system sensor histidine kinase PhoQ Salmonella enterica subsp. arizonae serovar 62:z4,z23:-- str. RSK2980 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 Z1_03247 VFG009135 41.2 7.95e-91 280.0 VF0809 VFC0272 kasB 3-oxoacyl-(acyl carrier protein) synthase II Mycobacterium tuberculosis RGTB327 Z1_03248 VFG011430 63.2 3.05e-25 89.0 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 Z1_03249 VFG038840 77.5 7.479999999999999e-128 361.0 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 Z1_03269 VFG007263 44.5 2.16e-187 545.0 VF0628 VFC0272 irgA ligand-gated channel protein Vibrio cholerae O1 biovar El Tor str. N16961 Z1_03274 VFG048863 41.8 1.72e-06 44.7 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 Z1_03280 VFG032106 42.5 2.05e-14 70.9 VF0068 VFC0083 iap/cwhA P60 extracellular protein, invasion associated protein Iap Listeria ivanovii subsp. ivanovii PAM 55 P60 Listeria monocytogenes Invasion Encoded by the iap (for invasion-associated protein) gene; not regulated by PrfA A modular protein containing two LysM domains, a bacterial Src homology 3 (SH3) domain and a C-terminal NLPC/P60 domain. The LysM domain is involved in degradation of bacterial cell wall. The function of SH3 domain is as yet unknown, but it may probably mediate interaction with host signalling molecules. Murein hydrolase activity required for normal septum formation and essential for cell viability; may play a role in intestinal invasion and in vivo survival Abstract(s) in PubMed Z1_03302 VFG042526 42.3 1.89e-20 88.6 AF/R1 VFC0001 afrR transcriptional activator AfrR Escherichia coli str. RDEC-1 Z1_03322 VFG043544 68.8 1.02e-168 474.0 VF1158 VFC0001 ompA porin OmpA Escherichia coli O157:H7 str. EDL933 Z1_03340 VFG043568 56.2 4.86e-132 382.0 VF0969 VFC0001 nmpC phosphoporin PhoE Salmonella enterica subsp. enterica serovar Typhimurium str. LT2 Z1_03344 VFG051986 78.0 3.8300000000000003e-63 208.0 VF1354 VFC0086 tke2 T6SS Rhs-type effector Tke2 Pseudomonas syringae pv. syringae B728a Z1_03352 VFG051985 66.1 3.5099999999999995e-46 159.0 VF1354 VFC0086 tke2 T6SS Rhs-type effector Tke2 Pseudomonas syringae pv. phaseolicola 1448A Z1_03355 VFG051982 42.1 3.92e-18 78.2 VF1354 VFC0086 tke2 T6SS Rhs-type effector Tke2 Pseudomonas putida F1 Z1_03364 VFG038407 41.5 1.96e-126 391.0 VF0480 VFC0086 vgrG3 VgrG protein Aeromonas hydrophila subsp. hydrophila ATCC 7966 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03365 VFG038370 90.1 5.37e-120 335.0 VF0480 VFC0086 hcp hemolysin co-regulated protein Aeromonas hydrophila ML09-119 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03366 VFG038379 60.4 9.44e-63 190.0 VF0480 VFC0086 vipA Type VI secretion system contractile sheath small subunit TssB/VipA Aeromonas salmonicida subsp. salmonicida A449 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03367 VFG038380 76.4 6.489999999999999e-288 787.0 VF0480 VFC0086 vipB Type VI secretion system contractile sheath large subunit TssC/VipB Aeromonas hydrophila subsp. hydrophila ATCC 7966 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03368 VFG038381 43.4 3.4500000000000004e-37 124.0 VF0480 VFC0086 atsG Type VI secretion system protein Aeromonas hydrophila subsp. hydrophila ATCC 7966 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03369 VFG038384 40.8 1.32e-145 433.0 VF0480 VFC0086 atsH Type VI secretion system protein Aeromonas salmonicida subsp. salmonicida A449 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03370 VFG038385 48.1 3.6600000000000004e-110 324.0 VF0480 VFC0086 atsI Type VI secretion system protein Aeromonas hydrophila subsp. hydrophila ATCC 7966 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03371 VFG038387 41.8 1.34e-97 298.0 VF0480 VFC0086 atsJ Type VI secretion system protein Aeromonas hydrophila subsp. hydrophila ATCC 7966 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03372 VFG038389 50.0 5.940000000000002e-57 176.0 VF0480 VFC0086 atsK Type VI secretion system protein Aeromonas hydrophila subsp. hydrophila ATCC 7966 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03373 VFG038391 46.4 1.37e-147 427.0 VF0480 VFC0086 atsL Type VI secretion system protein Aeromonas hydrophila subsp. hydrophila ATCC 7966 T6SS Aeromonas hydrophila Effector delivery system A phagetail-spike-like injectisome to translocate virulence determinants directly into the host cell cytoplasm; Four effectors of the T6SS have so far been characterized, Hcp1, Vgr1, Vgr2 and Vgr3; Hcp is a powerful effector substrate and once translocated into the targeted host cell cytoplasm, apoptosis ensues following caspase 3 activation; Hcp paralyzes macrophages to prevent phagocytosis;Vgr1 is an ADP-ribosylating toxin capable of interrupting the host cell cytoskeleton and inducing apoptosis Abstract(s) in PubMed Z1_03374 VFG035601 56.1 2e-92 272.0 VF1122 VFC0086 aec26 type IVB secretion system protein IcmH/DotU Escherichia coli O44:H18 042 Z1_03375 VFG035582 64.4 0.0 1102.0 VF1122 VFC0086 aec27/clpV type VI secretion system ATPase TssH Escherichia coli O83:H1 str. LF82 Z1_03377 VFG035552 47.2 1.04e-49 162.0 VF1122 VFC0086 aec28 type VI secretion system-associated protein TagO Escherichia coli UMNK88 Z1_03378 VFG035513 44.1 2.41e-121 363.0 VF1122 VFC0086 aec29 type VI secretion system protein TssA Escherichia coli O55:H7 str. CB9615 Z1_03379 VFG035493 49.5 0.0 1103.0 VF1122 VFC0086 aec30 type VI secretion system membrane subunit TssM Escherichia coli O103:H2 str. 12009 Z1_03382 VFG036078 40.9 2.2600000000000002e-29 112.0 VF1135 VFC0235 usp type VI secretion system tube protein Hcp Escherichia coli NA114 Z1_03393 VFG038845 70.9 1.3800000000000001e-118 338.0 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 Z1_03396 VFG013246 54.3 3.17e-117 341.0 VF0044 VFC0258 lpxK tetraacyldisaccharide 4'-kinase 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 Z1_03397 VFG013149 67.8 4.989999999999998e-274 759.0 VF0044 VFC0258 msbA lipid transporter ATP-binding/permease 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 Z1_03405 VFG042380 40.9 9.09e-15 76.6 VF1277 VFC0086 ABQ43328 MhaB2 Moraxella catarrhalis str. O35E Z1_03412 VFG049124 69.0 5.13e-178 497.0 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 Z1_03458 VFG048844 85.9 2.38e-294 801.0 VF0560 VFC0258 gndA NADP-dependent phosphogluconate 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 Z1_03464 VFG007583 47.2 1.42e-06 49.3 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 Z1_03508 VFG047512 51.0 9.68e-111 325.0 VF0552 VFC0272 bioB biotin synthase Francisella tularensis subsp. tularensis SCHU S4 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 Z1_03524 VFG036031 43.4 2.18e-69 245.0 VF1131 VFC0086 cdiA contact-dependent inhibition effector tRNA nuclease Escherichia coli CFT073 Z1_03534 VFG039074 41.3 1.26e-18 79.0 VF0499 VFC0083 ompA outer membrane protein OmpA Anaplasma centrale str. Israel 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 Z1_03538 VFG006291 52.6 2.62e-18 80.1 VF0895 VFC0272 exbB TonB-system energizer ExbB Neisseria gonorrhoeae FA 1090 Z1_03573 VFG000478 86.4 6.76e-96 273.0 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 Z1_03578 VFG042619 95.0 2.3e-114 322.0 UCA VFC0001 ucaA uroepithelial cell adherence major pilin UcaA Proteus mirabilis HI4320 Z1_03579 VFG042618 97.5 8.77e-169 464.0 UCA VFC0001 PMI_RS02645 fimbria/pilus periplasmic chaperone Proteus mirabilis HI4320 Z1_03580 VFG042617 99.1 0.0 1645.0 UCA VFC0001 PMI_RS02640 fimbrial biogenesis outer membrane usher protein Proteus mirabilis HI4320 Z1_03581 VFG042616 99.2 7.03e-262 710.0 UCA VFC0001 PMI_RS02635 type 1 fimbrial protein Proteus mirabilis HI4320 Z1_03582 VFG042615 94.1 1.17e-62 185.0 UCA VFC0001 PMI_RS02630 helix-turn-helix transcriptional regulator Proteus mirabilis HI4320 Z1_03672 VFG030314 41.5 8.059999999999999e-46 160.0 VF0840 VFC0258 adhD Putative zinc-type alcohol dehydrogenase AdhD (aldehyde reductase) Mycobacterium tuberculosis CAS/NITR204 Z1_03714 VFG013643 45.5 7.209999999999998e-230 662.0 VF0758 VFC0272 hemR TonB-dependent hemoglobin/transferrin/lactoferrin family receptor Haemophilus influenzae Rd KW20 Z1_03720 VFG036944 46.2 2.7e-103 310.0 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 Z1_03721 VFG036965 58.2 1.16e-210 592.0 VF0450 VFC0325 farB fatty acid efflux system protein FarB Neisseria meningitidis G2136 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 Z1_03733 VFG049189 83.8 0.0 1388.0 VF0783 VFC0086 clpV ATP-dependent chaperone ClpB Klebsiella oxytoca E718 Z1_03751 VFG018243 77.8 1.27e-95 274.0 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 Z1_03759 VFG010906 83.6 3.2600000000000004e-27 92.8 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