ライフサイエンスコーパス: virulence gene

1 ained the mTmV prophage, harbouring the sopE virulence gene.

2 ed to EPEC, but appear to have acquired ETEC virulence genes.

3 homology and number of core genes including virulence genes.

4 te hub enzymes and fermentation pathways and virulence genes.

5 11%) samples were also positive for the stx2 virulence genes.

6 eproduction, as well as several well-studied virulence genes.

7 exploit host cytosolic signals to upregulate virulence genes.

8 ic cells had enhanced expression of numerous virulence genes.

9 of unlinked chromosomal segments containing virulence genes.

10 They differed in number of virulence genes.

11 types ST73 and ST127, and multiple specific virulence genes.

12 cue that leads to expression of LEE-encoded virulence genes.

13 spA to positively regulate the expression of virulence genes.

14 chitecture and translocations of chromosomal virulence genes.

15 carry and disseminate superantigen and other virulence genes.

16 ways and reduces the expression of bacterial virulence genes.

17 ategorized into essential, non-essential and virulence genes.

18 d ORFs in the island included metabolism and virulence genes.

19 aurocholate that activates the expression of virulence genes.

20 st use of TraSH in GAS to identify potential virulence genes.

21 expression of early and late BvgA-regulated virulence genes.

22 SF sensor, RpfC, to coordinate expression of virulence genes.

23 sory genome is enriched with uncharacterized virulence genes.

24 or human disease via acquisition of distinct virulence genes.

25 cies is constrained by the colocalization of virulence genes.

26 stinal pathogenic E. coli (ExPEC)-associated virulence genes.

27 ed clustering of centromeres, telomeres, and virulence genes.

28 op codons were detected in the prfA and inlA virulence genes.

29 two (MglA-SspA)-based strategies to activate virulence genes.

30 ule that activates the expression of several virulence genes.

31 ates of MYXV that fall in known or potential virulence genes.

32 vironmental cues activates the expression of virulence genes.

33 ugh the acquisition of horizontally acquired virulence genes(4,5).

34 xperimentally validated, thereby identifying virulence genes, a molecule that triggers G2/M arrest an

35 le intracellular conditions that promote its virulence gene activity.

36 means of spreading antibiotic resistance and virulence genes among bacteria and therefore presents a

37 s study was to identify the common H. pylori virulence genes among dyspeptic Southwestern Saudi patie

38 phylotyping, ESBL genes, plasmid replicons, virulence genes, amplified fragment length polymorphism

39 ated the expression of the BcBOT and all the virulence genes analyzed when B. cinerea was grown alone

40 The data provide additional insights into virulence gene and epistatic interaction discovery in HS

41 lates SsrB, and SsrB~P relieves silencing of virulence genes and activates their transcription.

42 orizontally acquired genes such as bacterial virulence genes and antibiotic resistance genes.

43 zobium etli CFN42, harbors a complete set of virulence genes and can mediate plant genetic transforma

44 By exploiting the hypervariable nature of virulence genes and clustered regularly interspaced shor

45 e E. coli serogroup-specific gene with major virulence genes and developed a single-cell-based dPCR a

46 nt in a population before the acquisition of virulence genes and emergence of pathogenic clones remai

47 Virulence genes and hotspots can be visualized directly

48 ies are possibly linked to pathogen-specific virulence genes and how they may influence pathology and

49 ddition, DHMA induces the expression of EHEC virulence genes and increases attachment to intestinal e

50 gma factor, RpoN (sigma(54)), regulates many virulence genes and is linked to antibiotic resistance.

51 to persistent infection: down-regulation of virulence genes and reduced hemolysis and neutrophil che

52 phase was the induction of known B. quintana virulence genes and several previously unannotated genes

53 Multivariate analyses among H. pylori virulence genes and severity of hepatobiliary disease re

54 talities in direct proportion to the encoded virulence genes and showed similar signs of septicemia f

55 y revealed a significant association between virulence genes and the development of certain forms of

56 hese mutations result in the upregulation of virulence genes and the downregulation of the protease S

57 lates bore more antimicrobial resistance and virulence genes and were less diverse than isolates from

58 alence of Giardia lamblia genes, any E. coli virulence gene, and the specific E. coli virulence genes

59 characterized for antimicrobial resistance, virulence genes, and diversity.

60 ween bacterial physiology, the expression of virulence genes, and the underlying molecular mechanism

61 to adapt to changing conditions and express virulence genes appropriately.

62 locus of enterocyte effacement (LEE)-encoded virulence genes are activated and promote intestinal col

63 ains, regular PCR cannot confirm whether the virulence genes are carried by adulterant or nonadultera

64 Homologs of Agrobacterium virulence genes are found in many bacterial genomes, but

65 H. pylori virulence genes are highly prevalent and diverse among p

66 Virulence genes are regulated by a complex regulatory ne

67 rofiling, i.e., of antibiotic resistance and virulence genes, are crucial for effective infection con

68 iously identified regulator of P. aeruginosa virulence genes, as novel targets of prrF-mediated heme

69 vator that is required for the expression of virulence genes associated with invasion and cell-to-cel

70 oprL and toxA genes are the most predominant virulence genes associated with P. aeruginosa infection.

71 s of functional genes and pseudogenes (e.g., virulence genes) associated with bovine and human isolat

72 nctive geographic, temporal, resistance, and virulence gene associations; and establish a new laborat

73 conditions but also direct the expression of virulence genes at an appropriate time and place.

74 e how quorum sensing regulates expression of virulence genes at appropriate times, thereby enabling s

75 cement of the expression of CovRS-controlled virulence genes at the exponential growth phase; however

76 mage analysis, we analyzed the expression of virulence genes at the single cell level and related it

77 val and transfer of fitness enhancing and (a)virulence genes between bacteria.

78 The Bordetella virulence gene (BvgAS) phosphorelay-type TCS controls ex

79 The Bordetella virulence gene (BvgAS) two-component system, a paradigm

80 AraC Negative Regulators (ANR) suppress virulence genes by directly down-regulating AraC/XylS me

81 narrow host range, and potential transfer of virulence genes by generalized transduction.

82 evolved to integrate expression of the major virulence gene cagA with the flagellar regulatory circui

83 g the prevalence of H. pylori infections and virulence genes (cagA, dupA, and vacA); the relationship

84 The Helicobacter pylori virulence gene, cagA, and active forms of the vacuolatin

85 Major virulence genes carried by each of the top 7 STEC serogr

86 In P. falciparum, the heterochromatic virulence gene cluster had a strong repressive effect on

87 by clustering of the centromeres and lacked virulence gene clustering.

88 Internal virulence gene clusters exhibit domain-like structures i

89 e, and nutrition utilization genes, specific virulence gene communities have been accumulated in stx-

90 ts had transcript levels of CovRS-controlled virulence genes comparable to those of a covS mutant but

91 ity of E. coli isolates and their resistance/virulence gene content as a proxy measure of accessory g

92 tors include multidrug resistance, extensive virulence gene content, and ongoing transmission.

93 cluding resistance to fluoroquinolones, high virulence gene content, the possession of the type 1 fim

94 thogenic variants (pathovars) based on their virulence gene content.

95 are characterized by extensive variation in virulence gene content.

96 um falciparum, the clustering of a family of virulence genes correlates with their coordinated silenc

97 ave been no molecular analyses using defined virulence gene deletion mutants in that lineage as of ye

98 hanism enables a pathogen to express foreign virulence genes during infection without the need to evo

99 nse bile as an environmental cue to regulate virulence genes during infection.

100 Chromosomal virulence gene E (chvE) encodes a periplasmic-binding pr

101 ga toxin-producing E. coli (STEC) associated virulence genes (eaeA, stx1, stx2, and hlyA) in ten anim

102 The occurrence of E. coli virulence genes (ECVG) was equivalent across all sample

103 n amino acids and arginine biosynthesis) and virulence genes (eg, beta-toxin, delta-toxin) that defin

104 c mutations, including deletion of the major virulence gene encoding the NSs protein and introduction

105 sequencing revealed differences in putative virulence genes encoding aggregative adherence fimbriae,

106 e host environment and promote expression of virulence genes essential for adherence.

107 t can function as a ToxR agonist to modulate virulence gene expression and biofilm production in V. c

108 cetylase 2 (PfHda2), is a global silencer of virulence gene expression and controls the frequency of

109 e transcription factor that is essential for virulence gene expression and human colonization by Vibr

110 glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in

111 One mechanism by which PTS promotes virulence gene expression appears to be by modulating th

112 ns must sense their environment and regulate virulence gene expression appropriately.

113 S. aureus CodY activity grades metabolic and virulence gene expression as a function of ILV availabil

114 ult from strains with mutations that enhance virulence gene expression but reduce subsequent transmis

115 Here, we show that serotonin decreases virulence gene expression by enterohemorrhagic E. coli (

116 The PTS modulates virulence gene expression by regulating expression of tc

117 e Staphylococcus aureus Agr system regulates virulence gene expression by responding to cell populati

118 Unlike B. anthracis, much of the increased virulence gene expression can be attributed to loss of o

119 hat cell population density signals inducing virulence gene expression can be overridden by nutrient

120 mechanism of the mechanosensor GrlA, whereby virulence gene expression can be rapidly fine-tuned in r

121 effect that arises through heterogeneity in virulence gene expression can protect clonal populations

122 Virulence gene expression following host cell associatio

123 Bistable flagellar and virulence gene expression generates specialized Salmonel

124 e concentration of colonic arginine promotes virulence gene expression in C. rodentium Arginine is an

125 responses are required for downregulation of virulence gene expression in Citrobacter rodentium, an e

126 lular signalling machinery that controls the virulence gene expression in concert with population den

127 ty of these compounds to affect agr-mediated virulence gene expression in cultured S. aureus cells.

128 is of its ability to both attract and induce virulence gene expression in EHEC, we propose that DHMA

129 f of ArcA is sufficient to selectively alter virulence gene expression in P. gingivalis, and PGN_0294

130 on of Mga may allow the bacteria to modulate virulence gene expression in response to carbohydrate st

131 of how DSF-dependent microorganisms modulate virulence gene expression in response to changes in the

132 wo-component system (CpxRA), which regulates virulence gene expression in response to environmental s

133 t undergo dramatic changes in cell shape and virulence gene expression in response to host temperatur

134 Increased virulence gene expression in the DeltacccB and DeltaresB

135 ing (QS) systems are important regulators of virulence gene expression in the opportunistic human pat

136 Here, we show that heterogeneous virulence gene expression in this organism also promotes

137 Exogenously added arginine induces EHEC virulence gene expression in vitro.

138 EAEC virulence gene expression is controlled by the autoactiv

139 ected eukaryotic cells, where PrfA-regulated virulence gene expression is critical for survival.

140 How this organism regulates virulence gene expression is poorly understood.

141 We found that DSFs repressed virulence gene expression of enteric pathogens by intera

142 to be constitutively activated, we show that virulence gene expression significantly impairs the list

143 tious period by achieving low frequencies of virulence gene expression switching and sexual conversio

144 nsporter can increase the sensitivity of the virulence gene expression system to certain sugars that

145 We show that Bt enhances EHEC virulence gene expression through the transcription fact

146 ScsA directs overall Salmonella virulence gene expression under conditions that mimic th

147 quorum sensing is the main driving force for virulence gene expression when bacterial cell densities

148 potential of GAS is elevated (i.e. enhanced virulence gene expression), cellular responses mediated

149 host, where phiSa3 serves as a regulator of virulence gene expression, and increased fitness and vir

150 y, and that this was coincident with greater virulence gene expression, likely accounting for the mor

151 iated with elevated intracellular Salmonella virulence gene expression, rupture of the Salmonella-con

152 Some AIPs are agonists of virulence gene expression, while others are antagonists.

153 hogen that employs quorum sensing to control virulence gene expression.

154 rs that mediate the epigenetic regulation of virulence gene expression.

155 arginine transport (DeltaartP) had decreased virulence gene expression.

156 expression of toxT, the central activator of virulence gene expression.

157 an lead to highly selective dysregulation of virulence gene expression.

158 n, ChvE, play a critical role in controlling virulence gene expression.

159 ptation through sRNA-mediated fine-tuning of virulence gene expression.

160 y due to a decrease in energy generation and virulence gene expression.

161 at individual regulators play in controlling virulence gene expression.

162 res of the host response as cues to regulate virulence gene expression.

163 tion, conditions that also induce Salmonella virulence gene expression.

164 ll to process virulence factors and regulate virulence gene expression.

165 ase system (PEP-PTS) and for their impact on virulence gene expression.

166 osa to light represses biofilm formation and virulence gene expression.

167 2457T, including induced drug resistance and virulence gene expression.

168 enome, controls the repression of multi-copy virulence gene families and determines sexual stage comm

169 mechanism for optimizing the evolvability of virulence gene families in pathogens.

170 pyrosequencing data obtained from a malaria virulence gene family, where Multipass generates 20 % mo

171 ly P) state at P(fim3), the promoter for the virulence gene fim3 (fimbrial subunit), using gel retard

172 he preliminary results showed differences in virulence genes found in Yersinia pestis and Yersinia ps

173 her of the methods based on detection of the virulence genes from DNA in whole stools.

174 similar environmental strains could acquire virulence genes from the 2010 Haitian epidemic clone, in

175 nto a temperate phage genome, removing major virulence genes from the host chromosome, and expanding

176 e initiates transcription of cagA, the major virulence gene, from a promoter identified in this study

177 gene, which encodes the master regulator of virulence genes, has been previously implicated in regul

178 es that characterization of S. aureus CC and virulence genes helps to predict the likelihood of the o

179 Here, we analyzed phylogeny, virulence genes, host range, and aggressiveness of Pseud

180 reduced the expression of the VirF-dependent virulence genes icsA, virB, icsB, and ipaB in Shigella.

181 ination of ribosomal spacer PCR (RS-PCR) and virulence gene identification for typing of S. aureus st

182 or deleted for individual known pAA-encoded virulence genes (ie, aggR, aggA, and sepA).

183 onas aeruginosa activates expression of many virulence genes in a cell density-dependent manner by us

184 transcriptional regulator of plasmid-encoded virulence genes in Bacillus anthracis.

185 The Log10 concentrations of STEC virulence genes in cattle wastewater samples ranged from

186 entification and the detection of resistance/virulence genes in clinical settings.

187 H, member of the NusG/Spt5 family, activates virulence genes in Gram-negative pathogens.

188 rmosensing is critical for the expression of virulence genes in pathogenic bacteria that infect warm-

189 elp understand how Francisella regulates its virulence genes in response to host cell environments, a

190 e with C. albicans induces the expression of virulence genes in S. mutans (e.g., gtfB, fabM).

191 gmatic example is the bistable expression of virulence genes in Salmonella typhimurium, which leads t

192 spaced sites that controls the expression of virulence genes in several human pathogens.

193 sis revealed degradation events in important virulence genes in ST313 L3, which had not occurred in o

194 d a global perturbation in the expression of virulence genes in the DeltafakA strain.

195 s the expression of dozens of metabolism and virulence genes in the opportunistic pathogen Staphyloco

196 h, CM14 reduces HlyU-dependent expression of virulence genes in V. vulnificus.

197 s occurred in genes previously identified as virulence genes in whole-gene knockout studies.

198 cated in pathogenesis and that PafR controls virulence genes, in particular biofilm formation genes.

199 Three virulence genes including ply (pneumolysin) were upregul

200 activates transcription of a large number of virulence genes, including Aar, which in turn acts as a

201 us aureus is critical for regulation of many virulence genes, including hla, which encodes alpha-toxi

202 genomes, but overrepresented in a number of virulence genes, including motility-associated genes, an

203 lation in the expression of key pneumococcal virulence genes, including the gene for the pneumococcal

204 mmon set of genomic loci that includes known virulence genes, indicating that the Ryp factors directl

205 ile salt taurocholate, a host signal for the virulence gene induction of V. cholerae, induces an incr

206 to K. aerogenes isolates, including putative virulence genes involved in iron acquisition (n = 67), f

207 tes possess a unique combination of putative virulence genes involved in iron metabolism, protein sec

208 Expression of SPI-1 virulence genes is controlled by a complex hierarchy of

209 We show that Cas9, reprogrammed to target virulence genes, kills virulent, but not avirulent, Stap

210 s compared to other isogenic mutants lacking virulence genes known to be disproportionately associate

211 well as reduced expression of other critical virulence genes (Listeriolysin O, and two phospholipases

212 First, virulence genes may be acquired from other organisms.

213 tional factor CpxR controlling expression of virulence genes, notably those within the locus of enter

214 ly, CM14 decreases the expression of various virulence genes of other Vibrio species and thus attenua

215 Although the virulence genes of S. suis have been extensively studied

216 uencing, demonstrated that the EPEC and ETEC virulence genes of these hybrid isolates were differenti

217 The virulence genes of this pathogen are under a large amoun

218 Virulence genes on mobile DNAs such as genomic islands (

219 ng leading to cAMP-dependent upregulation of virulence genes on surface contact.

220 osa (P. aeruginosa), and the distribution of virulence genes (oprL, exoS, phzM, and toxA) and the ant

221 ctal culture isolates (n = 68) for any of 49 virulence genes or ST131 status (all P > .05).

222 PCR patterns were associated with a specific virulence gene pattern, as previously reported.

223 72% of prophages possessed the virulence genes pblA and/or pblB.

224 The tested strains harbored the virulence genes phoA, hly, tsh, eaeA, sta, and lt with a

225 0% of the total GAS genes, including several virulence genes potentially through the two-component re

226 Immunoblot assays further verified that the virulence gene products were produced and that the T3SS

227 oresis (PFGE) analysis, sequence typing, and virulence gene profiling.

228 We demonstrate that isolates lacking virulence genes promote beneficial plant growth, and tha

229 y by increasing DNA binding affinity for the virulence gene promoters that ToxT activates regardless

230 tome, including altered transcription of GAS virulence genes, providing a potential mechanism for the

231 al domain is involved in multiple aspects of virulence gene regulation and response to human host sig

232 is focused on providing a global picture of virulence gene regulation in P. aeruginosa.

233 These findings have implications for virulence gene regulation in Shigella and other pathogen

234 r quorum-sensing system, plays a key role in virulence gene regulation in Staphylococcus aureus, but

235 tion of an IS element has a direct impact on virulence gene regulation resulting in hypervirulence.

236 he assumed, although not proven, key role of virulence gene regulation systems in suppressing the cos

237 The molecular basis by which AdhE affects virulence gene regulation was found to be multifactorial

238 understanding GAS fitness mutations in vivo, virulence gene regulation, in vivo gene expression, and

239 ds a new layer of complexity to B. pertussis virulence gene regulation.

240 vealed previously unrecognized complexity of virulence gene regulation.

241 a SigD, making this signaling molecule a key virulence gene regulator in C. difficile.

242 MgrA is an important global virulence gene regulator in Staphylococcus aureus.

243 AtxA, the master virulence gene regulator of Bacillus anthracis, is a PRD

244 S) found that the gene encoding the multiple virulence gene regulator of GAS (mga) is highly polymorp

245 ed in the differential expression of several virulence genes relative to basal expression levels.

246 on of both invasion-associated effectors and virulence genes required for intracellular survival.

247 f centromeres, telomeres, ribosomal DNA, and virulence genes, resulting in a complex architecture tha

248 evealed the following risk factors for hvKP: virulence gene rmpA (odds ratio [OR], 16.92 [95% confide

249 the regulation of heat shock, cold shock and virulence genes, RNATs constitute an interesting potenti

250 the regulation by Cmr of the DosR-regulated virulence gene Rv2623 demonstrate the complexity of Cmr-

251 ere further characterised for resistance and virulence genes, SCCmec and spa typing.

252 ubpopulation of bacterial cells that express virulence genes shows increased survival after exposure

253 Sequencing of the virulence gene sic revealed that all outbreak isolates h

254 EHEC) functions to activate transcription of virulence genes silenced by the histone-like nucleoid-st

255 oli virulence gene, and the specific E. coli virulence genes stx1/2 with every log(10) increase in th

256 Among the virulence genes, stx2 (25%, 95% CI, 17-33%) was most pre

257 responsible for the activation of accessory virulence genes, such as aldA, tagA, acfA, acfD, tcpI, a

258 Although the majority of these constitute virulence genes, suggesting that CrgA is important in pa

259 rimary sequence of two major T. gondii mouse virulence genes, TgROP5 and TgROP18.

260 R genes, CC151, CC479 and CC133 carried more virulence genes than other CCs, and CC398 was associated

261 easons emerging serotypes tend to carry more virulence genes than other E. coli are not understood.

262 exposure to mucus triggers downregulation of virulence genes that are involved in quorum sensing, sid

263 to distinct host cell types and express key virulence genes that are relevant to the disease process

264 clusters of A + T-rich horizontally acquired virulence genes that are silenced by the nucleoid-associ

265 h amoeba causes the accumulation of distinct virulence genes that collectively allow replication in m

266 Several genes that encode toxins and other virulence genes that enhance pathogen dissemination and

267 tidase) in previously unrecognized S. aureus virulence genes that enhance pathogenesis when introduce

268 revealed the presence of several fragmented virulence genes that probably are nonfunctional, e.g., F

269 3, O111, O121, and O145, when carrying major virulence genes, the Shiga toxin genes stx (1) and stx (

270 cteria must often restrict the expression of virulence genes to host environments.

271 pportunistic human pathogen able to transfer virulence genes to other cells through the mobilization

272 dapts the expression of its broad arsenal of virulence genes to promote different types of disease ma

273 The major Vibrio cholerae virulence gene transcription activator, ToxT, is respons

274 crystal structure of the LytTR domain of the virulence gene transcription factor AgrA from Staphyloco

275 ch wHTH proteins are important regulators of virulence gene transcription in many pathogens; they als

276 ty acid incorporation into phospholipids and virulence gene transcription.

277 f bicarbonate explains the elevated level of virulence gene transcription.

278 cts, we found two host signals that activate virulence gene transcription.

279 role as a metabolic sensor for regulation of virulence gene transcription.

280 inhibitor GrlR was not sufficient to induce virulence gene transcription; mechanical stimuli were re

281 lus growth, Agrobacterium incubation medium, virulence genes, transformation and selection conditions

282 O157:H7 strain, activates the expression of virulence genes under gluconeogenic conditions, suggesti

283 lyses, and we did not succeed in identifying virulence genes unique to the IE strains.

284 erestingly, variability in the expression of virulence genes upon infection enhances colonization.

285 r the presence of seven clinically important virulence genes (VGs).

286 ps, sequence types (STs), H30, H30Rx, and 53 virulence genes (VGs).

287 Any virulence gene was associated with IBC/IIB.

288 The CagA virulence gene was found in 62% (145/234), dupA in 53.4%

289 Expression of T3SS and other virulence genes was reduced in ppGpp(0) mutants.

290 One set of virulence genes was required in nonvirally infected mice

291 In this study, 38 ExPEC-associated virulence genes were added to the existing E. coli Virul

292 gnificant differences in expression of known virulence genes were also detected, further suggesting a

293 Several virulence genes were associated with clinical characteri

294 Virulence genes were consistently enriched in highly cod

295 , and the pathogenicity island, SaPI5, while virulence genes were dramatically down-regulated.

296 yoelii In Plasmodium knowlesi, telomeres and virulence genes were more dispersed throughout the nucle

297 Phospho-AlgB represses biofilm and virulence genes, while KinB dephosphorylates and thereby

298 he examined strains harbored (oprL and toxA) virulence genes, while only 22.2% were positive for the

299 nization with colocalization of subtelomeric virulence genes, while the Toxoplasma gondii genome was

300 nome approach, we searched for P. aeruginosa virulence genes with multi-host relevance.