ライフサイエンスコーパス: virulence gene

1 of unlinked chromosomal segments containing virulence genes.

2 ule that activates the expression of several virulence genes.

3 They differed in number of virulence genes.

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

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

6 spA to positively regulate the expression of virulence genes.

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

8 chitecture and translocations of chromosomal virulence genes.

9 carry and disseminate superantigen and other virulence genes.

10 vironmental cues activates the expression of virulence genes.

11 ways and reduces the expression of bacterial virulence genes.

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

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

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

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

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

17 or human disease via acquisition of distinct virulence genes.

18 ng the efflux pump PecM in addition to other virulence genes.

19 15 (75%) samples were harboring two or more virulence genes.

20 /C resistance plasmids also carried putative virulence genes.

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

22 l regulators that modulate the expression of virulence genes.

23 ates from 20 rainwater tank samples harbored virulence genes.

24 e genetic elements carrying pvl and 30 other virulence genes.

25 homology and number of core genes including virulence genes.

26 a and precisely regulating the expression of virulence genes.

27 the plant by regulating the transcription of virulence genes.

28 ible for activating the transcription of the virulence genes.

29 croenvironment by changing the expression of virulence genes.

30 a group carrying several of the typical EAEC virulence genes.

31 transcriptional activation of the Ti plasmid virulence genes.

32 lecule that regulates the expression of many virulence genes.

33 te hub enzymes and fermentation pathways and virulence genes.

34 11%) samples were also positive for the stx2 virulence genes.

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

36 exploit host cytosolic signals to upregulate virulence genes.

37 ic cells had enhanced expression of numerous virulence genes.

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

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

40 Virulence gene ace was also detected in 14 (61%) rainwat

41 le intracellular conditions that promote its virulence gene activity.

42 onstrate that a covS inactivation results in virulence gene alterations and also suggest that the Cov

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

44 The apparent lack of significant virulence genes among MRSA ST398 strains, demonstrates t

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

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

47 spp. from 5 (25%) samples harbored a single virulence gene and 15 (75%) samples were harboring two o

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

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

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

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

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

53 These included several known virulence genes and genes involved in adaptive metabolis

54 h regard to the distribution of the putative virulence genes and genetic elements analyzed.

55 Virulence genes and hotspots can be visualized directly

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

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

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

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

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

61 ans according to mobile resistance elements, virulence genes, and genomic backbone.

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

63 is required to activate the transcription of virulence genes, and toxboxes in several virulence gene

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

65 trated in syntenic gene-rich blocks, whereas virulence genes are dispersed into highly dynamic, repea

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

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

68 lates were also tested for the presence of 6 virulence genes associated with Enterococcus related inf

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

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

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

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

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

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

75 n vitro, CodY represses the transcription of virulence genes, but it is not known if CodY also repres

76 all RNAs are essential for the expression of virulence genes, but little is known about this mechanis

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

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

79 poson mutagenesis to identify S. Enteritidis virulence genes by assay of invasiveness in human intest

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 od to systematically knock out (KO) putative virulence genes by site-specific integration into the FV

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

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

85 Internal virulence gene clusters exhibit domain-like structures i

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

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

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

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

90 are characterized by extensive variation in virulence gene content.

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

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

93 ants revealed no selection against any known virulence genes, demonstrating the transformation of the

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

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

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

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

98 ates also had mutations in the promoter of a virulence gene, eis, which increase its expression and c

99 on six housekeeping genes and two 'putative virulence' genes (eMLST) that provides improved high res

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

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

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

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

104 A complex regulatory network controls virulence gene expression and responds to various enviro

105 omponent of the regulatory network governing virulence gene expression and stress adaptation in B. ps

106 suggest that DNA methylation could regulate virulence gene expression and transcription elongation.

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

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

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

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

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

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

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

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

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

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

117 Virulence gene expression following host cell associatio

118 Bistable flagellar and virulence gene expression generates specialized Salmonel

119 The majority of virulence gene expression in Bordetella is regulated by

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

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

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

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

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

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

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

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

128 We have previously shown that QseC activates virulence gene expression in Salmonella enterica serovar

129 osphorelay regulatory cascade that modulates virulence gene expression in several pathogens.

130 Virulence gene expression in Staphylococcus aureus is ti

131 Increased virulence gene expression in the DeltacccB and DeltaresB

132 ner and that Rgg and LacD.1 directly control virulence gene expression in the exponential phase of gr

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

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

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

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

137 the FusKR signalling cascade, modulating the virulence gene expression of EHEC.

138 ing pathogens with drugs that interfere with virulence gene expression offers an effective alternativ

139 It is known that V. cholerae terminates virulence gene expression prior to escape from the host,

140 ce to suggest that the blockade of S. aureus virulence gene expression significantly attenuates infec

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

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

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

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

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

146 Virulence gene expression was down-regulated during the

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

148 lex transcriptional network that coordinates virulence gene expression with multiple cellular phenoty

149 ivo expression technology was used to assess virulence gene expression within these populations.

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

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

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

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

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

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

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

157 2457T, including induced drug resistance and virulence gene expression.

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

159 at individual regulators play in controlling virulence gene expression.

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

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

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

163 as hypoinfectious and failed to fully induce virulence gene expression.

164 hogens often rely on thermosensing to adjust virulence gene expression.

165 aureus, in which it is a global regulator of virulence gene expression.

166 kingdom chemical sensing systems to regulate virulence gene expression.

167 rug design aimed at repressing SloR-mediated virulence gene expression.

168 that in V. cholerae is the key regulator of virulence gene expression.

169 is broken, an essential step in terminating virulence gene expression.

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

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

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

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

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

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

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

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

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

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

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

181 There is also evidence that key virulence genes have been acquired by horizontal transfe

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

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

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

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

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

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

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

189 expression of ten characterized and putative virulence genes in nasopharyngeal colonization and pneum

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

191 s in response to salt-induced osmolarity and virulence genes in response to changes in metabolite con

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

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

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

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

196 roles, including the essential regulation of virulence genes in several human pathogens.

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

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

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

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

201 sion studies showed that stp1 also regulates virulence genes, including a hemolysin, superantigen-lik

202 s a global response regulator that activates virulence genes, including adhesin-encoding fim3 and fha

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

204 contrast, multiple known or suspected ExPEC virulence genes, including pap (P fimbriae), vat (vacuol

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

206 olic processes and diminishing expression of virulence genes, including type 1 pili.

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

208 W, almost completely abolished intracellular virulence gene induction and thus displayed the expected

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

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

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

212 race between host immune genes and parasite virulence genes is known as Red Queen dynamics.

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

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

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

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

217 s transcription of the coding region for the virulence gene mgtC, which is the most highly induced ho

218 es from the innate immune system to regulate virulence genes necessary for intracellular survival, gr

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

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

221 Virulence genes on mobile DNAs such as genomic islands (

222 icroarray showed variation in resistance and virulence genes on mobile genetic elements (MGEs) betwee

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

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

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

226 72% of prophages possessed the virulence genes pblA and/or pblB.

227 0% of the total GAS genes, including several virulence genes potentially through the two-component re

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

229 We also analyzed the virulence gene profiles of the isolated K. pneumoniae st

230 complex (ST/CC) were found to share similar virulence gene profiles.

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

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

233 of virulence genes, and toxboxes in several virulence gene promoters have been characterized.

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

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

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

237 Given the role of sRNA in virulence gene regulation and stress response, potential

238 pecific differences in agr autoinduction and virulence gene regulation by utilizing congenic strains,

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

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

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

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

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

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

245 To further our understanding of virulence gene regulation, an in silico approach was use

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

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

248 A global negative virulence gene regulator CsrRS of SDSE modulated the exp

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

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

251 on to SK, suggesting disruption of a general virulence gene regulatory network.

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

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

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

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

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

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

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

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

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

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

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

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

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

265 come and (i) presence of any of the 30 other virulence genes tested, (ii) presence of specific bacter

266 antial enteric comorbidities, had all of the virulence genes tested, but 66% of nonbacteremic, enteri

267 Among the 6 virulence genes tested, gelE and efaA were most prevalen

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

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

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

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

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

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

274 All MRSA ST398 isolates lacked accessory virulence genes that were detected in other ST/CC.

275 eased transcription of global regulators and virulence genes; these features are reminiscent of a str

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

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

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

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

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

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

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

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

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

285 ty acid incorporation into phospholipids and virulence gene transcription.

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

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

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

289 tes from urine were screened for 16 putative virulence genes using high-throughput dot-blot hybridiza

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

291 Any virulence gene was associated with IBC/IIB.

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

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

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

295 Virulence genes were consistently enriched in highly cod

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

297 Early in infection, virulence genes were expressed and required for pathogen

298 T398 lineage displayed the lowest content of virulence genes, which consisted mainly of genes detecte

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

300 neral mechanism for Mga regulation of target virulence genes within GAS and provides insight into rel