ライフサイエンスコーパス: exoenzyme

1 -nucleate due to inactivation of Rho with C3 exoenzyme.

2 be blocked by pretreating the cells with C3 exoenzyme.

3 ally antagonized by Clostridium botulinum C3 exoenzyme.

4 1 integrin or pretreatment of cells with C3 exoenzyme.

5 sis and secretion of a costly but beneficial exoenzyme.

6 Activation by RhoA was suppressed by the C3 exoenzyme.

7 s reversed by treatment of the cells with C3 exoenzyme.

8 ctin cytoskeleton, which was disrupted by C3 exoenzyme.

9 and beta-propeller phytase genes coding for exoenzymes.

10 li and/or extracellular secretion of several exoenzymes.

11 an adhesive pilus organelle and secretion of exoenzymes.

12 to substrates and release powerful catabolic exoenzymes.

13 nutrients, and more efficient use of costly exoenzymes.

14 were also not impaired for type II-dependent exoenzymes.

15 bare fallowed soils rely upon the action of exoenzymes.

16 s determined by intrastromally injecting the exoenzyme (20-200 ng) into the cornea.

17 Treatment of cells with C3-exoenzyme (a Rho GTPase-specific inhibitor), however, ab

18 C. botulinum C3 exoenzyme, a pharmacologic agent that specifically cause

19 Exposure of HUVECs to C3 exoenzyme, a selective inhibitor of Rho, markedly reduce

20 blocked by pretreatment of the cells with C3 exoenzyme, a specific inhibitor of the small G-protein,

21 The Rho inhibitory C3 exoenzyme abolished the effects of parallel flow.

22 Pretreatment of myocytes with C3 exoenzyme ADP-ribosylated Rho and inhibited the characte

23 C3 exoenzyme ADP-ribosylates and inactivates Rho with high

24 Rho-GDI and C3 exoenzyme also inhibited EGF-induced migration of IEC-6

25 C3 transferase exoenzyme, an inhibitor of Rho, abolished BK-induced NF-

26 Further, C3 exoenzyme, an inhibitor of Rho, blocked induction of int

27 -ordinately controls flagella synthesis, and exoenzyme and antibiotic production in X. nematophila.

28 which specifies an RNA regulator controlling exoenzyme and HarpinEcc production.

29 alpha(q) on this response is inhibited by C3 exoenzyme and requires phospholipase C activation.

30 tion of this site affects swarming motility, exoenzyme and secondary metabolite production in the hum

31 The Rho-specific inhibitor C3 exoenzyme and small interfering RNA to the Rho GDP/GTP e

32 des or treated with Clostridium botulinum C3 exoenzyme and then stimulated with fibronectin (FN) or c

33 Pf-5 also produces a broad spectrum of exoenzymes and natural products with antibiotic activity

34 nteraction (overflow metabolism, mixotrophy, exoenzymes and reactive oxygen species detoxification) c

35 regulating expression of virulence factors (exoenzymes and toxins) and by inducing inflammation.

36 am effectors {i.e., Rho-family functions (C3-exoenzyme) and Rho kinase [Y27632 (N-(4-pyridyl)-4-(1-am

37 tor Y-27632, permeable Rho/ROCK inhibitor c3-exoenzyme, and PKC activator PdBU was measured.

38 lic goods, including quorum-sensing signals, exoenzymes, and effectors.

39 cleotides by means of the following secreted exoenzymes: apyrase, 5'-nucleotidase, and adenosine deam

40 Aggregation and compaction induced by C3 exoenzyme are diminished by removal of extracellular Ca2

41 e in vivo functions of the type III-secreted exoenzymes are less well understood, particularly for th

42 ression of genes encoding several hydrolytic exoenzymes as well as an operon that may encode a novel

43 Addition of C3 exoenzyme at any time after addition of the bacteria blo

44 of Cdc42 and Rho, as well as recombinant C3 exoenzyme, attenuated the shear stress activation of c-J

45 The exoenzyme ATX can potentially regulate diverse processes

46 Treatment of the cells with C3 exoenzyme before AMF stimulation inhibited both the form

47 about the mechanisms by which the bacterial exoenzyme binds to and functions on the fungal surface t

48 Inactivation of Rho by C3 transferase exoenzyme blocked agonist-induced lymphocyte alpha4beta1

49 holine receptors, inactivating RhoA using C3 exoenzyme blocked the ability of ml receptors to suppres

50 C3 exoenzyme blocked the effects of Rho(Val-14) and induced

51 tions were inhibited with specific inhibitor exoenzyme C3 (C3) and confirmed by knockdown with small

52 Rho GTPases are specifically inactivated by exoenzyme C3 (C3) of Clostridium botulinum.

53 tants of MM1 expressing active and Botulinum exoenzyme C3 (C3)-sensitive (Val14), or active and C3-in

54 eurons, and inhibition of RhoA activity with exoenzyme C3 attenuated cell death, indicating that thro

55 RhoA by treatment with Clostridium botulinum exoenzyme C3 exotoxin or expression of dominant negative

56 Incubation of myocytes with exoenzyme C3 for 48 hours completely ADP-ribosylated Rho

57 Specific ADP-ribosylation of Rho1p by exoenzyme C3 inactivates glucan synthase activity specif

58 Exoenzyme C3 of Clostridium botulinum ADP-ribosylates Rh

59 rprisingly, pretreatment of the lysates with exoenzyme C3 shifted both resident and recruited RhoA fr

60 P2, dominant-negative Src, and Rho inhibitor exoenzyme C3 transferase each inhibited collagen I induc

61 The effect of a Rho protein inhibitor, exoenzyme C3 transferase, on tPA production was also det

62 eonine kinase inhibitors, cytochalasin D, or exoenzyme C3, a potent inhibitor of the small GTPase Rho

63 st, treatment of cells with a Rho inhibitor, exoenzyme C3, or cellular overexpression of dominant neg

64 iments, HK2 cells were treated with toxin B, exoenzyme C3, Y-27632, and HA1077.

65 so induced by a blockade of RhoA function by exoenzyme C3.

66 oA activation with Clostridium botulinium C3 exoenzyme (C3) or the blocking of ROCK activation with Y

67 The Rho ADP-ribosylating C3 exoenzyme (C3bot) is a bacterial protein toxin devoid of

68 nhibition of Rho, by either lovastatin or C3 exoenzyme, can increase the translational efficiency of

69 as the fungal metabolite brefeldin A, and C3 exoenzyme (Clostridium botulinum), implicating the activ

70 Of the 10 agents microinjected, C3 exoenzyme, constitutively active Cdc42, and dominant neg

71 avastatin, and ADP-ribosylation of Rho by C3 exoenzyme decreases PDGF-stimulated phosphatidylinositol

72 atment with 1.0 micro g/ml RhoA inhibitor C3 exoenzyme demonstrated that RhoA activity was necessary

73 ced force generation, whereas Y-27632 and c3 exoenzyme did not.

74 gative RhoA or the Rho-specific inhibitor C3 exoenzyme disrupted podosome structure as judged by loca

75 e RhoAAsn-19 or inactivation of RhoA with C3 exoenzyme does not affect PMA-induced myosin reorganizat

76 ructed, and microarray studies revealed that exoenzymes (Ecp protease and Geh lipase) and low-molecul

77 least in part, why this bacterially derived exoenzyme effectively modulates this virulent cross-king

78 The retention of exoenzymes effectively renders the biofilm matrix an ext

79 ocytes with a RhoA inhibitor, C3 transferase exoenzyme, effectively blocked LPS-induced IL-8 gene exp

80 ADP-ribosylation of Rho with C3 exoenzyme enhanced PIP5K binding by approximately eightf

81 C3 exoenzyme exhibited broad cytostatic activity toward a n

82 n stages, embryos were microinjected with C3 exoenzyme from Clostridium botulinum or with wild-type,

83 The addition of C3 exoenzyme from clostridium botulinum to specifically rib

84 cells were inactivated by treatment with C3 exoenzyme from Clostridium botulinum, the ability of Gal

85 Both constructs, as well as the C3 exoenzyme from Clostritium botulinum, partially reduced

86 directly, by inhibiting the transcription of exoenzyme genes; and (ii) indirectly, by preventing the

87 her analyses revealed that S. mutans-derived exoenzyme glucosyltransferase B (GtfB), which binds to t

88 be largely mediated by the S. mutans-derived exoenzyme glucosyltransferase B (GtfB); GtfB readily bin

89 present study demonstrates that a bacterial exoenzyme (GtfB) augments the C. albicans counterpart in

90 bitor piceatannol, and the RhoA inhibitor C3 exoenzyme had no effect, implying that neither tyrosine

91 studies, the Clostridium botulinum toxin C3 exoenzyme has been used to ADP-ribosylate and inactivate

92 ells was inhibited by pertussis toxin and C3 exoenzyme, implicating G(i/o)- and Rho-dependent pathway

93 f LPA molecular species and the level of ATX exoenzyme in bronchoalveolar lavage fluids of human pati

94 Clostridium botulinum C3 exoenzyme inactivates the small GTP-binding protein fami

95 ted protein kinase kinase inhibitors, and C3 exoenzyme inactivation of rho, suggesting mediation by E

96 ha(12) was inhibited by microinjection of C3 exoenzyme, indicating Rho dependence.

97 as blocked by preincubation of cells with C3 exoenzyme, indicating that the stimulation of PLD may in

98 ation or electroporation with recombinant C3 exoenzyme induces rapid aggregation and compaction of SC

99 emonstrate that treatment of T cells with C3 exoenzyme inhibits IL-2 transcription following ligation

100 ibosylation of rho by C3 ribosyltransferase (exoenzyme) inhibits IL-2 production due, in part, to the

101 Scrape loading Clostridium botulinum C3 exoenzyme into primary peripheral blood human T lymphocy

102 Among the Legionella type II-dependent exoenzymes is a p-nitrophenol phosphorylcholine (p-NPPC)

103 Metalation of membrane-bound and secreted exoenzymes is more problematic since metal concentration

104 This gene, hexA (hyperproduction of exoenzymes), is a close relative of the Erwinia chrysant

105 Previously, the exoenzyme laccase was believed to attack organic the mat

106 grading bacterial genera and the activity of exoenzyme lipase.

107 stic or endothelial cells with Y-27632 or C3 exoenzyme markedly reduced the rate of de-adhesion, whil

108 For some exoenzymes, metalation occurs in the cytosol, and metala

109 rsed by dominant negative N19RhoA and the C3 exoenzyme of Clostridium botulinum, further supporting a

110 Western blot analysis, and the effects of C3-exoenzyme on lovastatin-induced cytoskeletal changes wer

111 tion of Rho by the Rho-specific inhibitor C3 exoenzyme or by a dominant negative Rho A (RhoN19) inhib

112 inhibition of RhoA signaling with either C3 exoenzyme or dominant negative Rho blocked arachidonic a

113 We found that blockade of RhoA with C3 exoenzyme or inhibition of RhoA kinase by the specific i

114 Inhibition of Rho proteins with C3 exoenzyme or of Rho kinase with Y27632 attenuated TNF-al

115 eatment of endothelial cell networks with C3 exoenzyme or recombinant adenoviruses expressing dominan

116 ere abolished by either the Rho inhibitor C3 exoenzyme or Rho-kinase inhibitor Y-27632.

117 s that were abolished in cells expressing C3 exoenzyme or Rho19N.

118 C3 exoenzyme or rhoGDI, inhibitors of rhoA signaling, block

119 Interestingly, inactivation of RhoA with C3-exoenzyme or treatment with ROK inhibitors strongly inhi

120 rganic carbon and nitrogen recycling through exoenzymes or an overflow metabolism, in which the high

121 (CHO) cell model system of alphaIIbbeta3: C3 exoenzyme (or overexpression of dominant-negative N19Rho

122 the presence or absence of Rho inhibitor (C3 exoenzyme) or ROCK (Rho kinase) inhibitor (Y27632).

123 cquire nutrients, retain and protect eDNA or exoenzymes, or offer sorption sites for ions and hydroph

124 nt acquisition potential by diversifying the exoenzyme palette.

125 sease by secreting plant cell wall degrading exoenzymes (PCWDEs).

126 was not affected by Clostridium botulinum C3 exoenzyme, pertussis toxin, or cholera toxin.

127 py hexA expression resulted in repression of exoenzyme, pigment and antibiotic production and repress

128 of virulence factors, including degradative exoenzymes possibly involved in resistance to antimicrob

129 ansferase (C3) toxin, a Rho-ADP-ribosylating exoenzyme, potently inhibited migration.

130 nd starch-) and Streptococcus mutans-derived exoenzymes present in the pellicle and on microbial surf

131 ents of potential enzyme activities of eight exoenzymes probably involved in nutrient mobilization.

132 xA from even a low-copy plasmid can suppress exoenzyme production in Ecc and Eca and motility in Eca.

133 We show that exoenzyme production is overall advantageous only if ini

134 indicating that motility and FliA-regulated exoenzyme production were not essential for virulence.

135 Inactivation of fliA eliminated exoenzyme production which was restored by complementati

136 ed in multiple phenotypic changes, including exoenzyme production, motility and differential regulati

137 haracterize a role for EepR in regulation of exoenzyme production, stress survival, cytotoxicity to h

138 mutans gtfBC expression (responsible for Gtf exoenzymes production), enhancing Gtf activity essential

139 de variety of virulence determinants such as exoenzymes (proteases, lipases, nucleases) and downregul

140 Rho GTPase-specific Clostridium botulinum C3 exoenzyme, raising the possibility that it may be a misc

141 tive site loop near the central core, the C3 exoenzyme replaces the active site loop with an alpha-he

142 cycle is sufficiently long compared with the exoenzyme response time.

143 Using C-3 exoenzyme (RhoA inhibitor) or monodansylcadaverine (TGas

144 We used exoenzyme root tip assays and molecular identification t

145 s data indicated that Pseudomonas aeruginosa exoenzyme S (ExoS) ADP-ribosylated Ras at multiple sites

146 Pseudomonas aeruginosa exoenzyme S (ExoS) ADP-ribosylated Ras to a stoichiometr

147 Pseudomonas aeruginosa exoenzyme S (ExoS) ADP-ribosylates multiple eukaryotic t

148 Production of the ADP-ribosylating enzyme exoenzyme S (ExoS) by Pseudomonas aeruginosa has been as

149 d protein ligand, the ADP-ribosyltransferase Exoenzyme S (ExoS) from Pseudomonas aeruginosa.

150 Type III-mediated translocation of exoenzyme S (ExoS) into HT-29 epithelial cells by Pseudo

151 Pseudomonas aeruginosa delivers exoenzyme S (ExoS) into the intracellular compartment of

152 Exoenzyme S (ExoS) is a bifunctional Pa TTS effector pro

153 Exoenzyme S (ExoS) is a bifunctional toxin directly tran

154 Pseudomonas aeruginosa Exoenzyme S (ExoS) is a bifunctional type-III cytotoxin.

155 Exoenzyme S (ExoS) is a bifunctional virulence factor di

156 Exoenzyme S (ExoS) is a mono-ADP-ribosyltransferase secr

157 Pseudomonas aeruginosa exoenzyme S (ExoS) is a type III secretion (TTS) effecto

158 Exoenzyme S (ExoS) is an ADP-ribosyltransferase produced

159 Pseudomonas aeruginosa exoenzyme S (ExoS) is an ADP-ribosyltransferase that mod

160 Exoenzyme S (ExoS) is translocated into eukaryotic cells

161 studies reported that Pseudomonas aeruginosa exoenzyme S (ExoS) possessed an absolute requirement for

162 Type III-delivered exoenzyme S (ExoS) preferentially ADP-ribosylated membra

163 two mutations within Pseudomonas aeruginosa exoenzyme S (ExoS) showed that a E379D mutation inhibite

164 Exoenzyme S (ExoS), an ADP-ribosylating enzyme produced

165 n of 14-3-3zeta with another target protein, exoenzyme S (ExoS), an ADP-ribosyltransferase from Pseud

166 nal data suggest that Pseudomonas aeruginosa exoenzyme S (ExoS), an ADP-ribosyltransferase, is transl

167 f at least four different effector proteins, exoenzyme S (ExoS), ExoT, ExoU, and ExoY.

168 The exoenzyme S (ExoS)-producing Pseudomonas aeruginosa stra

169 two ADP-ribosyltransferases, exotoxin A and exoenzyme S (ExoS).

170 etained the requirement of factor activating exoenzyme S (FAS) activation for the expression of ADP-r

171 for the eukaryotic protein factor activating exoenzyme S (FAS) for expressing ADP-ribosyltransferase

172 eutralized the ability of 14-3-3 to activate exoenzyme S ADP-ribosyltransferase.

173 pparatus which is required for the export of exoenzyme S and potentially other co-ordinately regulate

174 udies prove that the 53- and 49-kDa forms of exoenzyme S are encoded by separate genes.

175 Thus, exoenzyme S could interfere with host cell physiology vi

176 Pseudomonas aeruginosa exoenzyme S double ADP-ribosylates Ras at Arg(41) and Ar

177 PAO-exsA::omega,, which lacks exoenzyme S expression, was fully virulent, causing at l

178 equence similarity to the ribosyltransferase exoenzyme S from Pseudomonas aeruginosa and the cytotoxi

179 t studies predict that the amino-terminus of exoenzyme S has limited primary amino acid homology with

180 Exoenzyme S is an ADP-ribosylating extracellular protein

181 Exoenzyme S is an extracellular ADP-ribosyltransferase o

182 The production of exoenzyme S is correlated with the ability of Pseudomona

183 sion of the ADP-ribosyltransferase domain of exoenzyme S is cytotoxic to eukaryotic cells.

184 Exoenzyme S is purified from culture supernatants as a n

185 Exoenzyme S of Pseudomonas aeruginosa (ExoS) is a member

186 he 53-kDa (Exo53) and 49-kDa (ExoS) forms of exoenzyme S of Pseudomonas aeruginosa are encoded by sep

187 Exoenzyme S of Pseudomonas aeruginosa is an ADP-ribosylt

188 ding ExsB and most of ExsB' severely reduced exoenzyme S production.

189 for ExsB and ExsB', however, did not affect exoenzyme S production.

190 cleotide sequence analysis of loci linked to exoenzyme S production.

191 388 was used to identify genes required for exoenzyme S production.

192 The exoenzyme S regulatory protein ExsA regulates a type III

193 Proteins encoded by the exoenzyme S regulon and the Yersinia Yop virulon show a

194 It will be important to understand how the exoenzyme S regulon contributes to pathogenesis and whet

195 The exoenzyme S regulon is a set of coordinately regulated v

196 Members of the exoenzyme S regulon represent only a portion of the viru

197 ogenic mutants of the Pseudomonas aeruginosa exoenzyme S regulon were compared to identify proteins c

198 e ExsA is a transcriptional regulator of the exoenzyme S regulon, chromosomal preparations from invas

199 rolled by ExsA and therefore was part of the exoenzyme S regulon.

200 in vitro cytotoxicity and expression of the exoenzyme S regulon.

201 trains were screened for their complement of exoenzyme S structural genes, exoS, encoding the 49-kDa

202 region that is co-ordinately regulated with exoenzyme S synthesis.

203 Expression of ExsC, ExsB, and ExsA (the exoenzyme S trans-regulatory locus) of Pseudomonas aerug

204 oRI fragment that is not contiguous with the exoenzyme S trans-regulatory operon.

205 t upon, exogenous FAS (for factor activating exoenzyme S), which indicated that serum contained endog

206 -53 catalyzed the FAS (for factor activating exoenzyme S)-dependent ADP-ribosylation of soybean tryps

207 on the levels of elastase, phospholipase C, exoenzyme S, and alkaline protease.

208 enetic relationship between the two forms of exoenzyme S, exoS (encoding the 49-kDa form) was used as

209 by ART3, ART4, ART5, Pseudomonas aeruginosa exoenzyme S, or cholera toxin A subunit.

210 The carboxyl-terminal 222 amino acids of exoenzyme S, which represent the FAS-dependent ADP-ribos

211 ion mutants were isolated which exhibited an exoenzyme S-deficient phenotype (388::Tn5Tc 469, 550, 34

212 yltransferase activity of the 53-kDa form of exoenzyme S.

213 as contributing to the catalytic activity of exoenzyme S.

214 med Exo53, which reacted to antisera against exoenzyme S.

215 th exoenzyme Y (ExoY) alone or together with exoenzymes S and T (ExoS/T/Y) generated the most virulen

216 is the first report of the factor-activating-exoenzyme-S-dependent ADP-ribosyltransferase activity of

217 h as bioluminescence, biofilm formation, and exoenzyme secretion.

218 The 1.7 A resolution C3 exoenzyme structure establishes the conserved features o

219 Importantly, the central core of the C3 exoenzyme structure is distinguished by the absence of a

220 d by pretreatment with pertussis toxin or C3 exoenzyme, suggesting requirements for both a Gi protein

221 is inhibited by inactivation of Rho with C3 exoenzyme, suggesting that myosin phosphorylation is nec

222 Exoenzyme T (ExoT) is a bifunctional type III cytotoxin

223 Autotaxin (ATX) is an exoenzyme that potently induces tumor cell motility, and

224 clusters for seven natural products and two exoenzymes that are produced by the bacterium under the

225 xanoyl)-L-homoserine lactone (OHHL), induces exoenzymes that degrade the plant cell wall by the patho

226 HEp-2 cells, a block in secretion of several exoenzymes that follow the type II secretion pathway, an

227 is further, platelets were incubated with C3 exoenzyme to adenine diphosphate (ADP)-ribosylate and in

228 arsenal of hemolysins, immunomodulators, and exoenzymes to cause disease.

229 recycling were inhibited by Toxin B and C(3) exoenzyme treatment in CHO and THP-1 cells, confirming a

230 Expression of exoenzyme U (ExoU) by P. aeruginosa is associated with a

231 acute infections express a potent cytotoxin, exoenzyme U (ExoU), that is delivered via the type III s

232 inosa isolates express the effector molecule exoenzyme U (ExoU), which we demonstrate is capable of i

233 xceptionally strong expression of toxins and exoenzymes, upregulation of fibrinogen-binding proteins,

234 express recombinant Clostridium botulinum C3 exoenzyme (using double subgenomic recombinant Sindbis v

235 controlling the production of antibiotic and exoenzyme virulence determinants in the phytopathogen, E

236 ified a gene important for the regulation of exoenzyme virulence factor synthesis in the plant pathog

237 nd Eca produce abnormally high levels of the exoenzyme virulence factors pectate lyase, cellulase and

238 Rac1, Cdc42 and their mutants, as well as C3 exoenzyme, we altered cytoskeletal organization under no

239 Pretreatment with Clostridium botulinum C3 exoenzyme which inactivates the small GTP-binding protei

240 The C3 exoenzyme, which ADP-ribosylates and inactivates Rho, fu

241 Preincubation of endothelial cells with C3 exoenzyme, which inactivated intracellular Rho-GTPase, b

242 Botulinum C3 exoenzyme, which inactivates Rho p21 (known to participa

243 eatment of SMCs with Clostridia botulinum C3 exoenzyme, which inhibits RhoA activation, decreased SMC

244 ons (i.e. hemolysins, pilins, adhesins), and exoenzymes with a potential mixotrophic goal (i.e. exopr

245 toxic amyloid release, yet intoxication with exoenzyme Y (ExoY) alone or together with exoenzymes S a

246 Exoenzyme Y (ExoY) is a type III secretion system effect

247 The promiscuous nucleotidyl cyclase, exoenzyme Y (ExoY), is one of the most common effectors

248 s summarized above suggested that BglA is an exoenzyme yielding Glc at each cleavage step.