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 bare fallowed soils rely upon the action of exoenzymes.

10 li and/or extracellular secretion of several exoenzymes.

11 an adhesive pilus organelle and secretion of exoenzymes.

12 and beta-propeller phytase genes coding for exoenzymes.

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

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

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

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

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

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

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

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

21 C3 exoenzyme ADP-ribosylates and inactivates Rho with high

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 The exoenzyme ATX can potentially regulate diverse processes

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

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

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

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

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

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

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

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

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

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

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

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

54 Exoenzyme C3 of Clostridium botulinum ADP-ribosylates Rh

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 C3 exoenzyme exhibited broad cytostatic activity toward a n

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 nt acquisition potential by diversifying the exoenzyme palette.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 We used exoenzyme root tip assays and molecular identification t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 Exoenzyme S (ExoS) is translocated into eukaryotic cells

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 Exoenzyme S is an ADP-ribosylating extracellular protein

168 Exoenzyme S is an extracellular ADP-ribosyltransferase o

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

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

171 Exoenzyme S is purified from culture supernatants as a n

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

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

174 Exoenzyme S of Pseudomonas aeruginosa is an ADP-ribosylt

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

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

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

178 388 was used to identify genes required for exoenzyme S production.

179 The exoenzyme S regulatory protein ExsA regulates a type III

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

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

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

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

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

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

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

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

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

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

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

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

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

193 -53 catalyzed the FAS (for factor activating exoenzyme S)-dependent ADP-ribosylation of soybean tryps

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

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

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

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

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

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

200 as contributing to the catalytic activity of exoenzyme S.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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