ライフサイエンスコーパス: CDT

1 CDT (Clostridium difficile transferase) is a binary, act

2 CDT activity requires the function of three genes: cdtA,

3 CDT consists of three protein subunits, CdtA, CdtB, and

4 CDT depolymerizes actin, causes formation of microtubule

5 CDT has limited sensitivity as a biomarker of heavy alco

6 CDT holotoxin containing these mutant forms of CdtB did

7 CDT is a potential virulence factor in H. pullorum that

8 CDT is a primary mechanism for the lateral propagation o

9 CDT is composed of three proteins, CdtA, CdtB, and CdtC.

10 CDT is encoded by three highly conserved genes, cdtA, -B

11 CDT leads to the collapse of the actin cytoskeleton and,

12 CDT proved safe to administer in vivo, and when incorpor

13 CDT should be employed for DVT patients who have severe

14 CDT treatment was also shown to cause HeLa cells to accu

15 CDT, the third C. difficile toxin, is a binary actin-ADP

16 CDT-like activities were no longer expressed by the reco

17 CDT-treated GMSM-K cells displayed cell cycle arrest at

18 CDTs are virulence factors secreted by a variety of path

19 addition of the Campylobacter jejuni 81-176 CDT to primary human fibroblasts resulted in formation o

20 In cells lacking CUL-4, CDT-1 levels fail to decrease during S phase and instead

21 A CDT and hemolysin double mutant was constructed and test

22 y infected with wild-type H. hepaticus and a CDT-deficient isogenic mutant.

23 eyi mutant restored its ability to express a CDT that killed both HeLa cells and HaCaT keratinocytes.

24 However, a CDT-negative H. hepaticus mutant had a significantly dim

25 nese hamster ovary cells characteristic of a CDT.

26 n, six human subjects were inoculated with a CDT mutant and parent at multiple sites.

27 osed to recombinant A. actinomycetemcomitans CDT.

28 oxic effects of the A. actinomycetemcomitans CDT.

29 sa, two cellodextrin transporters, CDT-1 and CDT-2, contribute to cellulose sensing.

30 ating that redundant regulation of CDC-6 and CDT-1 prevents rereplication.

31 origin recognition complex (ORC), CDC-6, and CDT-1.

32 p between DNase-related residues in CdtB and CDT biological activity.

33 red questionnaire of alcohol consumption and CDT analysis using the standardized reference measuremen

34 8 secretion requires functional flagella and CDT and depends on the activation of NF-kappaB through T

35 yi 35000HP, which produces LspA1, LspA2, and CDT.

36 markedly elevated levels of phospho-p53 and CDT-1.

37 ation of NF-kappaB through TLR signaling and CDT in human intestinal epithelial cells.

38 To determine if anti-CDT antibodies are produced in human infection, a toxin

39 released all three CDT proteins, as well as CDT activity and IL-8 activity, from membranes into supe

40 cose levels (p = 0.044) and better scores at CDT (p = 0.030).

41 e dehydrogenase antigen (GDH) and toxin A/B (CDT) tests in two algorithmic approaches for a tertiary

42 understanding about the interaction between CDT and its receptor LSR, which is key to the developmen

43 significant difference in mortality between CDT versus anticoagulation alone; however, the bleeding

44 nd mortality additionally produce the binary CDT toxin (Clostridium difficile transferase) that ADP-r

45 arbohydrate specificities were used to block CDT activity and the cell surface binding of CdtA-II(Ec)

46 GNA, and NPA partially or completely blocked CDT activity.

47 embrane preparations became positive in both CDT and IL-8 assays.

48 three CDT subunit proteins neutralized both CDT activity and the activity responsible for IL-8 relea

49 on a shuttle plasmid in trans restored both CDT activity and the ability to release IL-8 to membrane

50 manner indistinguishable from that caused by CDT treatment.

51 HeLa cells blocked killing of these cells by CDT holotoxin.

52 enorhabditis elegans, RBX-1 silencing causes CDT-1 accumulation, triggering DDR in intestinal cells,

53 cle arrest, and apoptosis of cultured cells, CDTs are proposed to enhance virulence by blocking cellu

54 Further, crude CDT preparations possess detectable DNase activity not a

55 nces were tested for their ability to detect CDT producers and to determine CDT type.

56 ity to detect CDT producers and to determine CDT type.

57 26 patients had a diagnostic CDT based on a threshold value of %CDT > 1.7 indicating

58 ndependently associated with non-diagnostic %CDT (</= 1.7).

59 important for intoxication by four different CDTs.

60 e that causes actin cytoskeletal disruption, CDT is typically produced by the major, hypervirulent st

61 ains a cyclopenta-[2,1-b:3,4-b']dithiophene (CDT) unit flanked by two benzo[2,1,3]thiadiazole (BT) fr

62 H. ducreyi CDT activity is encoded by a three-gene cluster (cdtABC)

63 s to yield a profile characteristic for each CDT.

64 Ec-CDT and Hd-CDT shared comparable in vitro DNase activiti

65 mechanisms of CDTs from Escherichia coli (Ec-CDT) and Haemophilus ducreyi (Hd-CDT), which share limit

66 7 (T22N), suggesting that Hd-CDT, but not Ec-CDT, is trafficked through late endosomal vesicles.

67 m and nucleus, while having no effects on Ec-CDT.

68 These results suggest that Ec-CDT and Hd-CDT are transported within cells by distinct

69 ompetitive binding studies suggested that Ec-CDT and Hd-CDT bind to discrete cell surface determinant

70 verely reduce cellobiose transport by either CDT-1 or CDT-2 when expressed individually do not greatl

71 C. elegans CDT-1 is present in G1-phase nuclei but disappears as ce

72 o make sound clinical judgments on employing CDT.

73 at Salmonella enterica serovar Typhi encodes CDT activity, which depends on the function of a CdtB ho

74 UBXN-3/FAF1 binds to the licensing factor CDT-1 and additional ubiquitylated proteins, thus promot

75 nd specific structural regions essential for CDT are identified.

76 e show that septins (SEPT) are essential for CDT-induced protrusion formation.

77 dtB position 95 was considered important for CDT activity.

78 receptor (LSR) is the host cell receptor for CDT, and our aim was to gain a deeper insight into the i

79 heterodimer, not TLR2/1, is responsible for CDT recognition, and that gene pathways including NF-kap

80 d cells to intoxication by three of the four CDTs tested.

81 se results provide evidence for a functional CDT in a human oral pathogen.

82 r positivity by LAMP plus another test (GDH, CDT, or the Premier C. difficile toxin A and B enzyme im

83 ication (LAMP), and algorithm 2 entailed GDH/CDT followed by cytotoxicity neutralization assay (CCNA)

84 lgorithm 1 entailed initial testing with GDH/CDT followed by loop-mediated isothermal amplification (

85 ication of BP-based materials in PET-guided, CDT-enhanced combination cancer therapy.

86 These results suggest that Ec-CDT and Hd-CDT are transported within cells by distinct pathways, p

87 binding studies suggested that Ec-CDT and Hd-CDT bind to discrete cell surface determinants.

88 Ec-CDT and Hd-CDT shared comparable in vitro DNase activities of the C

89 ruption of endosome acidification blocked Hd-CDT-mediated cell cycle arrest and toxin transport to th

90 ia coli (Ec-CDT) and Haemophilus ducreyi (Hd-CDT), which share limited amino acid sequence homology,

91 ant negative Rab7 (T22N), suggesting that Hd-CDT, but not Ec-CDT, is trafficked through late endosoma

92 s of evidence indicate that (i) H. hepaticus CDT plays a crucial role in the persistent colonization

93 esults provide a framework to understand how CDT functions at the host cell interface.

94 To better understand how CDT functions, we used cryo-electron microscopy to defin

95 However, CDT mutations did not affect the ability of 81-176 to in

96 y using an analogue of tachyplesin I (TP-I), CDT (KWFRVYRGIYRRR-NH(2)), in which all four cysteines w

97 Like TP-I, CDT shows antimicrobial activity and disrupts Escherichi

98 general groups, with distinct differences in CDT type and in their complement of virulence-associated

99 r cholesterol, also previously implicated in CDT binding, affected intoxication by only a subset of C

100 cts in host factors previously implicated in CDT binding, including glycoproteins, and glycosphingoli

101 ns and glycolipids, previously implicated in CDT-host interactions, were not required for intoxicatio

102 se-specific active site residues resulted in CDT preparations that lacked DNase activity and failed t

103 d be applied when ordering and interpreting %CDT results, particularly in women, patients with cirrho

104 rating cells that are treated with C. jejuni CDT.

105 jejuni 81-176 and an isogenic mutant lacking CDT activity (cdtB mutant) were inoculated into NF-kappa

106 huttle plasmid into a C. coli strain lacking CDT, membrane preparations became positive in both CDT a

107 was a significant difference in the mean log CDT ratio between those who received ondansetron (1 and

108 The national CDT utilization rates increased from 16.0% in 2005 to 34

109 body to the cdtC gene product can neutralize CDT activity in vitro.

110 on of nonexportable CDC-6 with nondegradable CDT-1, indicating that redundant regulation of CDC-6 and

111 toxin activity in these naturally occurring CDT-negative C. jejuni strains was then investigated at

112 The mechanism of action of CDT suggests that the infliction of limited damage could

113 ght into the molecular and cellular basis of CDT-host interactions.

114 enhanced efficacy through the combination of CDT and chemotherapy.

115 inal truncations of the binding component of CDT (CDTb), we found that amino acids 757-866 of CDTb ar

116 cture of CDTb, the cell-binding component of CDT.

117 cle arrest, all of which are consequences of CDT action.

118 directly linking Dox and TF, cytotoxicity of CDT resulted from nuclear entry by Dox, promoting double

119 ciable role for SKPT-1 in the degradation of CDT-1 during S phase, even in a sensitized ddb-1 mutant

120 ans DDB-1 is required for the degradation of CDT-1 during S phase.

121 in part, by facilitating the degradation of CDT-1.

122 B-suggesting that the varied distribution of CDT in bacteria implicates many human pathogens as posse

123 Low doses of CDT result in the formation of microtubule-based protrus

124 colonized chickens despite the expression of CDT in the avian gut as indicated by reverse transcripti

125 ults indicate that neither the expression of CDT, nor that of hemolysin, nor both are required for pu

126 ting OMV induction of IL-8 is independent of CDT.

127 al conditions reveal that the interaction of CDT with lipid membranes is an enthalpy-driven process.

128 Here we explore the interactions of CDT with TLR2 and the impact on host immunity during CDI

129 a useful model to further study the role of CDT and other aspects of C. jejuni pathogenesis.

130 isolates raised questions about the role of CDT in some cases of human campylobacteriosis.

131 To investigate the role of CDT in the pathogenesis of H. hepaticus, transposon muta

132 needed to assess whether standardization of CDT protocols across all institutions in the United Stat

133 o-electron microscopy (cryo-EM) structure of CDT, a bipartite toxin comprised of the proteins CDTa an

134 tablished that CdtB is the active subunit of CDT, exerting its effect as a nuclease that damages the

135 Correlations between the type of CDT produced, the presence of other virulence properties

136 eting of the receptor and cellular uptake of CDT.

137 ere has been a steady increase in the use of CDT in the treatment of patients with inferior vena cava

138 nce measurement technique, widespread use of CDT remains limited due to low sensitivity.

139 an explanation for the enhanced virulence of CDT-expressing C. difficile and demonstrate a mechanism

140 p is interrelated with institution volume of CDT is unknown.

141 that an increase in institutional volume of CDT was associated with lower in-hospital mortality and

142 Despite the widespread distribution of CDTs among several important human pathogens, our unders

143 Here, the intoxication mechanisms of CDTs from Escherichia coli (Ec-CDT) and Haemophilus ducr

144 g, affected intoxication by only a subset of CDTs tested.

145 iagnostic CDT based on a threshold value of %CDT > 1.7 indicating heavy alcohol consumption, yielding

146 duce cellobiose transport by either CDT-1 or CDT-2 when expressed individually do not greatly impact

147 ing fluorometry demonstrate that the peptide CDT binds and inserts into only negatively charged membr

148 the risk-benefit ratio of pharmacomechanical CDT for acute proximal DVT.

149 for adjudication of discrepant GDH-positive/CDT-negative results.

150 ce of toxigenic C. difficile in GDH-positive/CDT-negative specimens.

151 O-linked surface sugar attachments prevents CDT-II(Ec) intoxication.

152 nd other diarrheagenic bacteria that produce CDT.

153 pted cdtABC coding region no longer produced CDT activity.

154 r hepaticus, which, like C. jejuni, produces CDT.

155 cient for protection from a strain producing CDT.

156 ed degradation of the DNA licensing protein, CDT-1, and premature spermatogenesis.

157 from our lab has shown that TLR2 recognizes CDT to induce inflammation.

158 thal distending toxin (CDT), and recombinant CDT causes apoptosis of DC in vitro.

159 Although related CDTs may share host factors, they also exploit unique ho

160 or invasion and the second of which requires CDT.

161 topic liver tumor growth via synergistic SDT/CDT.

162 , which is largely abrogated by simultaneous CDT-1 silencing.

163 ntly, inactivation of UBXN-3/FAF1 stabilizes CDT-1 and CDC-45/GINS on chromatin, causing severe defec

164 s but negative for binary toxin (TcdA+/TcdB+/CDT- toxin production type), found only in Clade-1.

165 via standardized Current Dental Terminology (CDT) codes related to periodontal treatment.

166 7), better scores at the Clock Drawing Test (CDT) (p = 0.047) and worse scores at the Geriatric Depre

167 ox) and transferrin (TF) to CND (CND-Dox-TF, CDT) was 10-100 times more potent than Dox against DLBCL

168 ry bowel disease in IL-10(-/-) mice and that CDT contributes to the virulence of H. cinaedi.

169 of C. jejuni is NF-kappaB dependent and that CDT may have proinflammatory activity in vivo, as well a

170 amination of these mutants demonstrated that CDT represents the previously described granulating cyto

171 In addition, it has been established that CDT is a tripartite AB toxin in which CdtB is the active

172 Data indicate that CDT may be involved in chronic inflammatory responses, v

173 These results indicated that CDT treatment results in a failure to activate CDC2, whi

174 We therefore proposed that CDT is a tripartite toxin composed of CdtB as the enzyma

175 isogenic H. hepaticus mutants revealed that CDT expression is not required for colonization of the m

176 otoxin from Haemophilus ducreyi reveals that CDT consists of an enzyme of the DNase-I family, bound t

177 Here, we show that CDT enhances the virulence of two PCR-ribotype 027 strai

178 We show that CDT interacts with the extracellular, Ig-like domain of

179 Here we show that CDT-induced protrusions allow vesicle traffic and contai

180 The NMR data suggest that CDT binding to negatively charged bilayers induces a cha

181 rulence factors, recent studies suggest that CDT increases the severity of C. difficile infection in

182 trial (RCT) (the CaVenT trial) suggest that CDT is reasonably well tolerated and that it may provide

183 The data suggest that CDT may interfere with T-cell responses to H. ducreyi by

184 These results suggest that CDT plays a key immunomodulatory role that allows persis

185 The data suggest that CDT usurps conserved regulatory principles involved in m

186 and holotoxin-assembled CdtBs suggested that CDT intoxication is contingent upon holotoxin disassembl

187 cally associates with CDT-1, suggesting that CDT-1 is a direct substrate of the CUL-4/DDB-1 E3 comple

188 nderance of available evidence suggests that CDT (with anticoagulation) should be routinely considere

189 Here we demonstrate that CDTs from Haemophilus ducreyi, Aggregatibacter actinomyc

190 Finally, we establish that CDTs are likely to be potent genotoxins, as indicated by

191 The CDT activities of C. jejuni strains possessing both type

192 The CDT group had longer length of stay and higher hospital

193 The CDT method is shown to be capable of simultaneous regist

194 The CDT peptide does not cause hemolysis up to 200 microg/mL

195 The CDT uses radial basis function transforms with distances

196 on outside of the cluster did not affect the CDT activity.

197 Both wild-type H. hepaticus and the CDT-deficient mutant successfully colonized IL-10-/- mic

198 was not significantly different between the CDT and the anticoagulation groups (2.0% versus 1.4%; P=

199 In conclusion, the CDT of H. pullorum is responsible for major cytopathogen

200 is DNase activity may be responsible for the CDT-induced cell cycle arrest.

201 4%; P=0.02) were significantly higher in the CDT group.

202 and resource utilization were higher in the CDT group.

203 In the CDT-negative strains, two types of mutation were identif

204 However, by 4 months after infection, the CDT-deficient mutant was no longer detectable in IL-10-/

205 In view of the possible role of the CDT as a prominent A. actinomycetemcomitans virulence fa

206 The formation of the CDT complex relies on the interaction of an N-terminal a

207 by delivering the active CdtB subunit of the CDT directly into the cells.

208 othing is known about the composition of the CDT holotoxin or the function of CdtA and CdtC.

209 identified CdtB as the active subunit of the CDT holotoxin.

210 unctional equivalent of the B subunit of the CDT toxin.

211 Expression of the CDT-like activities in A. actinomycetemcomitans was stra

212 These effects were dependent on the CDT, as they were (1) not observed in response to a cdtB

213 Together, these data suggest that the CDT holotoxin has intrinsic DNase activity that is assoc

214 overall strain relatedness revealed that the CDT producers studied here can be divided into three gen

215 ies of HPLF and oral epithelial cells to the CDT has important implications for the role of this puta

216 reduced following prolonged exposure to the CDT.

217 Examples of registration using the CDT are presented.

218 /1,000 males and 269/1,000 females using the CDT code method).

219 hepaticus, while animals challenged with the CDT-deficient mutant developed significantly lower IgG2c

220 while animals originally challenged with the CDT-deficient mutant had minimal cecal inflammation at t

221 nts, animals that cleared infection with the CDT-deficient mutant were protected from rechallenge wit

222 not required for intoxication by any of the CDTs tested.

223 therapeutic agent for chemodynamic therapy (CDT), but also as a stimulus to activate release of anti

224 n sites and Mn(2+) for chemodynamic therapy (CDT), resulting in enhanced reactive oxygen species (ROS

225 ctures further enables chemodynamic therapy (CDT)-enhanced PTT.

226 These CDT-producing strains possessed various combinations of

227 ls of sodium deoxycholate released all three CDT proteins, as well as CDT activity and IL-8 activity,

228 ainst recombinant forms of each of the three CDT subunit proteins neutralized both CDT activity and t

229 The use of catheter-directed thrombolysis (CDT) in the treatment of acute proximal lower-extremity

230 and role of catheter-directed thrombolysis (CDT) in the treatment of inferior vena cava thrombosis i

231 uggests that catheter-directed thrombolysis (CDT) may enable prevention of the post-thrombotic syndro

232 ltures and occurred more rapidly compared to CDT-treated HeLa cells.

233 ions of the CdtA, CdtB, and CdtC proteins to CDT activity.

234 o detect the recently described binary toxin CDT and a deletion in the pathogenicity locus gene, tcdC

235 type III, were positive for the binary toxin CDT, and contained an 18-bp tcdC deletion.

236 xacerbated by the emergence of binary toxin (CDT)-producing hypervirulent C. difficile strains.

237 s ducreyi makes cytolethal distending toxin (CDT) and hemolysin.

238 ins, produces a cytolethal distending toxin (CDT) consisting of CdtA, CdtB, and CdtC.

239 a member of the cytolethal distending toxin (CDT) family of bacterial cytotoxins.

240 w member of the cytolethal distending toxin (CDT) family of bacterial toxins.

241 Cytolethal distending toxin (CDT) from the diarrheagenic bacterium Campylobacter jeju

242 y flagellum and cytolethal distending toxin (CDT) gene mutants, treatment of the supernatant with pro

243 irulence factor cytolethal distending toxin (CDT) in the pathogenesis of this organism, interleukin-1

244 Cytolethal distending toxin (CDT) induces cell cycle arrest and apoptosis in eukaryot

245 The tripartite cytolethal distending toxin (CDT) induces cell cycle arrest and apoptosis in eukaryot

246 Cytolethal distending toxin (CDT) is a multisubunit protein found in various gram-neg

247 Because cytolethal distending toxin (CDT) may be a virulence factor, IL-10(-/-) mice were als

248 The cytolethal distending toxin (CDT) of Actinobacillus actinomycetemcomitans is a typica

249 The cytolethal distending toxin (CDT) of Campylobacter jejuni was detectable, using an in

250 The cytolethal distending toxin (CDT) of Haemophilus ducreyi is comprised of the CdtA, Cd

251 scherichia coli cytolethal distending toxin (CDT) shares significant pattern-specific homology with m

252 ejuni encodes a cytolethal distending toxin (CDT) that causes cells to arrest in the G(2)/M transitio

253 esses a soluble cytolethal distending toxin (CDT) that is encoded by the cdtABC gene cluster and can

254 esses a soluble cytolethal distending toxin (CDT) that kills HeLa, HEp-2, and other human epithelial

255 tic locus for a cytolethal distending toxin (CDT) was identified in a polymorphic region of the chrom

256 ns that produce cytolethal distending toxin (CDT) were analyzed for their virulence-associated genes.

257 effects of the cytolethal distending toxin (CDT) were evaluated first by using a wild-type strain an

258 ein subunits of cytolethal distending toxin (CDT) were unable to induce IL-8.

259 strains express cytolethal distending toxin (CDT), and recombinant CDT causes apoptosis of DC in vitr

260 actors, such as cytolethal distending toxin (CDT), in vivo are poorly understood.

261 toxin, known as cytolethal distending toxin (CDT), that has the ability to control cell cycle progres

262 t toxin, termed cytolethal distending toxin (CDT), that induces cell cycle arrest, cytoplasm distenti

263 a toxin, called cytolethal distending toxin (CDT), which causes direct DNA damage leading to invocati

264 gens encode the cytolethal distending toxin (CDT), which causes host cells to arrest during their cel

265 , including the cytolethal distending toxin (CDT).

266 hemolysin and a cytolethal distending toxin (CDT).

267 a toxin called cytolethal distending toxin (CDT).

268 actors, such as cytolethal distending toxin (CDT).

269 scovered toxin, cytolethal distending toxin (CDT); and (c) a secreted chaperonin 60 with potent leuko

270 cdB) and the C. difficile transferase toxin (CDT)(2).

271 dB), and the C. difficile transferase toxin (CDT).

272 (TcdB), and C. difficile transferase toxin (CDT).

273 ains, such as R20291, produce a third toxin, CDT.

274 Cytolethal distending toxins (CDTs) are multisubunit proteins produced by a variety of

275 Cytolethal distending toxins (CDTs) are tripartite protein exotoxins produced by a div

276 Cytolethal distending toxins (CDTs) block cell division by arresting the eukaryotic ce

277 The cytolethal distending toxins (CDTs) compose a subclass of intracellularly acting genot

278 the family of cytolethal distending toxins (CDTs).

279 We used connected discourse tracking (CDT) as the measure of speech perception.

280 ex responsible for conjugative DNA transfer (CDT) between bacterial cells.

281 rd toxin, known as C. difficile transferase (CDT), is increasingly common.

282 ing toxin Clostridium difficile transferase (CDT).

283 ribosylating toxin C. difficile transferase (CDT).

284 Carbohydrate deficient transferrin (CDT) is the most specific serum biomarker of heavy alcoh

285 presents the Constrained Distance Transform (CDT), a novel method for interactive image registration.

286 in N. crassa, two cellodextrin transporters, CDT-1 and CDT-2, contribute to cellulose sensing.

287 Within 24 h of treatment, CDT caused HeLa cells to arrest with a 4N DNA content, i

288 The detection of two CDT-negative clinical isolates raised questions about th

289 reduced DNase activity relative to wild-type CDT.

290 ablish a novel yeast model for understanding CDT-associated disease.

291 rombosis, and 3649 patients (4.1%) underwent CDT.

292 vena cava thrombosis, 718 (26.9%) underwent CDT.

293 BLAST search of the protein data bank using CDT polypeptides as query sequences indicated that CdtB

294 s from individual microfossils (delta(34)S(V-CDT) +6.7 per thousand to +21.5 per thousand) show that

295 ound chromatin independently of ORC, whereas CDT-1 and MCM-2-7 DNA binding was interdependent.

296 To test whether CDT was required for pustule formation, six human subjec

297 DDB-1 physically associates with CDT-1, suggesting that CDT-1 is a direct substrate of th

298 bunits were able to effectively compete with CDT holotoxin in the HeLa cell binding assay.

299 caval deep vein thrombosis and treated with CDT from 2005 to 2010.

300 We compared patients treated with CDT plus anticoagulation with patients treated with anti