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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 depolymerizes actin, causes formation of microtubule
6 CDT has limited sensitivity as a biomarker of heavy alco
7 CDT holotoxin containing these mutant forms of CdtB did
8 CDT induces distension and eventual death of a number of
9 CDT is a potential virulence factor in H. pullorum that
10 CDT is a primary mechanism for the lateral propagation o
11 CDT is composed of three proteins, CdtA, CdtB, and CdtC.
12 CDT is encoded by three highly conserved genes, cdtA, -B
13 CDT leads to the collapse of the actin cytoskeleton and,
14 CDT should be employed for DVT patients who have severe
15 CDT treatment was also shown to cause HeLa cells to accu
16 CDT, the third C. difficile toxin, is a binary actin-ADP
17 CDT-like activities were no longer expressed by the reco
18 CDT-treated cells underwent a progressive accumulation o
19 CDT-treated GMSM-K cells displayed cell cycle arrest at
20 CDTs are virulence factors secreted by a variety of path
21 addition of the Campylobacter jejuni 81-176 CDT to primary human fibroblasts resulted in formation o
25 eyi mutant restored its ability to express a CDT that killed both HeLa cells and HaCaT keratinocytes.
35 red questionnaire of alcohol consumption and CDT analysis using the standardized reference measuremen
36 8 secretion requires functional flagella and CDT and depends on the activation of NF-kappaB through T
41 released all three CDT proteins, as well as CDT activity and IL-8 activity, from membranes into supe
42 e dehydrogenase antigen (GDH) and toxin A/B (CDT) tests in two algorithmic approaches for a tertiary
43 understanding about the interaction between CDT and its receptor LSR, which is key to the developmen
44 significant difference in mortality between CDT versus anticoagulation alone; however, the bleeding
45 nd mortality additionally produce the binary CDT toxin (Clostridium difficile transferase) that ADP-r
46 arbohydrate specificities were used to block CDT activity and the cell surface binding of CdtA-II(Ec)
49 three CDT subunit proteins neutralized both CDT activity and the activity responsible for IL-8 relea
50 on a shuttle plasmid in trans restored both CDT activity and the ability to release IL-8 to membrane
53 enorhabditis elegans, RBX-1 silencing causes CDT-1 accumulation, triggering DDR in intestinal cells,
54 cle arrest, and apoptosis of cultured cells, CDTs are proposed to enhance virulence by blocking cellu
55 found to be related to the Escherichia coli CDT proteins, yet the amino acid sequences have diverged
62 e that causes actin cytoskeletal disruption, CDT is typically produced by the major, hypervirulent st
63 ains a cyclopenta-[2,1-b:3,4-b']dithiophene (CDT) unit flanked by two benzo[2,1,3]thiadiazole (BT) fr
67 mechanisms of CDTs from Escherichia coli (Ec-CDT) and Haemophilus ducreyi (Hd-CDT), which share limit
71 ompetitive binding studies suggested that Ec-CDT and Hd-CDT bind to discrete cell surface determinant
72 verely reduce cellobiose transport by either CDT-1 or CDT-2 when expressed individually do not greatl
75 at Salmonella enterica serovar Typhi encodes CDT activity, which depends on the function of a CdtB ho
76 UBXN-3/FAF1 binds to the licensing factor CDT-1 and additional ubiquitylated proteins, thus promot
80 receptor (LSR) is the host cell receptor for CDT, and our aim was to gain a deeper insight into the i
83 r positivity by LAMP plus another test (GDH, CDT, or the Premier C. difficile toxin A and B enzyme im
84 ication (LAMP), and algorithm 2 entailed GDH/CDT followed by cytotoxicity neutralization assay (CCNA)
85 lgorithm 1 entailed initial testing with GDH/CDT followed by loop-mediated isothermal amplification (
86 These results suggest that Ec-CDT and Hd-CDT are transported within cells by distinct pathways, p
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
95 y using an analogue of tachyplesin I (TP-I), CDT (KWFRVYRGIYRRR-NH(2)), in which all four cysteines w
97 demonstrating that morphological changes in CDT-treated Chinese hamster ovary cells are coincident w
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 ation of the stress fiber-like structures in CDT-treated cells was accompanied by an apparent blockag
104 d be applied when ordering and interpreting %CDT results, particularly in women, patients with cirrho
106 jejuni 81-176 and an isogenic mutant lacking CDT activity (cdtB mutant) were inoculated into NF-kappa
107 huttle plasmid into a C. coli strain lacking CDT, membrane preparations became positive in both CDT a
108 was a significant difference in the mean log CDT ratio between those who received ondansetron (1 and
112 on of nonexportable CDC-6 with nondegradable CDT-1, indicating that redundant regulation of CDC-6 and
113 toxin activity in these naturally occurring CDT-negative C. jejuni strains was then investigated at
116 inal truncations of the binding component of CDT (CDTb), we found that amino acids 757-866 of CDTb ar
118 ciable role for SKPT-1 in the degradation of CDT-1 during S phase, even in a sensitized ddb-1 mutant
121 B-suggesting that the varied distribution of CDT in bacteria implicates many human pathogens as posse
123 colonized chickens despite the expression of CDT in the avian gut as indicated by reverse transcripti
124 ults indicate that neither the expression of CDT, nor that of hemolysin, nor both are required for pu
127 al conditions reveal that the interaction of CDT with lipid membranes is an enthalpy-driven process.
131 needed to assess whether standardization of CDT protocols across all institutions in the United Stat
132 tablished that CdtB is the active subunit of CDT, exerting its effect as a nuclease that damages the
135 ere has been a steady increase in the use of CDT in the treatment of patients with inferior vena cava
137 an explanation for the enhanced virulence of CDT-expressing C. difficile and demonstrate a mechanism
139 that an increase in institutional volume of CDT was associated with lower in-hospital mortality and
143 iagnostic CDT based on a threshold value of %CDT > 1.7 indicating heavy alcohol consumption, yielding
145 duce cellobiose transport by either CDT-1 or CDT-2 when expressed individually do not greatly impact
146 ing fluorometry demonstrate that the peptide CDT binds and inserts into only negatively charged membr
160 ntly, inactivation of UBXN-3/FAF1 stabilizes CDT-1 and CDC-45/GINS on chromatin, causing severe defec
163 of C. jejuni is NF-kappaB dependent and that CDT may have proinflammatory activity in vivo, as well a
164 amination of these mutants demonstrated that CDT represents the previously described granulating cyto
165 In addition, it has been established that CDT is a tripartite AB toxin in which CdtB is the active
170 isogenic H. hepaticus mutants revealed that CDT expression is not required for colonization of the m
171 otoxin from Haemophilus ducreyi reveals that CDT consists of an enzyme of the DNase-I family, bound t
176 trial (RCT) (the CaVenT trial) suggest that CDT is reasonably well tolerated and that it may provide
180 and holotoxin-assembled CdtBs suggested that CDT intoxication is contingent upon holotoxin disassembl
181 cally associates with CDT-1, suggesting that CDT-1 is a direct substrate of the CUL-4/DDB-1 E3 comple
182 nderance of available evidence suggests that CDT (with anticoagulation) should be routinely considere
192 was not significantly different between the CDT and the anticoagulation groups (2.0% versus 1.4%; P=
198 However, by 4 months after infection, the CDT-deficient mutant was no longer detectable in IL-10-/
207 overall strain relatedness revealed that the CDT producers studied here can be divided into three gen
208 ies of HPLF and oral epithelial cells to the CDT has important implications for the role of this puta
212 hepaticus, while animals challenged with the CDT-deficient mutant developed significantly lower IgG2c
213 while animals originally challenged with the CDT-deficient mutant had minimal cecal inflammation at t
214 nts, animals that cleared infection with the CDT-deficient mutant were protected from rechallenge wit
217 ls of sodium deoxycholate released all three CDT proteins, as well as CDT activity and IL-8 activity,
218 ainst recombinant forms of each of the three CDT subunit proteins neutralized both CDT activity and t
219 The use of catheter-directed thrombolysis (CDT) in the treatment of acute proximal lower-extremity
220 and role of catheter-directed thrombolysis (CDT) in the treatment of inferior vena cava thrombosis i
221 uggests that catheter-directed thrombolysis (CDT) may enable prevention of the post-thrombotic syndro
223 action developed slowly, a 2-min exposure to CDT resulted in an irreversible development of toxicity.
225 o detect the recently described binary toxin CDT and a deletion in the pathogenicity locus gene, tcdC
232 y flagellum and cytolethal distending toxin (CDT) gene mutants, treatment of the supernatant with pro
233 irulence factor cytolethal distending toxin (CDT) in the pathogenesis of this organism, interleukin-1
235 The tripartite cytolethal distending toxin (CDT) induces cell cycle arrest and apoptosis in eukaryot
243 scherichia coli cytolethal distending toxin (CDT) shares significant pattern-specific homology with m
244 ejuni encodes a cytolethal distending toxin (CDT) that causes cells to arrest in the G(2)/M transitio
245 esses a soluble cytolethal distending toxin (CDT) that is encoded by the cdtABC gene cluster and can
246 esses a soluble cytolethal distending toxin (CDT) that kills HeLa, HEp-2, and other human epithelial
247 tic locus for a cytolethal distending toxin (CDT) was identified in a polymorphic region of the chrom
248 ns that produce cytolethal distending toxin (CDT) were analyzed for their virulence-associated genes.
249 effects of the cytolethal distending toxin (CDT) were evaluated first by using a wild-type strain an
251 strains express cytolethal distending toxin (CDT), and recombinant CDT causes apoptosis of DC in vitr
253 toxin, known as cytolethal distending toxin (CDT), that has the ability to control cell cycle progres
254 t toxin, termed cytolethal distending toxin (CDT), that induces cell cycle arrest, cytoplasm distenti
255 a toxin, called cytolethal distending toxin (CDT), which causes direct DNA damage leading to invocati
256 gens encode the cytolethal distending toxin (CDT), which causes host cells to arrest during their cel
262 scovered toxin, cytolethal distending toxin (CDT); and (c) a secreted chaperonin 60 with potent leuko
276 presents the Constrained Distance Transform (CDT), a novel method for interactive image registration.
284 BLAST search of the protein data bank using CDT polypeptides as query sequences indicated that CdtB
285 s from individual microfossils (delta(34)S(V-CDT) +6.7 per thousand to +21.5 per thousand) show that
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