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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
22                      In cells lacking CUL-4, CDT-1 levels fail to decrease during S phase and instead
23                                            A CDT and hemolysin double mutant was constructed and test
24 y infected with wild-type H. hepaticus and a CDT-deficient isogenic mutant.
25 eyi mutant restored its ability to express a CDT that killed both HeLa cells and HaCaT keratinocytes.
26                                   However, a CDT-negative H. hepaticus mutant had a significantly dim
27 nese hamster ovary cells characteristic of a CDT.
28 n, six human subjects were inoculated with a CDT mutant and parent at multiple sites.
29 osed to recombinant A. actinomycetemcomitans CDT.
30 oxic effects of the A. actinomycetemcomitans CDT.
31 sa, two cellodextrin transporters, CDT-1 and CDT-2, contribute to cellulose sensing.
32 ating that redundant regulation of CDC-6 and CDT-1 prevents rereplication.
33 origin recognition complex (ORC), CDC-6, and CDT-1.
34 p between DNase-related residues in CdtB and CDT biological activity.
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
37 yi 35000HP, which produces LspA1, LspA2, and CDT.
38  markedly elevated levels of phospho-p53 and CDT-1.
39 ation of NF-kappaB through TLR signaling and CDT in human intestinal epithelial cells.
40                         To determine if anti-CDT antibodies are produced in human infection, a toxin
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)
47 GNA, and NPA partially or completely blocked CDT activity.
48 embrane preparations became positive in both CDT and IL-8 assays.
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
51 manner indistinguishable from that caused by CDT treatment.
52 HeLa cells blocked killing of these cells by CDT holotoxin.
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
56                               Further, crude CDT preparations possess detectable DNase activity not a
57 nces were tested for their ability to detect CDT producers and to determine CDT type.
58 ity to detect CDT producers and to determine CDT type.
59                 26 patients had a diagnostic CDT based on a threshold value of %CDT > 1.7 indicating
60 ndependently associated with non-diagnostic %CDT (</= 1.7).
61 important for intoxication by four different CDTs.
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
64                                   H. ducreyi CDT activity is encoded by a three-gene cluster (cdtABC)
65 s to yield a profile characteristic for each CDT.
66                                           Ec-CDT and Hd-CDT shared comparable in vitro DNase activiti
67 mechanisms of CDTs from Escherichia coli (Ec-CDT) and Haemophilus ducreyi (Hd-CDT), which share limit
68 7 (T22N), suggesting that Hd-CDT, but not Ec-CDT, is trafficked through late endosomal vesicles.
69 m and nucleus, while having no effects on Ec-CDT.
70                These results suggest that Ec-CDT and Hd-CDT are transported within cells by distinct
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
73                                   C. elegans CDT-1 is present in G1-phase nuclei but disappears as ce
74 o make sound clinical judgments on employing CDT.
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
77 nd specific structural regions essential for CDT are identified.
78 e show that septins (SEPT) are essential for CDT-induced protrusion formation.
79 dtB position 95 was considered important for CDT activity.
80 receptor (LSR) is the host cell receptor for CDT, and our aim was to gain a deeper insight into the i
81 d cells to intoxication by three of the four CDTs tested.
82 se results provide evidence for a functional CDT in a human oral pathogen.
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
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  jejuni strains produce significantly higher CDT titers than do C. coli strains.
94                                     However, CDT mutations did not affect the ability of 81-176 to in
95 y using an analogue of tachyplesin I (TP-I), CDT (KWFRVYRGIYRRR-NH(2)), in which all four cysteines w
96                                   Like TP-I, CDT shows antimicrobial activity and disrupts Escherichi
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
105 rating cells that are treated with C. jejuni CDT.
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
109 cell assay indicated that these strains make CDT.
110                                 The national CDT utilization rates increased from 16.0% in 2005 to 34
111 body to the cdtC gene product can neutralize CDT activity in vitro.
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
114                   The mechanism of action of CDT suggests that the infliction of limited damage could
115 ght into the molecular and cellular basis of CDT-host interactions.
116 inal truncations of the binding component of CDT (CDTb), we found that amino acids 757-866 of CDTb ar
117 cle arrest, all of which are consequences of CDT action.
118 ciable role for SKPT-1 in the degradation of CDT-1 during S phase, even in a sensitized ddb-1 mutant
119 ans DDB-1 is required for the degradation of CDT-1 during S phase.
120  in part, by facilitating the degradation of CDT-1.
121 B-suggesting that the varied distribution of CDT in bacteria implicates many human pathogens as posse
122                                 Low doses of CDT result in the formation of microtubule-based protrus
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
125  did not constitute a significant feature of CDT action.
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  a useful model to further study the role of CDT and other aspects of C. jejuni pathogenesis.
129  isolates raised questions about the role of CDT in some cases of human campylobacteriosis.
130                   To investigate the role of CDT in the pathogenesis of H. hepaticus, transposon muta
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
133             Correlations between the type of CDT produced, the presence of other virulence properties
134 eting of the receptor and cellular uptake of CDT.
135 ere has been a steady increase in the use of CDT in the treatment of patients with inferior vena cava
136 nce measurement technique, widespread use of CDT remains limited due to low sensitivity.
137 an explanation for the enhanced virulence of CDT-expressing C. difficile and demonstrate a mechanism
138 p is interrelated with institution volume of CDT is unknown.
139  that an increase in institutional volume of CDT was associated with lower in-hospital mortality and
140       Despite the widespread distribution of CDTs among several important human pathogens, our unders
141         Here, the intoxication mechanisms of CDTs from Escherichia coli (Ec-CDT) and Haemophilus ducr
142 g, affected intoxication by only a subset of CDTs tested.
143 iagnostic CDT based on a threshold value of %CDT > 1.7 indicating heavy alcohol consumption, yielding
144       [3H]thymidine incorporation studies on CDT-treated cells were consistent with a blockage of cel
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
147 the risk-benefit ratio of pharmacomechanical CDT for acute proximal DVT.
148  for adjudication of discrepant GDH-positive/CDT-negative results.
149 ce of toxigenic C. difficile in GDH-positive/CDT-negative specimens.
150  O-linked surface sugar attachments prevents CDT-II(Ec) intoxication.
151 nd other diarrheagenic bacteria that produce CDT.
152 pted cdtABC coding region no longer produced CDT activity.
153 r hepaticus, which, like C. jejuni, produces CDT.
154 cient for protection from a strain producing CDT.
155 ed degradation of the DNA licensing protein, CDT-1, and premature spermatogenesis.
156 thal distending toxin (CDT), and recombinant CDT causes apoptosis of DC in vitro.
157                             Although related CDTs may share host factors, they also exploit unique ho
158 or invasion and the second of which requires CDT.
159 , which is largely abrogated by simultaneous CDT-1 silencing.
160 ntly, inactivation of UBXN-3/FAF1 stabilizes CDT-1 and CDC-45/GINS on chromatin, causing severe defec
161 via standardized Current Dental Terminology (CDT) codes related to periodontal treatment.
162 ry bowel disease in IL-10(-/-) mice and that CDT contributes to the virulence of H. cinaedi.
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
166             Together, our data indicate that CDT affects F-actin assembly within target cells and may
167                           Data indicate that CDT may be involved in chronic inflammatory responses, v
168                 These results indicated that CDT treatment results in a failure to activate CDC2, whi
169                   We therefore proposed that CDT is a tripartite toxin composed of CdtB as the enzyma
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
172                           Here, we show that CDT enhances the virulence of two PCR-ribotype 027 strai
173                                 We show that CDT interacts with the extracellular, Ig-like domain of
174                            Here we show that CDT-induced protrusions allow vesicle traffic and contai
175                    The NMR data suggest that CDT binding to negatively charged bilayers induces a cha
176  trial (RCT) (the CaVenT trial) suggest that CDT is reasonably well tolerated and that it may provide
177                        The data suggest that CDT may interfere with T-cell responses to H. ducreyi by
178                   These results suggest that CDT plays a key immunomodulatory role that allows persis
179                        The data suggest that CDT usurps conserved regulatory principles involved in m
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
183                     Here we demonstrate that CDTs from Haemophilus ducreyi, Aggregatibacter actinomyc
184                   Finally, we establish that CDTs are likely to be potent genotoxins, as indicated by
185                                          The CDT activities of C. jejuni strains possessing both type
186                                          The CDT group had longer length of stay and higher hospital
187                                          The CDT method is shown to be capable of simultaneous regist
188                                          The CDT peptide does not cause hemolysis up to 200 microg/mL
189                                          The CDT uses radial basis function transforms with distances
190 on outside of the cluster did not affect the CDT activity.
191          Both wild-type H. hepaticus and the CDT-deficient mutant successfully colonized IL-10-/- mic
192  was not significantly different between the CDT and the anticoagulation groups (2.0% versus 1.4%; P=
193                           In conclusion, the CDT of H. pullorum is responsible for major cytopathogen
194 is DNase activity may be responsible for the CDT-induced cell cycle arrest.
195 4%; P=0.02) were significantly higher in the CDT group.
196  and resource utilization were higher in the CDT group.
197                                       In the CDT-negative strains, two types of mutation were identif
198    However, by 4 months after infection, the CDT-deficient mutant was no longer detectable in IL-10-/
199          In view of the possible role of the CDT as a prominent A. actinomycetemcomitans virulence fa
200 by delivering the active CdtB subunit of the CDT directly into the cells.
201 othing is known about the composition of the CDT holotoxin or the function of CdtA and CdtC.
202 identified CdtB as the active subunit of the CDT holotoxin.
203 unctional equivalent of the B subunit of the CDT toxin.
204                            Expression of the CDT-like activities in A. actinomycetemcomitans was stra
205          These effects were dependent on the CDT, as they were (1) not observed in response to a cdtB
206        Together, these data suggest that the CDT holotoxin has intrinsic DNase activity that is assoc
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
209  reduced following prolonged exposure to the CDT.
210           Examples of registration using the CDT are presented.
211 /1,000 males and 269/1,000 females using the CDT code method).
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
215  not required for intoxication by any of the CDTs tested.
216                                        These CDT-producing strains possessed various combinations of
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
222 ltures and occurred more rapidly compared to CDT-treated HeLa cells.
223 action developed slowly, a 2-min exposure to CDT resulted in an irreversible development of toxicity.
224 ions of the CdtA, CdtB, and CdtC proteins to CDT activity.
225 o detect the recently described binary toxin CDT and a deletion in the pathogenicity locus gene, tcdC
226 type III, were positive for the binary toxin CDT, and contained an 18-bp tcdC deletion.
227 s ducreyi makes cytolethal distending toxin (CDT) and hemolysin.
228 ins, produces a cytolethal distending toxin (CDT) consisting of CdtA, CdtB, and CdtC.
229 a member of the cytolethal distending toxin (CDT) family of bacterial cytotoxins.
230 w member of the cytolethal distending toxin (CDT) family of bacterial toxins.
231                 Cytolethal distending toxin (CDT) from the diarrheagenic bacterium Campylobacter jeju
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
234                 Cytolethal distending toxin (CDT) induces cell cycle arrest and apoptosis in eukaryot
235  The tripartite cytolethal distending toxin (CDT) induces cell cycle arrest and apoptosis in eukaryot
236                 Cytolethal distending toxin (CDT) is a multisubunit protein found in various gram-neg
237                 Cytolethal distending toxin (CDT) is a newly described toxin produced by a number of
238         Because cytolethal distending toxin (CDT) may be a virulence factor, IL-10(-/-) mice were als
239             The cytolethal distending toxin (CDT) of Actinobacillus actinomycetemcomitans is a typica
240             The cytolethal distending toxin (CDT) of Campylobacter jejuni was detectable, using an in
241             The cytolethal distending toxin (CDT) of Haemophilus ducreyi is comprised of the CdtA, Cd
242 at comprise the cytolethal distending toxin (CDT) of this enteric pathogen.
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
250 ein subunits of cytolethal distending toxin (CDT) were unable to induce IL-8.
251 strains express cytolethal distending toxin (CDT), and recombinant CDT causes apoptosis of DC in vitr
252 actors, such as cytolethal distending toxin (CDT), in vivo are poorly understood.
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
257 actors, such as cytolethal distending toxin (CDT).
258 hemolysin and a cytolethal distending toxin (CDT).
259  a toxin called cytolethal distending toxin (CDT).
260  a toxin called cytolethal distending toxin (CDT).
261 , including the cytolethal distending toxin (CDT).
262 scovered toxin, cytolethal distending toxin (CDT); and (c) a secreted chaperonin 60 with potent leuko
263  (TcdB), and C. difficile transferase toxin (CDT).
264 ains, such as R20291, produce a third toxin, CDT.
265                Cytolethal distending toxins (CDTs) are multisubunit proteins produced by a variety of
266                Cytolethal distending toxins (CDTs) are tripartite protein exotoxins produced by a div
267                Cytolethal distending toxins (CDTs) block cell division by arresting the eukaryotic ce
268            The cytolethal distending toxins (CDTs) compose a subclass of intracellularly acting genot
269  the family of cytolethal distending toxins (CDTs).
270        We used connected discourse tracking (CDT) as the measure of speech perception.
271 ex responsible for conjugative DNA transfer (CDT) between bacterial cells.
272 rd toxin, known as C. difficile transferase (CDT), is increasingly common.
273 ing toxin Clostridium difficile transferase (CDT).
274 ribosylating toxin C. difficile transferase (CDT).
275          Carbohydrate deficient transferrin (CDT) is the most specific serum biomarker of heavy alcoh
276 presents the Constrained Distance Transform (CDT), a novel method for interactive image registration.
277 in N. crassa, two cellodextrin transporters, CDT-1 and CDT-2, contribute to cellulose sensing.
278                    Within 24 h of treatment, CDT caused HeLa cells to arrest with a 4N DNA content, i
279                         The detection of two CDT-negative clinical isolates raised questions about th
280 reduced DNase activity relative to wild-type CDT.
281 ablish a novel yeast model for understanding CDT-associated disease.
282 rombosis, and 3649 patients (4.1%) underwent CDT.
283  vena cava thrombosis, 718 (26.9%) underwent CDT.
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
286 ound chromatin independently of ORC, whereas CDT-1 and MCM-2-7 DNA binding was interdependent.
287                              To test whether CDT was required for pustule formation, six human subjec
288             DDB-1 physically associates with CDT-1, suggesting that CDT-1 is a direct substrate of th
289 bunits were able to effectively compete with CDT holotoxin in the HeLa cell binding assay.
290  caval deep vein thrombosis and treated with CDT from 2005 to 2010.
291            We compared patients treated with CDT plus anticoagulation with patients treated with anti

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