ライフサイエンスコーパス: diphtheria toxin

1 ination of Foxp3+ Treg by treatment with Dx (diphtheria toxin).

2 e fused to the protein delivery machinery of diphtheria toxin.

3 nd specifically ablated by administration of diphtheria toxin.

4 variety of recombinant protein fragments of diphtheria toxin.

5 xpressing cells can be depleted by injecting diphtheria toxin.

6 IL-2 protein and as toxophore the truncated diphtheria toxin.

7 tly but selectively depleted by injection of diphtheria toxin.

8 y intracerebroventricular (ICV) injection of diphtheria toxin.

9 cific ablation of podocytes by administering diphtheria toxin.

10 ng of human interleukin-3 fused to truncated diphtheria toxin.

11 nine; DCs were depleted by administration of diphtheria toxin.

12 e called diphthamide, which is the target of diphtheria toxin.

13 electively deplete pDCs by administration of diphtheria toxin.

14 inooxy linkers bound to BSA or a recombinant diphtheria toxin.

15 D11c(+) cells was controlled by injection of diphtheria toxin.

16 AD(+)-dependent bacterial exotoxins, such as diphtheria toxin.

17 , a zoonotic bacterium that can also produce diphtheria toxin.

18 nsive islet infiltration upon treatment with diphtheria toxin.

19 immunity, only if Tregs were depleted using diphtheria toxin.

20 ma cells before depleting myeloid cells with diphtheria toxin.

21 genic mice were treated with intraperitoneal diphtheria toxin (5 ng/g b.wt.) in the presence or absen

22 nstrate that the fusion of Rad51 promoter to diphtheria toxin A (DTA) gene kills a variety of cancer

23 rprisingly, donor LC engraftment in Langerin-diphtheria toxin A (DTA) transgenic hosts was independen

24 e, we present the design and validation of a diphtheria toxin A (DTA)-encoding lentiviral vector expr

25 GPAIS) challenge in rat insulin promoter and diphtheria toxin A (RIP-DTA) mice.

26 have been ablated by targeted expression of diphtheria toxin A chain (DTA) under the control of the

27 the lethal factor amino-terminal domain and diphtheria toxin A chain expedited translocation.

28 on was validated by assessing the effects of diphtheria toxin A chain expression.

29 oter/gene were used to express an attenuated diphtheria toxin A chain in transgenic mice.

30 T domain aids the membrane translocation of diphtheria toxin A chain.

31 on, utilizing temporally controlled targeted diphtheria toxin A expression, results in failure of neu

32 Interestingly, neutropenic lysozyme 2-diphtheria toxin A mice exhibited striking EG and amplif

33 s) via Cre-dependent viral expression of the diphtheria toxin A subunit (DT-A) in hemiparkinsonian tr

34 ression of the potent translation inhibitor, diphtheria toxin A subunit, from the Arabidopsis (Arabid

35 loped genetically modified mice that express diphtheria toxin A under control of a loxP-flanked stop

36 deficient in LCs by virtue of expression of diphtheria toxin A under the control of a BAC (bacterial

37 in mice for 25 d via neuronal expression of diphtheria toxin A-chain, producing both a neuroinflamma

38 ectories of the conformational transition of diphtheria toxin, a particularly challenging example, sh

39 ataxin-3-orexin, and doxycycline-controlled-diphtheria-toxin-A-orexin.

40 engineered human Langerin-DTR mice in which diphtheria toxin ablates LCs without affecting Langerin(

41 ) cells, and donor Foxp3+ Treg depletion, by diphtheria toxin administration to DEREG donor mice whos

42 be specifically depleted from the brain upon diphtheria toxin administration.

43 splantation carrying a conditional allele of diphtheria toxin alpha subunit and cell-specific express

44 utively ablated because of expression of the diphtheria toxin alpha subunit within developing DCs.

45 selective ablation of PPARgamma(+) cells by diphtheria toxin also causes high bone mass due to decre

46 ted with increased fatality risk, are due to diphtheria toxin, an exotoxin produced by the pathogen t

47 switch to tightly regulate the expression of diphtheria toxin and Cre recombinase, respectively.

48 ch are required for the cytotoxic effects of diphtheria toxin and exotoxin A.

49 (T) domain plays a key role in the action of diphtheria toxin and is responsible for transferring the

50 We found that diphtheria toxin and its nontoxic mutant, called CRM197,

51 en shown to repress the transcription of the diphtheria toxin and other genes associated with ferrous

52 hMAb binds to the receptor-binding domain of diphtheria toxin and physically blocks the toxin from bi

53 teins that include the key virulence factors diphtheria toxin and the adhesive pili.

54 anthracis, toxin B of Clostridium difficile, diphtheria toxin, and exotoxin A of Pseudomonas aerugino

55 ng method to attach the catalytic subunit of diphtheria toxin as a toxic warhead to CTA1, thus conver

56 cific damage in mice of either sex either by diphtheria toxin-based ablation of >50% of mature DG gra

57 e used a transgenic mouse system that allows diphtheria toxin-based depletion of pericytes.

58 Denileukin diftitox (DAB-IL-2, Ontak) is a diphtheria-toxin-based fusion protein that depletes CD25

59 educed vascular leak, is a second-generation diphtheria-toxin-based fusion protein with promise as a

60 ction, reperfused myocardial infarction, and diphtheria toxin cardiomyocyte ablation), there is a shi

61 The delivery of the diphtheria toxin catalytic domain (DTA) from acidified e

62 The translocation of the diphtheria toxin catalytic domain from the lumen of earl

63 detrimental effects of anthrax lethal toxin, diphtheria toxin, cholera toxin, Pseudomonas aeruginosa

64 as their bovine serum albumin or recombinant diphtheria toxin conjugates.

65 ugars (OAg) of LPS to the nontoxic mutant of diphtheria toxin (CRM(197)).

66 etane grafting of the genetically detoxified diphtheria toxin CRM197 improves significantly the immun

67 (HiD); and the cross-reactive material from diphtheria toxin (CRM197).

68 Injection of diphtheria toxin deleted YFP(+) cells from Foxl1-Cre;Ros

69 fically depleted CD4(+)Foxp3(+) T cells in a diphtheria toxin-dependent manner.

70 Selective ablation of mitotic neurons using diphtheria toxin (DT) and a retrovirus vector encoding D

71 r 2 (eEF2) is the target of ADP ribosylating diphtheria toxin (DT) and Pseudomonas exotoxin A (PE).

72 tively sensitive to exogenously administered diphtheria toxin (DT) by targeted expression of the diph

73 In adult wild-type mice, administration of diphtheria toxin (DT) caused no significant hair cell lo

74 However, diphtheria toxin (DT) crosses the blood-brain barrier, w

75 We have employed a hormone-inducible diphtheria toxin (DT) expression system in Saccharomyces

76 wild-type Tf, we showed enhanced delivery of diphtheria toxin (DT) from these mutants to a monolayer

77 rated the first functional siRNA delivery by diphtheria toxin (DT) in vitro, marking an important ste

78 y timed local (subconjunctival) injection of diphtheria toxin (DT) into mice that express high-affini

79 mouse models in which the administration of diphtheria toxin (DT) leads to specific depletion of reg

80 We generated mice in which administration of diphtheria toxin (DT) led to specific ablation of PYY-ex

81 nsists of interleukin 3 fused to a truncated diphtheria toxin (DT) molecule.

82 We inserted diphtheria toxin (DT) receptor (DTR) cDNA into the 3' UT

83 a gene knock-in strategy inserting the human diphtheria toxin (DT) receptor (DTR) into the endogenous

84 Hair cells express the human diphtheria toxin (DT) receptor behind the Pou4f3 promote

85 to the splenic marginal zone of naive CD11b-diphtheria toxin (DT) receptor bone marrow-chimeric mice

86 we used the DEREG mouse, which expresses the diphtheria toxin (DT) receptor under control of the Treg

87 used transgenic mice that express the human diphtheria toxin (DT) receptor under the control of the

88 d in mature, transgenic mice where the human diphtheria toxin (DT) receptor was expressed behind the

89 neural crest-derived cells (ENCDCs) express diphtheria toxin (DT) receptor.

90 ned CBA/CaJ male mice, engineered to express diphtheria toxin (DT) receptors in hair cells, by system

91 acrophages was achieved by administration of diphtheria toxin (DT) to CD11b-DTR mice.

92 Administration of diphtheria toxin (DT) to these mice resulted in nearly c

93 Tg) mice but not in CLEC4C-DTR-Tg mice after diphtheria toxin (DT) treatment.

94 ic tyrosinase promoter, under the control of diphtheria toxin (DT), we eliminated and/or halted diffe

95 he throat and upper airways and the produced diphtheria toxin (DT), which binds to the elongation fac

96 glycemia after induction of a more complete, diphtheria toxin (DT)-induced beta-cell loss, a situatio

97 Unexpectedly, OT-I cell injection into diphtheria toxin (DT)-treated beta(2)m --> K14-OVA x Lan

98 cTECs sensitive to the cytotoxic effects of diphtheria toxin (DT).

99 morphogenesis and maturation is disrupted by diphtheria toxin (DT).

100 can be selectively ablated by the action of diphtheria toxin (DT).

101 ecifically ablated from adult mice using the diphtheria toxin (DT)/DT-receptor system and the connexi

102 ynthetic antigen was conjugated to a mutated diphtheria toxin (DT, CRM197) with different copy number

103 lectively deplete human stromal cells (using diphtheria toxin, DT) without affecting mouse cancer cel

104 eration, we used Cre-activated expression of diphtheria toxin (DTA) in the Ascl3-expressing (Ascl3+)

105 ed with CRE-dependent AAV vectors expressing diphtheria toxin (DTA) to selectively ablate FC SST neur

106 Previous diphtheria toxin (DTA)-mediated ablation studies showed

107 sruption of the notochord and floor plate by diphtheria toxin (DTA)-mediated cell ablation did not di

108 addition to Stx, the phage-encoded exotoxin, diphtheria toxin (Dtx) expressed by Corynebacterium diph

109 in conjunction with mice expressing GFP and diphtheria toxin (DTx) receptor (DTR) under control of t

110 We have used CD11c-diphtheria toxin (DTx) receptor mice to deplete CD11c(+)

111 inating SCs followed by local application of diphtheria toxin (DTX).

112 Some mice were given injections of diphtheria toxin during the recovery phase to delete Fox

113 ent of NFATc1-DTR mouse embryoid bodies with diphtheria toxin efficiently ablated endocardial cells,

114 esponse and type 2 diabetes mellitus (T2DM), diphtheria toxin-expressing (DT) mice that specifically

115 To overcome this, Ucp1-Cre was used to drive diphtheria toxin expression in cells expressing UCP1 (Uc

116 odon in the Rosa26(DTA/+) allele and induces diphtheria toxin fragment A (DTA) expression.

117 specific CreER allele to drive expression of diphtheria toxin fragment A (DTA).

118 Denileukin diftitox (DD), a diphtheria toxin fragment IL-2 fusion protein, is though

119 ral crest lineage using a Wnt1-Cre-activated diphtheria toxin fragment-A cell-killing system was empl

120 ble cytoplasmic reconstitution of functional diphtheria toxin from engineered intein-flanked fragment

121 In vivo administration of LPS or an IL-2/diphtheria toxin fusion protein (Ontak) to chronically S

122 6 were culture-negative but PCR-positive for diphtheria toxin gene, 1 was culture-positive without fu

123 inducible Caspase-8 protein and an inducible diphtheria toxin gene, results in new neurons.

124 transformation method by the introduction of diphtheria toxin genes into the transformation vector as

125 d potent human neutralizing antibody against diphtheria toxin holds promise as a potential therapeuti

126 family includes ADP-ribosyltransferases with diphtheria toxin homology (ARTD).

127 The 18 human ADP-ribose transferases with diphtheria toxin homology include ARTD1/PARP1, a cancer

128 depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced AML diseas

129 an anti-CD25 immunotoxin (interleukin-2 with diphtheria toxin [IL-2-DT]), or two combinations of both

130 haDKRC::DTA mice that expressed an inducible diphtheria toxin in adult cycling cardiomyocytes and exa

131 Transient expression of diphtheria toxin in beta cells of old mice resulted in i

132 pressing either tetanus toxin light chain or diphtheria toxin in gal4-defined neural circuits, we wer

133 ique hMAbs were tested for neutralization of diphtheria toxin in in vitro cytotoxicity assays with a

134 Five days after administering diphtheria toxin in these adult mice, changes were obser

135 In these albumin-deficient rats, exposure to diphtheria toxin induced an increase in albumin GSC and

136 use, a model of hyperglycemia resulting from diphtheria toxin induced beta cell ablation.

137 tracer uptake in 2 models of cardiac injury (diphtheria toxin induced cardiomyocyte ablation and repe

138 ischemia/reperfusion (I/R) injury or a novel diphtheria toxin-induced (DT-induced) model of selective

139 Diphtheria toxin-induced depletion of Tregs significantl

140 state was perturbed by coronary ligation or diphtheria toxin-induced macrophage depletion in CD11b(D

141 microglia exert beneficial effects during a diphtheria toxin-induced neuronal lesion, but impede rec

142 model, PMN(DTR) mice, in which injection of diphtheria toxin induces selective neutrophil ablation.

143 Within 2 weeks of diphtheria toxin injection, heterozygous Pmch(DTR/+) mic

144 and efficient depletion of Foxp3(+) Tregs by diphtheria toxin injection, we observed that transient F

145 Diphthamide, the target of diphtheria toxin, is a post-translationally modified his

146 Diphthamide, the target of diphtheria toxin, is a unique posttranslational modifica

147 Diphthamide, the target of diphtheria toxin, is a unique posttranslational modifica

148 sing a Rosa26 conditional allele, expressing diphtheria toxin, led to crypt loss.

149 ied as a potent but unselective inhibitor of diphtheria toxin-like ADP-ribosyltransferase 3 (ARTD3).

150 The diphtheria toxin-like ADP-ribosyltransferases (ARTDs) ar

151 Diphtheria toxin-mediated ablation of lysozyme M-positiv

152 o acutely and selectively eliminate them via diphtheria toxin-mediated ablation.

153 answer this question, we used Cre-dependent, diphtheria toxin-mediated cell ablation to selectively r

154 Using a progressive, time-controllable, diphtheria toxin-mediated cell ablation/dysfunction tech

155 Using diphtheria toxin-mediated depletion models in mice, we s

156 Importantly, diphtheria toxin-mediated depletion of IL-7-producing st

157 In this study, an established model of diphtheria toxin-mediated depletion of resident pulmonar

158 Diphtheria toxin-mediated selective depletion of MCs or

159 Diphtheria toxin-mediated, acute ablation of hypothalami

160 After pericyte ablation with diphtheria toxin, mice showed acute blood-brain barrier

161 nd that limited podocyte renewal occurs in a diphtheria toxin model of acute podocyte ablation.

162 and covalently linked to recombinant CRM197 diphtheria toxin mutant (CRM197) to produce CPS-CRM197.

163 hesized and attached via a chain linker to a diphtheria toxin mutant carrier protein.

164 calizes to tumors in vivo and rVAR2 fused to diphtheria toxin or conjugated to hemiasterlin compounds

165 lls was assessed by selective depletion with diphtheria toxin or depleting anti-CD20 monoclonal antib

166 isting of interleukin-3 fused to a truncated diphtheria toxin payload.

167 vidity of immunoglobulin (Ig) G specific for diphtheria toxin, pertussis toxin, filamentous hemagglut

168 Screens for sensitivity to a cholera-diphtheria toxin provide broad insights into the mechani

169 a fusion protein of interleukin 2 (IL-2) and diphtheria toxin, provides a means of targeting Treg cel

170 onate (sLC), inducible depletion using CD11b diphtheria toxin receptor (CD11b DTR) transgenic mice, a

171 pletion of this population in CD11B promoter-diphtheria toxin receptor (CD11B-DTR) transgenic mice ca

172 onstituted with bone marrow cells from CD11c-diphtheria toxin receptor (CD11c-DTR) and CCR5(-/-) or C

173 mouse strains that either express the human diphtheria toxin receptor (DTR) coupled to the CD11b pro

174 Cs from LNs based on their expression of the diphtheria toxin receptor (DTR) directed by the gene enc

175 Many such models rely on transgenic diphtheria toxin receptor (DTR) expression driven by DC-

176 e adult mouse utricle by inserting the human diphtheria toxin receptor (DTR) gene into the Pou4f3 gen

177 Lgr5-expressing cells in mice using a human diphtheria toxin receptor (DTR) gene knocked into the Lg

178 tance, using B6.Foxp3(DTR) mice that express diphtheria toxin receptor (DTR) in Foxp3(+) cells.

179 via transgenic expression of a high-affinity diphtheria toxin receptor (DTR) is a new and powerful ap

180 In these mice, the diphtheria toxin receptor (DTR) is expressed under contr

181 Conditional expression of diphtheria toxin receptor (DTR) is widely used for tissu

182 Murine Langerin-diphtheria toxin receptor (DTR) mice allow for the induc

183 ular junction (NMJ) by using mice expressing diphtheria toxin receptor (DTR) preferentially in tSCs c

184 We attempted to create a model that used diphtheria toxin receptor (DTR) to ablate specific cell

185 in vivo, we targeted expression of the human diphtheria toxin receptor (DTR) to the gene for MCH (Pmc

186 1c-enhanced green fluorescent protein (EGFP)-diphtheria toxin receptor (DTR) transgene was associated

187 used several murine models, including BDCA-2-diphtheria toxin receptor (DTR) transgenic and IFN-alpha

188 cy to various APCs, together with the use of diphtheria toxin receptor (DTR) transgenic mouse strains

189 s were eliminated in newly generated SiglecH-diphtheria toxin receptor (DTR)-transgenic (Tg) mice but

190 Expression of the human diphtheria toxin receptor (hDTR) gene under the regulato

191 e induced limited podocyte depletion using a diphtheria toxin receptor (hDTR) transgenic rat.

192 el transgenic mouse model in which the human diphtheria toxin receptor (huDTR) is selectively express

193 m1cre mice were bred to homozygous inducible diphtheria toxin receptor (iDTR) mice to generate mice e

194 using the human diphtheria receptor system (diphtheria toxin receptor [DTR]) expressed in Lysmd1-cre

195 cendants (Foxl1-Cre;Rosa(YFP/iDTR)-inducible diphtheria toxin receptor [iDTR] mice).

196 By using B6/Langerin-diphtheria toxin receptor chimeric mice and LC ablation,

197 We generated mice that express the diphtheria toxin receptor exclusively in podocytes, allo

198 Using CX3CR1(CreER) to drive diphtheria toxin receptor expression in microglia, we fo

199 To test this hypothesis, we used a diphtheria toxin receptor expression system to selective

200 at ablation of Paneth cells in mice, using a diphtheria toxin receptor gene inserted into the P-lysoz

201 nondiabetic mice conditionally expressing a diphtheria toxin receptor in mural cells.

202 ria toxin (DT) by targeted expression of the diphtheria toxin receptor in oligodendrocytes.

203 Using Langerin-diphtheria toxin receptor mice and established mouse mod

204 organs (liver, spleen, and kidneys) in CD11c-diphtheria toxin receptor mice but not in wild-type mice

205 ished hepatic metastases in transgenic CD11b-diphtheria toxin receptor mice by intrasplenic injection

206 n, in either Mac1-deficient mice or in CD11b-diphtheria toxin receptor mice in which CD11b-positive c

207 etion of Treg during MCMV infection in Foxp3-diphtheria toxin receptor mice or in wild-type mice reca

208 epithelial debridement wound model and CD11c-diphtheria toxin receptor mice that express a CD11c prom

209 Selective Treg ablation in Foxp3-diphtheria toxin receptor mice with ischemic cardiomyopa

210 g monocytes only in CCR2 promoter-controlled diphtheria toxin receptor mice, whereas neutrophil numbe

211 otein (EGFP) knock-in mice and Langerin-EGFP-diphtheria toxin receptor mice--three dimensional rotati

212 CD11b/Gr1(mid) subset in a transgenic CD11b-diphtheria toxin receptor mouse model markedly reduced t

213 e have generated a transgenic strain, Clec9A-diphtheria toxin receptor that allows us to ablate in vi

214 Therefore, the diphtheria toxin receptor transgene was specifically exp

215 depletion of dendritic cells (DCs) in CD11c-diphtheria toxin receptor transgenic mice followed by in

216 and reconstitution in CD11b promoter-driven diphtheria toxin receptor transgenic mice revealed that

217 phtheria toxin treatment of sensitized CD11c-diphtheria toxin receptor transgenic mice to deplete CD1

218 We generated diphtheria toxin receptor transgenic mice to selectively

219 We used CD11b-diphtheria toxin receptor transgenic mice to transiently

220 nduced acute lung injury, wild-type or CD11c-diphtheria toxin receptor transgenic mice were treated w

221 To test the involvement of DCs, CD11c-diphtheria toxin receptor transgenic mice were used to d

222 Adult male wild-type C57BL/6 mice, Foxp3-diphtheria toxin receptor transgenic mice, and tumor nec

223 We also used a CD11c-diphtheria toxin receptor transgenic mouse model system

224 We used mice expressing Diphtheria toxin receptor under control of the Foxp3 pro

225 t C57BL/6-DEREG mice expressing a transgenic diphtheria toxin receptor under the Foxp3 promoter, tran

226 ndocardial-specific ablation model using the diphtheria toxin receptor under the regulatory elements

227 se line, using the Cre/loxP system, in which diphtheria toxin receptor was selectively expressed in m

228 ing CD (cluster of differentiation) 169-DTR (diphtheria toxin receptor) and CCR2-DTR mice, we further

229 Foxp3-GFP-DTR (human diphtheria toxin receptor) C57BL/6 mice allow eliminatio

230 tein, cluster of differentiation 11c (CD11c)/diphtheria toxin receptor, and IL-17 receptor A(-/-) mic

231 donor mice whose Foxp3+ Treg cells expressed diphtheria toxin receptor, restored rejection with eithe

232 11c promoter driving expression of the human diphtheria toxin receptor, we found that selective deple

233 Exploiting a transgene encoding the human diphtheria toxin receptor, we punctually and specificall

234 or mice that express a CD11c promoter-driven diphtheria toxin receptor, we showed that DCs migrate al

235 We developed a diphtheria toxin receptor-based strategy to selectively

236 1 knockout mice; DEREG mice, which express a diphtheria toxin receptor-enhanced green fluorescent pro

237 induced responses in CD11c promoter-directed diphtheria toxin receptor-expressing mice that were depl

238 r macrophages and in CD11b promoter-directed diphtheria toxin receptor-expressing mice that were depl

239 We used immunophenotyping techniques and diphtheria toxin receptor-expressing, chemokine receptor

240 the number of macrophages in mice following diphtheria toxin receptor-mediated cell ablation of panc

241 rgy induction to CD4 memory T cells, because diphtheria toxin receptor-transgenic mice that were cond

242 ith type II AEC-restricted expression of the diphtheria toxin receptor.

243 with iDTR mice carrying Cre-dependent human diphtheria toxin receptor.

244 ress both green fluorescence protein and the diphtheria toxin receptor.

245 mice expressing the CCR2 promoter-controlled diphtheria toxin receptor.

246 y podocyte-specific transgenic expression of diphtheria toxin receptor.

247 ogenic insult using a conditional, inducible diphtheria-toxin receptor expression strategy in mice.

248 Diphtheria-toxin receptor expression was induced among g

249 nction, we eliminated DCS cells by using the diphtheria-toxin receptor gene knocked into the murine R

250 To confirm this, we used a CD11b-diphtheria toxin-receptor (DTR) transgenic mouse model.

251 ke reaction, we generated K14-OVA x Langerin-diphtheria-toxin-receptor (Langerin-DTR) Tg mice to allo

252 d a combinatorial viral technique to express diphtheria toxin receptors in specific neuron population

253 The metal-ion-activated diphtheria toxin repressor (DtxR) is responsible for the

254 a membrane-anchored metal ion permease and a diphtheria toxin repressor (DtxR)-like transcriptional r

255 The diphtheria toxin repressor contains an SH3-like domain t

256 We found that a single injection of diphtheria toxin resulted in an initial peak of proteinu

257 Exposure of PdxCre;R26DTR mice to diphtheria toxin resulted in extensive ablation of acina

258 an langerin were used to drive expression of diphtheria toxin, resulting in absence of LC, suggest th

259 Diphtheria toxin robustly depleted circulating monocytes

260 Using Slc6a3(DTR/+) diphtheria-toxin-sensitive mice, we demonstrate that a p

261 velopment, including rituximab, epratuzumab, diphtheria toxin-single chain Fv (DC2219), belimumab, at

262 on of NTS PPG neurons by viral expression of diphtheria toxin subunit A substantially reduced active

263 r nanoparticulate delivery of DNA encoding a diphtheria toxin suicide protein (DT-A).

264 Furthermore, using the diphtheria toxin system to selectively eliminate APCs th

265 Diphtheria toxin T domain aids the membrane translocatio

266 The diphtheria toxin T domain helps translocate the A chain

267 The diphtheria toxin T domain translocates the catalytic C d

268 enzymatically inactive and nontoxic form of diphtheria toxin that contains a single amino acid subst

269 plasm (BPDCN) using an engineered version of diphtheria toxin that is targeted to malignant cells via

270 Its name refers to the target function for diphtheria toxin, the disease-causing agent that, throug

271 Thus, in contrast to diphtheria toxin, the formation of a membrane-competent

272 ring with a bacterial ADP-ribosyltransferase diphtheria toxin, the observed rate constant of sirtuin-

273 izures were frequent, mice were treated with diphtheria toxin to ablate peri-insult generated newborn

274 on of CD11c(high) cells by administration of diphtheria toxin to CD11c.DOG mice.

275 We used diphtheria toxin to deplete DCs to study their functiona

276 ol of intracerebroventricular application of diphtheria toxin to efficiently ablate hypothalamic cell

277 d (TT) or the cross-reactive mutant (CRM) of diphtheria toxin to form detoxified LOS (dLOS)-TT, dLOS-

278 Administration of diphtheria toxin to HBUS mice accelerated development of

279 We used diphtheria toxin to kill all mouse postmitotic sensory n

280 We induced autonomous expression of diphtheria toxin to kill articular surface chondrocytes

281 In vivo targeting of diphtheria toxin to kill Tregs leads to a lower fraction

282 ontributes to lung fibrosis, we administered diphtheria toxin to transgenic mice with type II AEC-res

283 c mice that express an attenuated version of diphtheria toxin (Tox176) linked to a modified Pax6 prom

284 switching in several systems, including the diphtheria toxin translocation (T) domain, which is resp

285 cdB and the well-characterized alpha-helical diphtheria toxin translocation domain provide insights i

286 A single systemic diphtheria toxin treatment 2 d before HSV-1 corneal infe

287 In this study, we used diphtheria toxin treatment of sensitized CD11c-diphtheri

288 In chimeric CD11c-DTR mice, diphtheria toxin treatment results in enhanced neutrophi

289 e, using doxycycline-inducible expression of diphtheria toxin, triggers a significant compensatory pr

290 d to those conjugated to tetanus (TT) or the diphtheria toxin variant, CRM.

291 embrane insertion pathway of the T-domain of diphtheria toxin was studied using site-selective fluore

292 x (DD), a fusion protein comprising IL-2 and diphtheria toxin, was initially expected to enhance anti

293 ecifically ablated through administration of diphtheria toxin, we demonstrate that natural Tregs are

294 sing Tregs that can be depleted in vivo with diphtheria toxin, we show that injected cells are requir

295 e lamina propria by injecting HBUS mice with diphtheria toxin, which binds transgenic HBEGF expressed

296 ansport and also provided protection against diphtheria toxin, which enters the cytosol from early en

297 ndritic cells (dDCs) after administration of diphtheria toxin, which results in reduced CHS.

298 al switching is essential for functioning of diphtheria toxin, which undergoes a membrane insertion/t

299 X-expressing neurons after administration of diphtheria toxin while leaving the neural precursor pool

300 ono-ADP-ribosyltransferase proteins, such as diphtheria toxin, with the exception of a unique loop th