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1 ination of Foxp3+ Treg by treatment with Dx (diphtheria toxin).
2 variety of recombinant protein fragments of diphtheria toxin.
3 xpressing cells can be depleted by injecting diphtheria toxin.
4 IL-2 protein and as toxophore the truncated diphtheria toxin.
5 tly but selectively depleted by injection of diphtheria toxin.
6 y intracerebroventricular (ICV) injection of diphtheria toxin.
7 cific ablation of podocytes by administering diphtheria toxin.
8 nine; DCs were depleted by administration of diphtheria toxin.
9 e called diphthamide, which is the target of diphtheria toxin.
10 electively deplete pDCs by administration of diphtheria toxin.
11 nsive islet infiltration upon treatment with diphtheria toxin.
12 inooxy linkers bound to BSA or a recombinant diphtheria toxin.
13 D11c(+) cells was controlled by injection of diphtheria toxin.
14 immunity, only if Tregs were depleted using diphtheria toxin.
15 ma cells before depleting myeloid cells with diphtheria toxin.
16 s in activation of anthrax, pseudomonas, and diphtheria toxins.
17 genic mice were treated with intraperitoneal diphtheria toxin (5 ng/g b.wt.) in the presence or absen
18 nstrate that the fusion of Rad51 promoter to diphtheria toxin A (DTA) gene kills a variety of cancer
19 rprisingly, donor LC engraftment in Langerin-diphtheria toxin A (DTA) transgenic hosts was independen
20 ased in insulin-resistant uncoupling protein-diphtheria toxin A (UCP-DTA) transgenic mice, a murine m
21 have been ablated by targeted expression of diphtheria toxin A chain (DTA) under the control of the
24 that directs cone-specific expression of the diphtheria toxin A chain was used to ablate cone photore
27 on, utilizing temporally controlled targeted diphtheria toxin A expression, results in failure of neu
29 s) via Cre-dependent viral expression of the diphtheria toxin A subunit (DT-A) in hemiparkinsonian tr
30 ression of the potent translation inhibitor, diphtheria toxin A subunit, from the Arabidopsis (Arabid
31 loped genetically modified mice that express diphtheria toxin A under control of a loxP-flanked stop
32 deficient in LCs by virtue of expression of diphtheria toxin A under the control of a BAC (bacterial
33 in mice for 25 d via neuronal expression of diphtheria toxin A-chain, producing both a neuroinflamma
34 ectories of the conformational transition of diphtheria toxin, a particularly challenging example, sh
36 engineered human Langerin-DTR mice in which diphtheria toxin ablates LCs without affecting Langerin(
39 le we show that the translocation pathway of diphtheria toxin allows much larger molecules to be tran
40 splantation carrying a conditional allele of diphtheria toxin alpha subunit and cell-specific express
41 utively ablated because of expression of the diphtheria toxin alpha subunit within developing DCs.
42 selective ablation of PPARgamma(+) cells by diphtheria toxin also causes high bone mass due to decre
45 (T) domain plays a key role in the action of diphtheria toxin and is responsible for transferring the
47 tox (Ontak), a recombinant fusion protein of diphtheria toxin and ligand, IL-2, binds to the IL-2 rec
48 en shown to repress the transcription of the diphtheria toxin and other genes associated with ferrous
49 hMAb binds to the receptor-binding domain of diphtheria toxin and physically blocks the toxin from bi
50 thamide, which serves as the only target for diphtheria toxin and Pseudomonas aeruginosa exotoxin A.
52 anthracis, toxin B of Clostridium difficile, diphtheria toxin, and exotoxin A of Pseudomonas aerugino
53 ng method to attach the catalytic subunit of diphtheria toxin as a toxic warhead to CTA1, thus conver
57 detrimental effects of anthrax lethal toxin, diphtheria toxin, cholera toxin, Pseudomonas aeruginosa
58 CD4+/CD25+ Tregs using the recombinant IL-2 diphtheria toxin conjugate DAB(389)IL-2 (also known as d
61 etane grafting of the genetically detoxified diphtheria toxin CRM197 improves significantly the immun
64 Selective ablation of mitotic neurons using diphtheria toxin (DT) and a retrovirus vector encoding D
65 r 2 (eEF2) is the target of ADP ribosylating diphtheria toxin (DT) and Pseudomonas exotoxin A (PE).
66 tively sensitive to exogenously administered diphtheria toxin (DT) by targeted expression of the diph
67 In adult wild-type mice, administration of diphtheria toxin (DT) caused no significant hair cell lo
71 wild-type Tf, we showed enhanced delivery of diphtheria toxin (DT) from these mutants to a monolayer
73 y timed local (subconjunctival) injection of diphtheria toxin (DT) into mice that express high-affini
74 mouse models in which the administration of diphtheria toxin (DT) leads to specific depletion of reg
75 We generated mice in which administration of diphtheria toxin (DT) led to specific ablation of PYY-ex
77 a gene knock-in strategy inserting the human diphtheria toxin (DT) receptor (DTR) into the endogenous
78 hages in atherosclerosis, we developed CD11b-diphtheria toxin (DT) receptor (DTR) transgenic mice, wh
80 to the splenic marginal zone of naive CD11b-diphtheria toxin (DT) receptor bone marrow-chimeric mice
81 arance using a transgenic mouse model (CD11c-diphtheria toxin (DT) receptor GFP) that allows for thei
82 -Tg(.Itgax-DTR/EGFP.57)Lan/J) expressing the diphtheria toxin (DT) receptor on the CD11c promoter (DC
83 we used the DEREG mouse, which expresses the diphtheria toxin (DT) receptor under control of the Treg
84 used transgenic mice that express the human diphtheria toxin (DT) receptor under the control of the
85 HSV-1 infection was investigated using CD11c-diphtheria toxin (DT) receptor-green fluorescent protein
86 ned CBA/CaJ male mice, engineered to express diphtheria toxin (DT) receptors in hair cells, by system
90 ic tyrosinase promoter, under the control of diphtheria toxin (DT), we eliminated and/or halted diffe
91 be the development and characterization of a diphtheria toxin (DT)-based antigen delivery system.
92 ction when engaged by physiological ligands, diphtheria toxin (DT)-C3d fusion protein and C3dg-strept
93 glycemia after induction of a more complete, diphtheria toxin (DT)-induced beta-cell loss, a situatio
98 ecifically ablated from adult mice using the diphtheria toxin (DT)/DT-receptor system and the connexi
99 ynthetic antigen was conjugated to a mutated diphtheria toxin (DT, CRM197) with different copy number
100 lectively deplete human stromal cells (using diphtheria toxin, DT) without affecting mouse cancer cel
101 eration, we used Cre-activated expression of diphtheria toxin (DTA) in the Ascl3-expressing (Ascl3+)
102 ed with CRE-dependent AAV vectors expressing diphtheria toxin (DTA) to selectively ablate FC SST neur
104 sruption of the notochord and floor plate by diphtheria toxin (DTA)-mediated cell ablation did not di
105 addition to Stx, the phage-encoded exotoxin, diphtheria toxin (Dtx) expressed by Corynebacterium diph
106 in conjunction with mice expressing GFP and diphtheria toxin (DTx) receptor (DTR) under control of t
109 esponse and type 2 diabetes mellitus (T2DM), diphtheria toxin-expressing (DT) mice that specifically
113 ral crest lineage using a Wnt1-Cre-activated diphtheria toxin fragment-A cell-killing system was empl
114 In vivo administration of LPS or an IL-2/diphtheria toxin fusion protein (Ontak) to chronically S
115 a rapid tool to confirm the presence of the diphtheria toxin gene (tox) in an isolate or specimen.
117 transformation method by the introduction of diphtheria toxin genes into the transformation vector as
118 riggered membrane insertion, the T domain of diphtheria toxin helps translocate the catalytic domain
119 d potent human neutralizing antibody against diphtheria toxin holds promise as a potential therapeuti
121 The 18 human ADP-ribose transferases with diphtheria toxin homology include ARTD1/PARP1, a cancer
122 depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced AML diseas
124 pressing either tetanus toxin light chain or diphtheria toxin in gal4-defined neural circuits, we wer
125 ique hMAbs were tested for neutralization of diphtheria toxin in in vitro cytotoxicity assays with a
128 In these albumin-deficient rats, exposure to diphtheria toxin induced an increase in albumin GSC and
130 ischemia/reperfusion (I/R) injury or a novel diphtheria toxin-induced (DT-induced) model of selective
131 state was perturbed by coronary ligation or diphtheria toxin-induced macrophage depletion in CD11b(D
132 microglia exert beneficial effects during a diphtheria toxin-induced neuronal lesion, but impede rec
133 11b promoter such that the administration of diphtheria toxin induces ablation of nearly 97% of resid
134 model, PMN(DTR) mice, in which injection of diphtheria toxin induces selective neutrophil ablation.
142 ied as a potent but unselective inhibitor of diphtheria toxin-like ADP-ribosyltransferase 3 (ARTD3).
146 answer this question, we used Cre-dependent, diphtheria toxin-mediated cell ablation to selectively r
148 Using a progressive, time-controllable, diphtheria toxin-mediated cell ablation/dysfunction tech
155 and covalently linked to recombinant CRM197 diphtheria toxin mutant (CRM197) to produce CPS-CRM197.
158 calizes to tumors in vivo and rVAR2 fused to diphtheria toxin or conjugated to hemiasterlin compounds
159 lls was assessed by selective depletion with diphtheria toxin or depleting anti-CD20 monoclonal antib
160 vidity of immunoglobulin (Ig) G specific for diphtheria toxin, pertussis toxin, filamentous hemagglut
162 a fusion protein of interleukin 2 (IL-2) and diphtheria toxin, provides a means of targeting Treg cel
163 onate (sLC), inducible depletion using CD11b diphtheria toxin receptor (CD11b DTR) transgenic mice, a
164 pletion of this population in CD11B promoter-diphtheria toxin receptor (CD11B-DTR) transgenic mice ca
165 onstituted with bone marrow cells from CD11c-diphtheria toxin receptor (CD11c-DTR) and CCR5(-/-) or C
166 mouse strains that either express the human diphtheria toxin receptor (DTR) coupled to the CD11b pro
167 Cs from LNs based on their expression of the diphtheria toxin receptor (DTR) directed by the gene enc
169 e adult mouse utricle by inserting the human diphtheria toxin receptor (DTR) gene into the Pou4f3 gen
170 Lgr5-expressing cells in mice using a human diphtheria toxin receptor (DTR) gene knocked into the Lg
172 via transgenic expression of a high-affinity diphtheria toxin receptor (DTR) is a new and powerful ap
176 We attempted to create a model that used diphtheria toxin receptor (DTR) to ablate specific cell
177 in vivo, we targeted expression of the human diphtheria toxin receptor (DTR) to the gene for MCH (Pmc
178 1c-enhanced green fluorescent protein (EGFP)-diphtheria toxin receptor (DTR) transgene was associated
179 used several murine models, including BDCA-2-diphtheria toxin receptor (DTR) transgenic and IFN-alpha
180 s were eliminated in newly generated SiglecH-diphtheria toxin receptor (DTR)-transgenic (Tg) mice but
183 nerated transgenic mice expressing the human diphtheria toxin receptor (hDTR, encoded by HBEGF) from
184 el transgenic mouse model in which the human diphtheria toxin receptor (huDTR) is selectively express
185 m1cre mice were bred to homozygous inducible diphtheria toxin receptor (iDTR) mice to generate mice e
186 using the human diphtheria receptor system (diphtheria toxin receptor [DTR]) expressed in Lysmd1-cre
194 , a transgenic rat strain in which the human diphtheria toxin receptor is specifically expressed in p
196 organs (liver, spleen, and kidneys) in CD11c-diphtheria toxin receptor mice but not in wild-type mice
197 ished hepatic metastases in transgenic CD11b-diphtheria toxin receptor mice by intrasplenic injection
198 n, in either Mac1-deficient mice or in CD11b-diphtheria toxin receptor mice in which CD11b-positive c
199 etion of Treg during MCMV infection in Foxp3-diphtheria toxin receptor mice or in wild-type mice reca
200 epithelial debridement wound model and CD11c-diphtheria toxin receptor mice that express a CD11c prom
201 g monocytes only in CCR2 promoter-controlled diphtheria toxin receptor mice, whereas neutrophil numbe
202 otein (EGFP) knock-in mice and Langerin-EGFP-diphtheria toxin receptor mice--three dimensional rotati
203 CD11b/Gr1(mid) subset in a transgenic CD11b-diphtheria toxin receptor mouse model markedly reduced t
204 ectly test this hypothesis, we expressed the diphtheria toxin receptor specifically on either B lymph
205 e have generated a transgenic strain, Clec9A-diphtheria toxin receptor that allows us to ablate in vi
207 apidly killing peptide-pulsed DCs carrying a diphtheria toxin receptor transgene with timed injection
208 depletion of dendritic cells (DCs) in CD11c-diphtheria toxin receptor transgenic mice followed by in
209 and reconstitution in CD11b promoter-driven diphtheria toxin receptor transgenic mice revealed that
210 phtheria toxin treatment of sensitized CD11c-diphtheria toxin receptor transgenic mice to deplete CD1
213 nduced acute lung injury, wild-type or CD11c-diphtheria toxin receptor transgenic mice were treated w
216 olerance was assessed by combining the CD11c-diphtheria toxin receptor transgenic system, in which DC
218 l macrophage ablation mice express the human diphtheria toxin receptor under the control of the CD11b
219 t C57BL/6-DEREG mice expressing a transgenic diphtheria toxin receptor under the Foxp3 promoter, tran
220 se line, using the Cre/loxP system, in which diphtheria toxin receptor was selectively expressed in m
222 tein, cluster of differentiation 11c (CD11c)/diphtheria toxin receptor, and IL-17 receptor A(-/-) mic
223 11c promoter driving expression of the human diphtheria toxin receptor, we found that selective deple
224 Exploiting a transgene encoding the human diphtheria toxin receptor, we punctually and specificall
225 or mice that express a CD11c promoter-driven diphtheria toxin receptor, we showed that DCs migrate al
227 induced responses in CD11c promoter-directed diphtheria toxin receptor-expressing mice that were depl
228 r macrophages and in CD11b promoter-directed diphtheria toxin receptor-expressing mice that were depl
229 We used immunophenotyping techniques and diphtheria toxin receptor-expressing, chemokine receptor
230 the number of macrophages in mice following diphtheria toxin receptor-mediated cell ablation of panc
231 rgy induction to CD4 memory T cells, because diphtheria toxin receptor-transgenic mice that were cond
236 ogenic insult using a conditional, inducible diphtheria-toxin receptor expression strategy in mice.
238 nction, we eliminated DCS cells by using the diphtheria-toxin receptor gene knocked into the murine R
240 ke reaction, we generated K14-OVA x Langerin-diphtheria-toxin-receptor (Langerin-DTR) Tg mice to allo
241 d a combinatorial viral technique to express diphtheria toxin receptors in specific neuron population
244 om Bacillus anthracis and is a member of the diphtheria toxin repressor (DtxR) family of proteins.
248 a membrane-anchored metal ion permease and a diphtheria toxin repressor (DtxR)-like transcriptional r
250 rms substituted in domain IV confer dominant diphtheria toxin resistance, which correlates with an in
253 an langerin were used to drive expression of diphtheria toxin, resulting in absence of LC, suggest th
255 ed to specific recognition of the A chain by diphtheria toxin's translocation pathway because the tra
256 velopment, including rituximab, epratuzumab, diphtheria toxin-single chain Fv (DC2219), belimumab, at
263 enzymatically inactive and nontoxic form of diphtheria toxin that contains a single amino acid subst
264 plasm (BPDCN) using an engineered version of diphtheria toxin that is targeted to malignant cells via
265 Its name refers to the target function for diphtheria toxin, the disease-causing agent that, throug
267 ring with a bacterial ADP-ribosyltransferase diphtheria toxin, the observed rate constant of sirtuin-
268 oyed at source by the targeted expression of diphtheria toxin, the remaining cells take over and the
269 izures were frequent, mice were treated with diphtheria toxin to ablate peri-insult generated newborn
272 ol of intracerebroventricular application of diphtheria toxin to efficiently ablate hypothalamic cell
273 d (TT) or the cross-reactive mutant (CRM) of diphtheria toxin to form detoxified LOS (dLOS)-TT, dLOS-
277 ontributes to lung fibrosis, we administered diphtheria toxin to transgenic mice with type II AEC-res
278 c mice that express an attenuated version of diphtheria toxin (Tox176) linked to a modified Pax6 prom
279 switching in several systems, including the diphtheria toxin translocation (T) domain, which is resp
280 cdB and the well-characterized alpha-helical diphtheria toxin translocation domain provide insights i
281 we constructed a gene encoding a portion of diphtheria toxin transmembrane helix 1, T1, which carrie
285 either B lymphocytes or macrophages and used diphtheria toxin treatment to deplete these specific cel
286 e, using doxycycline-inducible expression of diphtheria toxin, triggers a significant compensatory pr
288 embrane insertion pathway of the T-domain of diphtheria toxin was studied using site-selective fluore
289 x (DD), a fusion protein comprising IL-2 and diphtheria toxin, was initially expected to enhance anti
290 ecifically ablated through administration of diphtheria toxin, we demonstrate that natural Tregs are
291 selectively ablated by minute injections of diphtheria toxin, we depleted renal inflammatory macroph
292 sing Tregs that can be depleted in vivo with diphtheria toxin, we show that injected cells are requir
293 protected cells from anthrax edema toxin and diphtheria toxin, which also require an acidic environme
294 ansport and also provided protection against diphtheria toxin, which enters the cytosol from early en
296 al switching is essential for functioning of diphtheria toxin, which undergoes a membrane insertion/t
297 X-expressing neurons after administration of diphtheria toxin while leaving the neural precursor pool
298 which DC can be depleted via treatment with diphtheria toxin, with a TCR-transgenic adoptive transfe
299 ono-ADP-ribosyltransferase proteins, such as diphtheria toxin, with the exception of a unique loop th
300 receptor transgene with timed injections of diphtheria toxin without altering the course of an accom
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