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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
22  the lethal factor amino-terminal domain and diphtheria toxin A chain expedited translocation.
23 oter/gene were used to express an attenuated diphtheria toxin A chain in transgenic mice.
24 that directs cone-specific expression of the diphtheria toxin A chain was used to ablate cone photore
25  T domain aids the membrane translocation of diphtheria toxin A chain.
26 off system is used to regulate expression of diphtheria toxin A chain.
27 on, utilizing temporally controlled targeted diphtheria toxin A expression, results in failure of neu
28        Interestingly, neutropenic lysozyme 2-diphtheria toxin A mice exhibited striking EG and amplif
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
35  ataxin-3-orexin, and doxycycline-controlled-diphtheria-toxin-A-orexin.
36  engineered human Langerin-DTR mice in which diphtheria toxin ablates LCs without affecting Langerin(
37 be specifically depleted from the brain upon diphtheria toxin administration.
38           The membrane-inserting T domain of diphtheria toxin aids the low-pH-triggered translocation
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
43 switch to tightly regulate the expression of diphtheria toxin and Cre recombinase, respectively.
44 ch are required for the cytotoxic effects of diphtheria toxin and exotoxin A.
45 (T) domain plays a key role in the action of diphtheria toxin and is responsible for transferring the
46                                We found that diphtheria toxin and its nontoxic mutant, called CRM197,
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.
51 teins that include the key virulence factors diphtheria toxin and the adhesive pili.
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
54 e used a transgenic mouse system that allows diphtheria toxin-based depletion of pericytes.
55                          The delivery of the diphtheria toxin catalytic domain (DTA) from acidified e
56                     The translocation of the diphtheria toxin catalytic domain from the lumen of earl
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
59 as their bovine serum albumin or recombinant diphtheria toxin conjugates.
60 ugars (OAg) of LPS to the nontoxic mutant of diphtheria toxin (CRM(197)).
61 etane grafting of the genetically detoxified diphtheria toxin CRM197 improves significantly the immun
62                                 Injection of diphtheria toxin deleted YFP(+) cells from Foxl1-Cre;Ros
63 fically depleted CD4(+)Foxp3(+) T cells in a diphtheria toxin-dependent manner.
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
68                                              Diphtheria toxin (DT) contains separate domains for rece
69                                     However, diphtheria toxin (DT) crosses the blood-brain barrier, w
70         We have employed a hormone-inducible diphtheria toxin (DT) expression system in Saccharomyces
71 wild-type Tf, we showed enhanced delivery of diphtheria toxin (DT) from these mutants to a monolayer
72                                              Diphtheria toxin (DT) injection causes transient DC depl
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
76                                  We inserted diphtheria toxin (DT) receptor (DTR) cDNA into the 3' UT
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
79                 Hair cells express the human diphtheria toxin (DT) receptor behind the Pou4f3 promote
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
87 acrophages was achieved by administration of diphtheria toxin (DT) to CD11b-DTR mice.
88                            Administration of diphtheria toxin (DT) to these mice resulted in nearly c
89 Tg) mice but not in CLEC4C-DTR-Tg mice after diphtheria toxin (DT) treatment.
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
94       Unexpectedly, OT-I cell injection into diphtheria toxin (DT)-treated beta(2)m --> K14-OVA x Lan
95  cTECs sensitive to the cytotoxic effects of diphtheria toxin (DT).
96 morphogenesis and maturation is disrupted by diphtheria toxin (DT).
97  can be selectively ablated by the action of diphtheria toxin (DT).
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
103                                     Previous diphtheria toxin (DTA)-mediated ablation studies showed
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
107                           We have used CD11c-diphtheria toxin (DTx) receptor mice to deplete CD11c(+)
108           Some mice were given injections of diphtheria toxin during the recovery phase to delete Fox
109 esponse and type 2 diabetes mellitus (T2DM), diphtheria toxin-expressing (DT) mice that specifically
110 odon in the Rosa26(DTA/+) allele and induces diphtheria toxin fragment A (DTA) expression.
111 specific CreER allele to drive expression of diphtheria toxin fragment A (DTA).
112                  Denileukin diftitox (DD), a diphtheria toxin fragment IL-2 fusion protein, is though
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.
116 inducible Caspase-8 protein and an inducible diphtheria toxin gene, results in new neurons.
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
120 family includes ADP-ribosyltransferases with diphtheria toxin homology (ARTD).
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
123                      Transient expression of diphtheria toxin in beta cells of old mice resulted in i
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
126 gerin(+) DCs were depleted by treatment with diphtheria toxin in Lang-DTREGFP knock-in mice.
127                Five days after administering diphtheria toxin in these adult mice, changes were obser
128 In these albumin-deficient rats, exposure to diphtheria toxin induced an increase in albumin GSC and
129 use, a model of hyperglycemia resulting from diphtheria toxin induced beta cell ablation.
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.
135                            Within 2 weeks of diphtheria toxin injection, heterozygous Pmch(DTR/+) mic
136              In Corynebacterium diphtheriae, diphtheria toxin is encoded by the tox gene of some temp
137         In particular, the folded A chain of diphtheria toxin is readily translocated by that toxin b
138                   Diphthamide, the target of diphtheria toxin, is a post-translationally modified his
139                   Diphthamide, the target of diphtheria toxin, is a unique posttranslational modifica
140                   Diphthamide, the target of diphtheria toxin, is a unique posttranslational modifica
141 sing a Rosa26 conditional allele, expressing diphtheria toxin, led to crypt loss.
142 ied as a potent but unselective inhibitor of diphtheria toxin-like ADP-ribosyltransferase 3 (ARTD3).
143                                          The diphtheria toxin-like ADP-ribosyltransferases (ARTDs) ar
144                                              Diphtheria toxin-mediated ablation of lysozyme M-positiv
145 o acutely and selectively eliminate them via diphtheria toxin-mediated ablation.
146 answer this question, we used Cre-dependent, diphtheria toxin-mediated cell ablation to selectively r
147  diabetes mellitus of the NOD mouse by using diphtheria toxin-mediated cell ablation.
148      Using a progressive, time-controllable, diphtheria toxin-mediated cell ablation/dysfunction tech
149                                        Using diphtheria toxin-mediated depletion models in mice, we s
150                                 Importantly, diphtheria toxin-mediated depletion of IL-7-producing st
151       In this study, an established model of diphtheria toxin-mediated depletion of resident pulmonar
152                                              Diphtheria toxin-mediated selective depletion of MCs or
153                                              Diphtheria toxin-mediated, acute ablation of hypothalami
154 nd that limited podocyte renewal occurs in a diphtheria toxin model of acute podocyte ablation.
155  and covalently linked to recombinant CRM197 diphtheria toxin mutant (CRM197) to produce CPS-CRM197.
156 hesized and attached via a chain linker to a diphtheria toxin mutant carrier protein.
157               Regions of both colicin Ia and diphtheria toxin N-terminal to the channel-forming domai
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
161         Screens for sensitivity to a cholera-diphtheria toxin provide broad insights into the mechani
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
168          Many such models rely on transgenic diphtheria toxin receptor (DTR) expression driven by DC-
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
171 tance, using B6.Foxp3(DTR) mice that express diphtheria toxin receptor (DTR) in Foxp3(+) cells.
172 via transgenic expression of a high-affinity diphtheria toxin receptor (DTR) is a new and powerful ap
173                           In these mice, the diphtheria toxin receptor (DTR) is expressed under contr
174                    Conditional expression of diphtheria toxin receptor (DTR) is widely used for tissu
175                              Murine Langerin-diphtheria toxin receptor (DTR) mice allow for the induc
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
181                      Expression of the human diphtheria toxin receptor (hDTR) gene under the regulato
182 e induced limited podocyte depletion using a diphtheria toxin receptor (hDTR) transgenic rat.
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
187 cendants (Foxl1-Cre;Rosa(YFP/iDTR)-inducible diphtheria toxin receptor [iDTR] mice).
188                         By using B6/Langerin-diphtheria toxin receptor chimeric mice and LC ablation,
189           We generated mice that express the diphtheria toxin receptor exclusively in podocytes, allo
190                 Using CX3CR1(CreER) to drive diphtheria toxin receptor expression in microglia, we fo
191           To test this hypothesis, we used a diphtheria toxin receptor expression system to selective
192  nondiabetic mice conditionally expressing a diphtheria toxin receptor in mural cells.
193 ria toxin (DT) by targeted expression of the diphtheria toxin receptor in oligodendrocytes.
194 , a transgenic rat strain in which the human diphtheria toxin receptor is specifically expressed in p
195                               Using Langerin-diphtheria toxin receptor mice and established mouse mod
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
206                               Therefore, the diphtheria toxin receptor transgene was specifically exp
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
211                                 We generated diphtheria toxin receptor transgenic mice to selectively
212                                We used CD11b-diphtheria toxin receptor transgenic mice to transiently
213 nduced acute lung injury, wild-type or CD11c-diphtheria toxin receptor transgenic mice were treated w
214        To test the involvement of DCs, CD11c-diphtheria toxin receptor transgenic mice were used to d
215                         We also used a CD11c-diphtheria toxin receptor transgenic mouse model system
216 olerance was assessed by combining the CD11c-diphtheria toxin receptor transgenic system, in which DC
217                      We used mice expressing Diphtheria toxin receptor under control of the Foxp3 pro
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
221                         Foxp3-GFP-DTR (human diphtheria toxin receptor) C57BL/6 mice allow eliminatio
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
226                               We developed a diphtheria toxin receptor-based strategy to selectively
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
232 ith type II AEC-restricted expression of the diphtheria toxin receptor.
233 mice expressing the CCR2 promoter-controlled diphtheria toxin receptor.
234 y podocyte-specific transgenic expression of diphtheria toxin receptor.
235 ress both green fluorescence protein and the diphtheria toxin receptor.
236 ogenic insult using a conditional, inducible diphtheria-toxin receptor expression strategy in mice.
237                                              Diphtheria-toxin receptor expression was induced among g
238 nction, we eliminated DCS cells by using the diphtheria-toxin receptor gene knocked into the murine R
239             To confirm this, we used a CD11b-diphtheria toxin-receptor (DTR) transgenic mouse model.
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
242                                    Using the diphtheria toxin-related fusion protein toxin DAB(389)IL
243                           Upon activation of diphtheria toxin repressor (DtxR) by transition metals,
244 om Bacillus anthracis and is a member of the diphtheria toxin repressor (DtxR) family of proteins.
245                                          The diphtheria toxin repressor (DtxR) is a metal ion-activat
246                                          The diphtheria toxin repressor (DtxR) is an Fe(II)-activated
247                      The metal-ion-activated diphtheria toxin repressor (DtxR) is responsible for the
248 a membrane-anchored metal ion permease and a diphtheria toxin repressor (DtxR)-like transcriptional r
249                                          The diphtheria toxin repressor contains an SH3-like domain t
250 rms substituted in domain IV confer dominant diphtheria toxin resistance, which correlates with an in
251          We found that a single injection of diphtheria toxin resulted in an initial peak of proteinu
252            Exposure of PdxCre;R26DTR mice to diphtheria toxin resulted in extensive ablation of acina
253 an langerin were used to drive expression of diphtheria toxin, resulting in absence of LC, suggest th
254                                              Diphtheria toxin robustly depleted circulating monocytes
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
257 r nanoparticulate delivery of DNA encoding a diphtheria toxin suicide protein (DT-A).
258                       Furthermore, using the diphtheria toxin system to selectively eliminate APCs th
259                                              Diphtheria toxin T domain aids the membrane translocatio
260                                          The diphtheria toxin T domain helps translocate the A chain
261                                          The diphtheria toxin T domain translocates the catalytic C d
262  effect on the pH-triggered insertion of the diphtheria toxin T-domain.
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
266                         Thus, in contrast to diphtheria toxin, the formation of a membrane-competent
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
270 on of CD11c(high) cells by administration of diphtheria toxin to CD11c.DOG mice.
271                                      We used diphtheria toxin to deplete DCs to study their functiona
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-
274                                      We used diphtheria toxin to kill all mouse postmitotic sensory n
275          We induced autonomous expression of diphtheria toxin to kill articular surface chondrocytes
276                         In vivo targeting of diphtheria toxin to kill Tregs leads to a lower fraction
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
282                            A single systemic diphtheria toxin treatment 2 d before HSV-1 corneal infe
283                       In this study, we used diphtheria toxin treatment of sensitized CD11c-diphtheri
284                  In chimeric CD11c-DTR mice, diphtheria toxin treatment results in enhanced neutrophi
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
287 d to those conjugated to tetanus (TT) or the diphtheria toxin variant, CRM.
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
295 ndritic cells (dDCs) after administration of diphtheria toxin, which results in reduced CHS.
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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