コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 tein kinase) and Madd (MAP kinase-activating death domain).
2 anslated region (3'UTR) of SODD (silencer of death domains).
3 ciated ICH-1/CED-3 homologous protein with a death domain.
4 5(NTR) primarily via helix 4 of the p75(NTR) death domain.
5 sequence, previously defined as an essential death domain.
6 the TNFR superfamily, contains a cytoplasmic death domain.
7 hologue in that it contains an intracellular death domain.
8 nant-negative mutation of the Fas-associated death domain.
9 eraction of CaM with DR5 is localized at DR5 death domain.
10 modular interaction within their C-terminal death domains.
11 of four FADD death domains bound to four Fas death domains.
12 he proapoptotic Bcl-2 proteins via their BH3 death domains.
13 IPK1 kinase domain from the intermediate and death domains.
17 adaptor molecule (TRADD), the Fas-associated death domain adaptor molecule (FADD), caspase-8, TNFR-as
18 ISC involving TNF-alpha, the TNFR-associated death domain adaptor molecule (TRADD), the Fas-associate
20 in glioblastoma multiforme (GBM) specimens, death-domain adaptor protein Insuloma-Glucagonoma protei
21 o-1 signals through the FADD (Fas-associated death domain) adaptor protein, which recruits and activa
23 hough a direct interaction between the MALT1 death domain and Bcl10 cannot be detected via immunoprec
24 addition, full-length E6 binds to the TNF R1 death domain and can also bind to and accelerate the deg
25 Once stimulated, Fas recruits Fas-associated death domain and caspase-8 for the assembly of the death
26 et levels including p53-induced protein with death domain and cyclin-dependent kinase inhibitor, p21.
28 tes DAPK1, which interacts with TSC2 via its death domain and phosphorylates TSC2 via its kinase doma
29 of complexes that incorporate Fas-associated death domain and RIP1, which appear essential for kinase
31 ferent RIP mutants further revealed that the death domain and the kinase activity of RIP are not requ
33 with TNF receptor (TNFR) 1, TNFR-associated death domain and TRAF2 plasmids; NF-kappaB activated by
34 intact in Nup98, p53-induced protein with a death domain and UNC5C-like, deteriorated in many ZU5 do
35 evels of Fas-ligand, Fas, and Fas-associated death domain, and enhanced activation of procaspase-8 an
37 tment of TRAF-2, Fas-associated protein with death domain, and TNF receptor-associated protein with d
38 well as S215LKD and S296LAE motifs of TRADD-death domain) are phosphorylated, and this is required f
39 osis factor receptor-associated protein with death domain as an upstream regulator and transforming g
40 SXXE/D motifs (i.e., S381DHE motif of TNFR1-death domain as well as S215LKD and S296LAE motifs of TR
43 ntal retardation syndrome X-linked (ATRX) or death-domain associated protein (DAXX) have been shown t
44 promyelocytic leukemia protein (PML), Sp100, death-domain associated protein (Daxx), and so forth] an
48 osttranslational level through modulation of death domain-associated protein (DAXX), which disrupted
49 promyelocytic leukemia protein (PML), SP100, death domain-associated protein (Daxx)] and variable pro
52 hromatin remodeler that forms a complex with Death domain-associated protein 6 (DAXX) to deposit the
53 plasmacytoid DCs, which was associated with Death domain-associated protein 6 upregulation and B lym
55 X-linked chromatin remodeler (ATRX), a DAXX (death domain-associated protein) interacting protein, is
59 matin remodeling complex consisting of DAXX (death-domain-associated protein) and ATRX (alpha thalass
60 cleotide-binding protein, alpha stimulating, death-domain-associated protein, alpha thalassemia/menta
61 n MADD dissociation from, and Fas-associated death domain association with DR4, which allows death-in
63 which results in the motions of the receptor death domain being uncoupled from the motions of the tra
67 protein 1)-FADD (Fas-associated protein with death domain)-caspase 8 and RIP1-RIP3, a process that is
70 fully formed and isolated the human Fas-FADD death domain complex and report the 2.7 A crystal struct
73 pase-2 PIDDosome (p53-induced protein with a death domain) complexes were detected in dying cells, an
74 that modifies conserved arginine residues in death domain-containing host proteins with N-acetylgluco
76 we had reported on a role for Fas-associated death domain-containing protein (FADD) in the control of
77 iological role of endogenous MAPK-activating death domain-containing protein (MADD), a splice variant
78 aspase 8 recruitment to FADD (Fas-associated death domain-containing protein) in TNF-induced signalli
79 ndeed, SseK1 caused the GlcNAcylation of the death domain-containing proteins FADD and TRADD, whereas
81 inhibited by using a neutralizing Ab against death domain-containing receptor-3 (DR3) or a truncated
84 e DNA-PKcs and promoted by the p53-inducible death-domain-containing protein PIDD within a large nucl
86 nd receptor interacting protein adaptor with death domain (CRADD)/receptor interacting protein-associ
87 uces dimerization and the recruitment of the death domain (DD) adaptor protein MyD88 into an oligomer
90 We have tested the relevance of the p75(NTR) death domain (DD) and the highly conserved transmembrane
91 ing that the death effector domain (DED) and death domain (DD) are aligned with one another in an ort
92 e crystal structure of the MyD88-IRAK4-IRAK2 death domain (DD) complex, which surprisingly reveals a
94 the membrane-proximal adaptor MyD88 through death domain (DD) interactions, forming the oligomeric M
95 nvestigated mutant mice lacking the p75(NTR) death domain (DD) or a highly conserved transmembrane (T
96 ers of apoptosis and cell death that recruit death domain (DD) proteins FADD and TRADD and caspases t
97 death domain (DD) superfamily comprising the death domain (DD) subfamily, the death effector domain (
101 with the CARD of caspase-2 and a C-terminal death domain (DD) that interacts with the DD in PIDD.
103 assembly via ATM phosphorylation of the PIDD death domain (DD), which enables RAIDD recruitment to PI
105 he expression of most genes was induced by a death domain (DD)-dependent mechanism, since they were n
113 that alters the oligomeric structure of the death domain, de-stabilizes DAPK-1 binding to ERK, and p
116 (intrinsic) pathways, as both Fas-associated death domain dominant negative transgenic mice and mice
119 f doxazosin on recruitment of Fas-associated death domain (FADD) and procaspase-8 to the Fas receptor
121 IP from the complex to interact with the Fas death domain (FADD) and trigger the Fas-dependent pathwa
122 osis factor receptor 1 and to Fas-associated death domain (FADD) and, in doing so, prevents E6-expres
124 cted ablation of Fas-associated protein with death domain (FADD) combined with receptor-interacting p
125 in caspase 8 or Fas-associating protein with death domain (FADD) for the extrinsic pathway and in cel
127 eath-receptor adapter protein Fas-associated death domain (FADD) in apoptosis, it is intriguing that
128 cantly decreased Fas-associated protein with death domain (FADD) in the hippocampus, a key signaling
130 osis when the adaptor protein Fas-associated death domain (FADD) is lost or disabled by phosphorylati
131 to demonstrate that increased Fas-associated death domain (FADD) mRNA and protein were significantly
132 -8, -9, Fas, and Fas-associated protein with Death Domain (FADD) mRNA in conjunctiva were measured by
133 thway can be activated by the Fas-associated death domain (FADD) of the adaptor protein but is distin
134 d loss of either Fas-associated protein with death domain (FADD) or caspase-8 is known to sensitize t
135 us Jurkat lines that lack the Fas-associated death domain (FADD) or receptor-interacting protein kina
136 -1-induced apoptosis requires fas-associated death domain (FADD) since dominant-negative FADD express
137 interact with adaptor protein Fas-associated death domain (FADD) via the death domain, which recruits
138 C complex (caspase-8, Fas and Fas-associated death domain (FADD)) was observed within 30 min by immun
139 he death adaptor Fas-associated protein with death domain (FADD), and that in primary neuronal cultur
143 knockdown of the Fas-associated protein with death domain (FADD), the adaptor that mediates downstrea
144 odifies the host proteins Fas-associated via death domain (FADD), TNFRSF1A-associated via death domai
145 he TNFR1 complex II component Fas-associated death domain (FADD), which allowed a shift from TNF-indu
146 ent genomic amplifications of Fas-associated death domain (FADD), with or without Baculovirus inhibit
148 was significantly lessened in Fas-associated death domain (FADD)-deficient or caspase-8-deficient cou
149 ic pathways that regulate Fas-associated via death domain (FADD)-dependent signalling and other less
150 ion of cellular caspase 8 and Fas-associated death domain (FADD)-like apoptosis regulator-like inhibi
151 l-2), Bcl-x, A1, and cellular Fas-associated death domain (FADD)-like interleukin-1beta-converting en
155 a dominant negative mutant of Fas-associated death domain (FADD-DN) or Bid-/- and in mice with defect
157 flurane reduces neutrophil apoptosis via Fas death domain-Fas-associated death domain interaction.
162 n N-terminal Ser/Thr kinase and a C-terminal death domain, has emerged as a key regulatory molecule i
163 s the essential structural role of the IRAK4 death domain in receptor proximal signaling for mediatin
165 g a dominant-negative form of Fas-associated death domain in which the mice were resistant to apoptot
166 embrane, which in turn recruit IRAKs via the death domains in these proteins to form the Myddosome co
167 established that Act1-like proteins contain DEATH-domains in basal animals, such as Hydra and primit
169 on to depicting a previously unknown mode of death domain interactions, these results further uncover
170 Upon ligand binding and via its N-terminal death domain, IRAK4 is recruited to an oligomeric recept
173 f a dominant-negative form of Fas-associated death domain led to a reduction in the ability of apigen
174 f cellular FADD (Fas-associated protein with death domain)-like interleukin-1beta-converting enzyme i
175 in lower levels of Bcl-xL or Fas-associated death domain-like IL-1beta-converting enzyme inhibitor p
176 cell lines, including Bcl-xL, Fas-associated death domain-like IL-1beta-converting enzyme inhibitor p
178 olic protein c-FLIP (cellular Fas-associated death domain-like interleukin 1beta-converting enzyme in
179 -2, Bcl-xL, survivin, and antiFas-associated death domain-like interleukin-1 beta-converting enzyme-i
180 s due to the high levels of c-Fas-associated death domain-like interleukin-1-converting enzyme inhibi
181 ng protein (RIP) and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-in
182 tes (PEA-15/PED) and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-in
184 We also modelled a newly identified putative death domain, located N-terminal to the caspase-like dom
188 ession of a dominant-negative Fas-associated death domain mutant or silencing of DR5 expression using
189 ther the death domain adaptor Fas-associated death domain nor the apoptosis-initiating protease caspa
196 itation, FRET data strongly suggest that the death domain of MALT1 contributes significantly to the a
198 ng a fetal brain two-hybrid library with the death domain of the p75 neurotrophin receptor (NTR), we
199 both by pharmacologic inhibition of the cell death domain of the p75 neurotrophin receptor (TAT-Pep5)
200 on constants for the interaction between the death domains of dMyD88 and Tube and of Pelle and a pref
201 otypic protein interactions comprised of the death domains of Fas and FADD is at the centre of DISC f
203 ), which contains one of the most potent BH3 death domains of the BCL-2 protein family, to restore BH
205 that Jurkat variants lacking Fas-associated death domain or procaspase-8 undergo tipifarnib-induced
207 rotein complex of p53-induced protein with a death domain (PIDD), receptor-interacting protein-associ
210 or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epitheli
213 hway (WT) and a corresponding Fas-associated death domain protein (FADD) KO cell line were exposed to
214 gnal transduction mediated by Fas-associated death domain protein (FADD) represents a paradigm of cor
215 in LPS signaling such as the Fas-associated death domain protein (FADD), IkappaB kinase epsilon (IKK
217 of caspases 3, 8, and 9, the Fas-associated death domain protein (FADD), reactive oxygen species (RO
218 nant negative mutated form of Fas-associated death domain protein (FADD), which blocks caspase activa
219 not interfere with the TRADD-Fas-associated death domain protein (FADD)-procaspase-8 interaction.
221 ctions of p38 MAP kinase, p53, p53-inducible death domain protein (PIDD), and caspase-2 as shown by m
222 proteins, including TNF-receptor-associated death domain protein (TRADD) and receptor-interacting pr
224 racts with TNF receptor 1 (TNFR1)-associated death domain protein (TRADD), a death adaptor essential
225 In TNF-treated cells, TNFR1, TNFR-associated death domain protein (TRADD), Fas-associated death domai
226 TNF receptor 1 (TNFR1) and TNFR1-associated death domain protein (TRADD), suggesting that the core p
227 hile RIPK1 ablation induced TNFR1-associated death domain protein (TRADD)-dependent hepatocyte apopto
228 l death, the requirements for Fas-associated death domain protein and caspase-9 were different betwee
229 tical to TRADD for recruiting Fas-associated death domain protein and receptor-interacting protein ki
230 f dominant-negative mutant of Fas-associated death domain protein or a caspase-8 inhibitor completely
231 rminal ileum via Fas-associated protein with death domain protein repression along with decreased T-c
233 formed by Fas receptor, FADD (Fas-associated death domain protein) and caspase 8 is a pivotal trigger
234 ent of large amounts of FADD (FAS-associated death domain protein) and procaspase 8, leading to direc
235 or its adaptor protein FADD (Fas-associated death domain protein) develop a hyperautophagic morpholo
236 ent in the proapoptotic Bid (BH3-interacting death domain protein) gene (Bid KO) resist apoptosis and
238 modest reduction in levels of Fas-associated death domain protein, and procaspase 8 recruited to the
239 death domain protein (TRADD), Fas-associated death domain protein, and receptor-interacting protein k
240 nti-apoptotic isoform (MAP-kinase activating death domain protein, MADD), which effectively redirects
241 n-activated protein kinase (MAPK) activating death domain protein, regulates various cellular functio
242 ated factors (TRAFs) and the TNFR-associated death domain protein, respectively, and activate NF-kapp
243 on activated by TNFR type 1, TNFR-associated death domain protein, TNFR-associated factor 2, NF-kappa
244 induced by TNF-alpha, TNFR1, TNFR-associated death domain protein, TNFR-associated factor 2, TGF-beta
245 ha, TNF receptor-1 (TNFR1), TNFR1-associated death domain protein, TNFR-associated factor-2, NF-kappa
246 ketone, and dominant negative Fas-associated death domain protein, we found that deletion of these ki
247 s caspase-8-, caspase-9-, and Fas-associated death domain protein-deficient Jurkat cells, to assess w
248 ression of HHV8-encoded viral Fas-associated death domain protein-like IL-1beta-converting enzyme inh
249 IAP1, Bcl-x(L), A1/Bfl-1 and Fas-associated death domain protein-like IL-1beta-converting enzyme-inh
250 RIP1 participates in the Fas-associated death domain protein-mediated recruitment of caspase-8 t
251 y inhibited in caspase-8- and Fas-associated death domain protein-negative Jurkat cells, though apopt
253 domain through which it interacts with other death-domain proteins to promote cellular responses.
254 uroblastomas using responses to distinct BH3 death domains providing a BH3 response profile and direc
257 L1A is a TNF-like cytokine that binds to the death-domain receptor (DR)3 and provides costimulatory s
258 cholesterol biosynthesis, and apoptosis via death domain receptors, were overrepresented biological
260 involved in regulating necroptosis, and the death domain regulates RIP1 recruitment to the intracell
262 associated Ich-1/CED homologous protein with death domain) remained susceptible to heat-induced apopt
265 af-1-like proteins that are each linked to a death domain, suggesting that echinoderms have evolved u
266 cruitment domains (CARDs) are members of the death domain superfamily and contain six antiparallel he
273 rg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of F
274 the prostate by virtue of its intracellular death domain that can initiate apoptosis and inhibit gro
275 pro-death function via its alpha-helical BH3 death domain that has the dual capacity to inhibit antia
276 erized by a cytoplasmic region known as the "death domain" that enables the receptors to initiate cyt
278 tocyte-intrinsic Fas-associated protein with death domain, TNF-related apoptosis-inducing ligand rece
279 r activity induced by TNFR1, TNFR-associated death domain, TNFR-associated factor 2, and IkappaBalpha
283 FR associated factor (TRAF), TNFR associated death domain (TRADD) and Fas-associated death domain (FA
286 of tumor necrosis factor receptor-associated death domain (TRADD) was reduced in androgen deprivation
288 death domain (FADD), TNFRSF1A-associated via death domain (TRADD), and receptor-interacting serine/th
289 was inhibited by DN-TNF receptor-associated death domain (TRADD), DN-TNF receptor-associated factor
290 d binding of RIP1 to TNFRSF1A-associated via death domain (TRADD), two crucial signal adaptors for NF
291 show that TNF receptor 1 (TNFR1)-associated death domain (TRADD)-dependent TNFR1 signaling in epider
292 ty induced by TNFR1, TNF receptor-associated death domain, TRAF2, TAK1, NF-kappaB-inducing kinase, an
293 ace Fas receptor (FAS), FASL, FAS-associated death domain, tumor necrosis factor-related apoptosis-in
294 sic pathway involving Fas and Fas-associated death domain up-regulation, caspase-8 activation, and BI
296 1 protein harboring a N1347S mutation in the death domain was also defective in binding to ERK in cel
298 n Fas-associated death domain (FADD) via the death domain, which recruits downstream signaling protei
300 either to itself or to FADD (Fas-associated death domain), with the large version of E6 able to inhi