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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.
14             We refer to this short region as death domain-1 (DD1).
15           TLIS variants cluster in the CRADD death domain, a platform for interaction with other deat
16                                  Neither the death domain adaptor Fas-associated death domain nor the
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
19 pression of Fas, FasL, or the Fas-associated death domain adaptor protein (FADD).
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
22                 Proapoptotic BH3-interacting death domain agonist (BID) regulates apoptosis and the D
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.
27 mplex involving DR4/TRAIL R1, Fas-associated death domain and FLICE-inhibitory protein proteins.
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
30 located mostly at the junction of the second death domain and the C-terminal domain.
31 ferent RIP mutants further revealed that the death domain and the kinase activity of RIP are not requ
32 caspases in two fragments, one harboring the death domain and the other the Toll-IL-1R domain.
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
36                 Expression of Fas-associated death domain, and not Fas, Fas ligand, or caspase protei
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
41           They further establish Silencer of Death Domains as a novel target for miR-26a, which funct
42                 We previously identified the death domain associated protein (Daxx) and the alpha-tha
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
45                            Here we show that death domain-associated protein (Daxx) acts to negativel
46          On exit from mitosis, Sp100 and Fas death domain-associated protein (Daxx) entered the daugh
47                           Here, we show that death domain-associated protein (Daxx) is required for M
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
50                                              Death domain-associated protein 6 (Daxx) is a transcript
51        As a multifunctional nuclear protein, death domain-associated protein 6 (Daxx) regulates a wid
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
54                                 Mutations in death domain-associated protein gene (DAXX) or ATR-X gen
55 X-linked chromatin remodeler (ATRX), a DAXX (death domain-associated protein) interacting protein, is
56 dependent interaction between CHIP and Daxx (death domain-associated protein).
57 echanism involving the adaptor protein DAXX (death domain-associated protein).
58 tal retardation syndrome X-linked (ATRX) and death-domain-associated protein (DAXX).
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
62                                Moreover, the death domain at C-terminal of p100 is identified as bein
63 which results in the motions of the receptor death domain being uncoupled from the motions of the tra
64  shows a tetrameric arrangement of four FADD death domains bound to four Fas death domains.
65 in, and TNF receptor-associated protein with death domain but not NIK or TRAF-6 proteins.
66 strate that GSK-3 mediates activation of the death domain caspase by GMF overexpression.
67 protein 1)-FADD (Fas-associated protein with death domain)-caspase 8 and RIP1-RIP3, a process that is
68        Moreover, knockdown of Fas-associated death domain, caspase-8, and DR4, respectively, suppress
69                   Here, we localize the cell death domain (CDD) to the N-terminal 62 amino acids of B
70 fully formed and isolated the human Fas-FADD death domain complex and report the 2.7 A crystal struct
71 y, which indicates the formation of the PIDD death domain complex.
72 Tube) and heterotrimeric (dMyD88-Tube-Pelle) death domain complexes.
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
75                              It requires the death domain-containing kinase RIP1 and, in certain inst
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
80  level by the independent association of two death domain-containing proteins, RIP1 and TRADD.
81 inhibited by using a neutralizing Ab against death domain-containing receptor-3 (DR3) or a truncated
82                  Death receptor 5 (DR5) is a death domain-containing transmembrane receptor that trig
83             CRADD (also known as RAIDD) is a death-domain-containing adaptor protein that oligomerize
84 e DNA-PKcs and promoted by the p53-inducible death-domain-containing protein PIDD within a large nucl
85 omain, a platform for interaction with other death-domain-containing proteins including PIDD.
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
88           MyD88 is composed of an N-terminal death domain (DD) and a C-terminal Toll/IL-1 receptor (T
89 ane would bind to the interphase between Fas death domain (DD) and Fas-associated DD (FADD).
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
93 have carried out a phi-value analysis of the death domain (DD) from human FADD.
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 (
98                                          The death domain (DD) superfamily comprising the death domai
99                              Proteins of the death domain (DD) superfamily mediate assembly of oligom
100              PYDs, like other members of the death domain (DD) superfamily, are postulated to mediate
101  with the CARD of caspase-2 and a C-terminal death domain (DD) that interacts with the DD in PIDD.
102                        The assembly of MyD88 death domain (DD) with TRAF3 (anti-viral/anti-inflammato
103 assembly via ATM phosphorylation of the PIDD death domain (DD), which enables RAIDD recruitment to PI
104                                    Homotypic death domain (DD)-DD interactions are important in the a
105 he expression of most genes was induced by a death domain (DD)-dependent mechanism, since they were n
106 eptor superfamily that possess a cytoplasmic death domain (DD).
107 RH2/PLAIDD is a p75 homologue and contains a death domain (DD).
108                                   RIPK1 is a death-domain (DD) containing kinase involved in regulati
109          Biochemical evidence implicates the death-domain (DD) protein PIDD as a molecular switch cap
110 nally and rapidly increase the levels of the death domain (DD1) region of NRIF3.
111                                      A novel death domain (DD1) was mapped to a 30-amino acid region
112                                              Death domains (DDs) mediate assembly of oligomeric compl
113  that alters the oligomeric structure of the death domain, de-stabilizes DAPK-1 binding to ERK, and p
114            These modular proteins consist of death domains, death effector domains, caspase recruitme
115        We found that the consecutive ZU5-UPA-death domain domain organization is commonly used in hum
116 (intrinsic) pathways, as both Fas-associated death domain dominant negative transgenic mice and mice
117           We show that an opening of the Fas death domain exposes the FADD binding site and simultane
118 ptor molecules Fas-associated protein with a death domain (FADD) and IMD.
119 f doxazosin on recruitment of Fas-associated death domain (FADD) and procaspase-8 to the Fas receptor
120 dephosphorylates fas-associated protein with death domain (FADD) and regulates cell growth.
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
123 so show that MUC1-CD binds to Fas-associated death domain (FADD) at the death effector domain.
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
126              In addition, the Fas-associated death domain (FADD) gene was also deleted in the one fam
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
129                               Fas-associated death domain (FADD) is an adaptor molecule for the death
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
140 reonine kinase 1 (RIPK1), and Fas-associated death domain (FADD), but not RIPK3.
141                 We found that Fas-associated death domain (FADD), first described as an apoptotic pro
142 wn of caspase-8, Fas-associated protein with death domain (FADD), or Bid.
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
147                               Fas-associated death domain (FADD)-deficient Jurkat cells were resistan
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
152 ther with the adaptor protein Fas-associated death domain (FADD).
153 h adaptor protein termed Fas-associated with death domain (FADD).
154 ated death domain (TRADD) and Fas-associated death domain (FADD).
155 a dominant negative mutant of Fas-associated death domain (FADD-DN) or Bid-/- and in mice with defect
156 ), including the Fas-associated protein with death-domain (FADD) and caspase-8.
157 flurane reduces neutrophil apoptosis via Fas death domain-Fas-associated death domain interaction.
158                      The structure reveals a death domain fold with a short alpha3 helix that is butt
159 RP12 PYD adopts a typical six-helical bundle death domain fold.
160 he NLRP7 PYD adopts a six-alpha-helix bundle death domain fold.
161 activation in several complexes by homotypic death domain-fold interactions.
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
164          Deletion of either kinase domain or death domain in the T cell compartment reduced the T cel
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
168 poptosis via Fas death domain-Fas-associated death domain interaction.
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
171                                          The death domain kinase receptor interacting protein 1 (RIP1
172                      Here we report that the death domain kinase, RIP (receptor-interacting protein),
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
177                     FLIP (Fas-associated via death domain-like interleukin 1beta-converting enzyme in
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
183       The latent KSHV protein 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
185 ligomeric nature of the purified recombinant death domain miniprotein.
186            The N1347S mutation prevented the death domain module binding stably to ERK in vitro and i
187                      Accordingly, the N1347S death domain module is defective in vivo in the formatio
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
190 ovel mutation (N1347S) was identified in the death domain of DAPK-1.
191 dentified through its ability to bind to the death domain of Fas (CD95).
192          Our data show that CaM binds to the death domain of Fas (FasDD) with an apparent dissociatio
193 mapped to the B-box domain of PML moiety and death domain of Fas.
194          We demonstrated that GRK2 binds the death domain of MALT1 and inhibits MALT1 scaffolding and
195             We now provide evidence that the death domain of MALT1 and the CARD of Bcl10 also contrib
196 itation, FRET data strongly suggest that the death domain of MALT1 contributes significantly to the a
197 nction for the COOH-terminal leucine repeats/death domain of Par-4 in mediating apoptosis.
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
202 we found no interaction between the isolated death domains of Pelle and dMyD88.
203 ), which contains one of the most potent BH3 death domains of the BCL-2 protein family, to restore BH
204                                    The MyD88 death domain, on the other hand, was required for NF-kB
205  that Jurkat variants lacking Fas-associated death domain or procaspase-8 undergo tipifarnib-induced
206             It also regulates the associated death domain pathway and caspase 8-mediated events.
207 rotein complex of p53-induced protein with a death domain (PIDD), receptor-interacting protein-associ
208 enes, including p53-inducible protein with a death domain (Pidd).
209                               Fas-associated death domain protein (FADD) and caspase-8 (casp8) are vi
210 or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epitheli
211                  Knockdown of Fas-associated death domain protein (FADD) by either siRNA or overexpre
212                               Fas-associated death domain protein (FADD) constitutes an essential com
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
216 utation in FADD, encoding the Fas-associated death domain protein (FADD), in the patients.
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.
220                           The Fas-associated death domain protein (FADD)/Mort1 is a signaling adaptor
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
223                              TNFR-associated death domain protein (TRADD) is a key effector protein o
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
232         Knock down of CD95 or Fas-associated death domain protein suppressed drug combination toxicit
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
237  SseK2 glycosylated the FADD (Fas-associated death domain protein).
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
252                   However, signaling through death-domain proteins does not explain how TNFR1 induces
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
255 ciation and protein interactions via its two Death Domains, PYD and CARD.
256 ciated ICH-1/CED-3 homologous protein with a death domain (RAIDD), and procaspase-2.
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
259 ceptor DR4 thereby preventing Fas-associated death domain recruitment.
260  involved in regulating necroptosis, and the death domain regulates RIP1 recruitment to the intracell
261 r-346 is required for full activity, and the death domain regulates the activation of IRAK4.
262 associated Ich-1/CED homologous protein with death domain) remained susceptible to heat-induced apopt
263 fic interaction module for the alpha-helical death domain signal transduction.
264                 This is significant, because death domain signaling is driven by electrostatic contac
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
267  that has been observed in DED/DED and other death domain superfamily interactions.
268                                              Death domain superfamily members typically act as adapto
269                                        Seven death domain superfamily members were tested for crystal
270 nonical six-helix (H1-H6) bundle fold in the death domain superfamily.
271  contain N-terminal domains belonging to the death domain superfamily.
272            In this paper, we report that the death domain SXXE/D motifs (i.e., S381DHE motif of TNFR1
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
277           The type 1 TNFR (TNFR1) contains a death domain through which it interacts with other death
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
280 ical effect of decoy receptors that lack the death domain to trigger apoptosis.
281 l prion-like fibers through their respective death domains to propagate downstream signaling.
282 alpha Greek key protein FADD (Fas-associated death domain) to investigate this question.
283 FR associated factor (TRAF), TNFR associated death domain (TRADD) and Fas-associated death domain (FA
284                      TNF receptor-associated death domain (TRADD) is an essential mediator of TNF rec
285                          The TNFR-associated death domain (TRADD) protein has been suggested to be a
286 of tumor necrosis factor receptor-associated death domain (TRADD) was reduced in androgen deprivation
287  (TNF-alpha), TNF receptor (TNFR)-associated death domain (TRADD), and caspases.
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
295                        In reporter assays, a death domain variant, S34Y, was found to be inactive.
296 1 protein harboring a N1347S mutation in the death domain was also defective in binding to ERK in cel
297                                        RIP's death domain was critical for RIP and Fas association to
298 n Fas-associated death domain (FADD) via the death domain, which recruits downstream signaling protei
299 redicted to be exposed on the surface of the death domain, which we termed the WR motif.
300  either to itself or to FADD (Fas-associated death domain), with the large version of E6 able to inhi

 
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