ライフサイエンスコーパス: death domain

1 anslated region (3'UTR) of SODD (silencer of death domains).

2 sequence, previously defined as an essential death domain.

3 the TNFR superfamily, contains a cytoplasmic death domain.

4 hologue in that it contains an intracellular death domain.

5 nant-negative mutation of the Fas-associated death domain.

6 of TNF receptor 1 to TNF receptor-associated death domain.

7 eraction of CaM with DR5 is localized at DR5 death domain.

8 ciated ICH-1/CED-3 homologous protein with a death domain.

9 5(NTR) primarily via helix 4 of the p75(NTR) 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 We refer to this short region as death domain-1 (DD1).

14 TLIS variants cluster in the CRADD death domain, a platform for interaction with other deat

15 Neither the death domain adaptor Fas-associated death domain nor the

16 adaptor molecule (TRADD), the Fas-associated death domain adaptor molecule (FADD), caspase-8, TNFR-as

17 ISC involving TNF-alpha, the TNFR-associated death domain adaptor molecule (TRADD), the Fas-associate

18 pression of Fas, FasL, or the Fas-associated death domain adaptor protein (FADD).

19 in glioblastoma multiforme (GBM) specimens, death-domain adaptor protein Insuloma-Glucagonoma protei

20 o-1 signals through the FADD (Fas-associated death domain) adaptor protein, which recruits and activa

21 Proapoptotic BH3-interacting death domain agonist (BID) regulates apoptosis and the D

22 hough a direct interaction between the MALT1 death domain and Bcl10 cannot be detected via immunoprec

23 addition, full-length E6 binds to the TNF R1 death domain and can also bind to and accelerate the deg

24 Once stimulated, Fas recruits Fas-associated death domain and caspase-8 for the assembly of the death

25 et levels including p53-induced protein with death domain and cyclin-dependent kinase inhibitor, p21.

26 The death domain and death effector domain are two common mo

27 mplex involving DR4/TRAIL R1, Fas-associated death domain and FLICE-inhibitory protein proteins.

28 of complexes that incorporate Fas-associated death domain and RIP1, which appear essential for kinase

29 located mostly at the junction of the second death domain and the C-terminal domain.

30 ferent RIP mutants further revealed that the death domain and the kinase activity of RIP are not requ

31 caspases in two fragments, one harboring the death domain and the other the Toll-IL-1R domain.

32 with TNF receptor (TNFR) 1, TNFR-associated death domain and TRAF2 plasmids; NF-kappaB activated by

33 intact in Nup98, p53-induced protein with a death domain and UNC5C-like, deteriorated in many ZU5 do

34 evels of Fas-ligand, Fas, and Fas-associated death domain, and enhanced activation of procaspase-8 an

35 Expression of Fas-associated death domain, and not Fas, Fas ligand, or caspase protei

36 tment of TRAF-2, Fas-associated protein with death domain, and TNF receptor-associated protein with d

37 well as S215LKD and S296LAE motifs of TRADD-death domain) are phosphorylated, and this is required f

38 osis factor receptor-associated protein with death domain as an upstream regulator and transforming g

39 SXXE/D motifs (i.e., S381DHE motif of TNFR1-death domain as well as S215LKD and S296LAE motifs of TR

40 They further establish Silencer of Death Domains as a novel target for miR-26a, which funct

41 ating the ligand-binding region from the two death domains, as observed for other receptor family mem

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 plasmacytoid DCs, which was associated with Death domain-associated protein 6 upregulation and B lym

53 Mutations in death domain-associated protein gene (DAXX) or ATR-X gen

54 dependent interaction between CHIP and Daxx (death domain-associated protein).

55 echanism involving the adaptor protein DAXX (death domain-associated protein).

56 tal retardation syndrome X-linked (ATRX) and death-domain-associated protein (DAXX).

57 matin remodeling complex consisting of DAXX (death-domain-associated protein) and ATRX (alpha thalass

58 cleotide-binding protein, alpha stimulating, death-domain-associated protein, alpha thalassemia/menta

59 n MADD dissociation from, and Fas-associated death domain association with DR4, which allows death-in

60 Moreover, the death domain at C-terminal of p100 is identified as bein

61 which results in the motions of the receptor death domain being uncoupled from the motions of the tra

62 shows a tetrameric arrangement of four FADD death domains bound to four Fas death domains.

63 in, and TNF receptor-associated protein with death domain but not NIK or TRAF-6 proteins.

64 strate that GSK-3 mediates activation of the death domain caspase by GMF overexpression.

65 protein 1)-FADD (Fas-associated protein with death domain)-caspase 8 and RIP1-RIP3, a process that is

66 Moreover, knockdown of Fas-associated death domain, caspase-8, and DR4, respectively, suppress

67 Here, we localize the cell death domain (CDD) to the N-terminal 62 amino acids of B

68 fully formed and isolated the human Fas-FADD death domain complex and report the 2.7 A crystal struct

69 y, which indicates the formation of the PIDD death domain complex.

70 Tube) and heterotrimeric (dMyD88-Tube-Pelle) death domain complexes.

71 pase-2 PIDDosome (p53-induced protein with a death domain) complexes were detected in dying cells, an

72 that modifies conserved arginine residues in death domain-containing host proteins with N-acetylgluco

73 It requires the death domain-containing kinase RIP1 and, in certain inst

74 we had reported on a role for Fas-associated death domain-containing protein (FADD) in the control of

75 iological role of endogenous MAPK-activating death domain-containing protein (MADD), a splice variant

76 ependent on the p53-responsive gene, PIDD, a death domain-containing protein that was induced by cisp

77 aspase 8 recruitment to FADD (Fas-associated death domain-containing protein) in TNF-induced signalli

78 ndeed, SseK1 caused the GlcNAcylation of the death domain-containing proteins FADD and TRADD, whereas

79 level by the independent association of two death domain-containing proteins, RIP1 and TRADD.

80 inhibited by using a neutralizing Ab against death domain-containing receptor-3 (DR3) or a truncated

81 Death receptor 5 (DR5) is a death domain-containing transmembrane receptor that trig

82 CRADD (also known as RAIDD) is a death-domain-containing adaptor protein that oligomerize

83 e DNA-PKcs and promoted by the p53-inducible death-domain-containing protein PIDD within a large nucl

84 omain, a platform for interaction with other death-domain-containing proteins including PIDD.

85 nd receptor interacting protein adaptor with death domain (CRADD)/receptor interacting protein-associ

86 uces dimerization and the recruitment of the death domain (DD) adaptor protein MyD88 into an oligomer

87 MyD88 is composed of an N-terminal death domain (DD) and a C-terminal Toll/IL-1 receptor (T

88 We have tested the relevance of the p75(NTR) death domain (DD) and the highly conserved transmembrane

89 ing that the death effector domain (DED) and death domain (DD) are aligned with one another in an ort

90 e crystal structure of the MyD88-IRAK4-IRAK2 death domain (DD) complex, which surprisingly reveals a

91 have carried out a phi-value analysis of the death domain (DD) from human FADD.

92 the membrane-proximal adaptor MyD88 through death domain (DD) interactions, forming the oligomeric M

93 nvestigated mutant mice lacking the p75(NTR) death domain (DD) or a highly conserved transmembrane (T

94 death domain (DD) superfamily comprising the death domain (DD) subfamily, the death effector domain (

95 The death domain (DD) superfamily comprising the death domai

96 Proteins of the death domain (DD) superfamily mediate assembly of oligom

97 PYDs, like other members of the death domain (DD) superfamily, are postulated to mediate

98 with the CARD of caspase-2 and a C-terminal death domain (DD) that interacts with the DD in PIDD.

99 The assembly of MyD88 death domain (DD) with TRAF3 (anti-viral/anti-inflammato

100 assembly via ATM phosphorylation of the PIDD death domain (DD), which enables RAIDD recruitment to PI

101 Homotypic death domain (DD)-DD interactions are important in the a

102 he expression of most genes was induced by a death domain (DD)-dependent mechanism, since they were n

103 eptor superfamily that possess a cytoplasmic death domain (DD).

104 RH2/PLAIDD is a p75 homologue and contains a death domain (DD).

105 Biochemical evidence implicates the death-domain (DD) protein PIDD as a molecular switch cap

106 nally and rapidly increase the levels of the death domain (DD1) region of NRIF3.

107 A novel death domain (DD1) was mapped to a 30-amino acid region

108 Death domains (DDs) mediate assembly of oligomeric compl

109 assembled via homotypic associations between death domains (DDs) of Fas and FADD and between death ef

110 that alters the oligomeric structure of the death domain, de-stabilizes DAPK-1 binding to ERK, and p

111 These modular proteins consist of death domains, death effector domains, caspase recruitme

112 hway that is characterized by Fas-associated death domain-dependent (FADD-dependent) caspase-8 activa

113 We found that the consecutive ZU5-UPA-death domain domain organization is commonly used in hum

114 (intrinsic) pathways, as both Fas-associated death domain dominant negative transgenic mice and mice

115 We show that an opening of the Fas death domain exposes the FADD binding site and simultane

116 significant effect on Fas and Fas-associated death domain (FADD) adapter protein levels.

117 ptor molecules Fas-associated protein with a death domain (FADD) and IMD.

118 f doxazosin on recruitment of Fas-associated death domain (FADD) and procaspase-8 to the Fas receptor

119 dephosphorylates fas-associated protein with death domain (FADD) and regulates cell growth.

120 osis factor receptor 1 and to Fas-associated death domain (FADD) and, in doing so, prevents E6-expres

121 so show that MUC1-CD binds to Fas-associated death domain (FADD) at the death effector domain.

122 cted ablation of Fas-associated protein with death domain (FADD) combined with receptor-interacting p

123 in caspase 8 or Fas-associating protein with death domain (FADD) for the extrinsic pathway and in cel

124 In addition, the Fas-associated death domain (FADD) gene was also deleted in the one fam

125 eath-receptor adapter protein Fas-associated death domain (FADD) in apoptosis, it is intriguing that

126 Fas-associated death domain (FADD) is an adaptor molecule for the death

127 osis when the adaptor protein Fas-associated death domain (FADD) is lost or disabled by phosphorylati

128 to demonstrate that increased Fas-associated death domain (FADD) mRNA and protein were significantly

129 -8, -9, Fas, and Fas-associated protein with Death Domain (FADD) mRNA in conjunctiva were measured by

130 thway can be activated by the Fas-associated death domain (FADD) of the adaptor protein but is distin

131 d loss of either Fas-associated protein with death domain (FADD) or caspase-8 is known to sensitize t

132 us Jurkat lines that lack the Fas-associated death domain (FADD) or receptor-interacting protein kina

133 -1-induced apoptosis requires fas-associated death domain (FADD) since dominant-negative FADD express

134 interact with adaptor protein Fas-associated death domain (FADD) via the death domain, which recruits

135 C complex (caspase-8, Fas and Fas-associated death domain (FADD)) was observed within 30 min by immun

136 omplex (DISC) comprising Fas, Fas-associated death domain (FADD), and caspase-8/10 is assembled via h

137 he death adaptor Fas-associated protein with death domain (FADD), and that in primary neuronal cultur

138 ry complex formation required Fas-associated death domain (FADD), as well as caspase-8 activity.

139 reonine kinase 1 (RIPK1), and Fas-associated death domain (FADD), but not RIPK3.

140 We found that Fas-associated death domain (FADD), first described as an apoptotic pro

141 wn of caspase-8, Fas-associated protein with death domain (FADD), or Bid.

142 knockdown of the Fas-associated protein with death domain (FADD), the adaptor that mediates downstrea

143 odifies the host proteins Fas-associated via death domain (FADD), TNFRSF1A-associated via death domai

144 he TNFR1 complex II component Fas-associated death domain (FADD), which allowed a shift from TNF-indu

145 ent genomic amplifications of Fas-associated death domain (FADD), with or without Baculovirus inhibit

146 Fas-associated death domain (FADD)-deficient Jurkat cells were resistan

147 was significantly lessened in Fas-associated death domain (FADD)-deficient or caspase-8-deficient cou

148 ic pathways that regulate Fas-associated via death domain (FADD)-dependent signalling and other less

149 ion of cellular caspase 8 and Fas-associated death domain (FADD)-like apoptosis regulator-like inhibi

150 l-2), Bcl-x, A1, and cellular Fas-associated death domain (FADD)-like interleukin-1beta-converting en

151 itor of apoptosis (XIAP), and 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 pression of dominant-negative Fas-associated death domain failed to protect cells from the flavopirid

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 g a dominant-negative form of Fas-associated death domain in which the mice were resistant to apoptot

165 embrane, which in turn recruit IRAKs via the death domains in these proteins to form the Myddosome co

166 established that Act1-like proteins contain DEATH-domains in basal animals, such as Hydra and primit

167 on to depicting a previously unknown mode of death domain interactions, these results further uncover

168 The death domain kinase receptor interacting protein 1 (RIP1

169 Here we report that the death domain kinase, RIP (receptor-interacting protein),

170 f a dominant-negative form of Fas-associated death domain led to a reduction in the ability of apigen

171 f cellular FADD (Fas-associated protein with death domain)-like interleukin-1beta-converting enzyme i

172 FLIP, inhibition of caspase 8/Fas-associated death domain-like IL-1-converting enzyme and activation

173 HHV-8-encoded viral Fas-associated death domain-like IL-1-converting enzyme inhibitory prot

174 in lower levels of Bcl-xL or Fas-associated death domain-like IL-1beta-converting enzyme inhibitor p

175 cell lines, including Bcl-xL, Fas-associated death domain-like IL-1beta-converting enzyme inhibitor p

176 olic protein c-FLIP (cellular Fas-associated death domain-like interleukin 1beta-converting enzyme in

177 -2, Bcl-xL, survivin, and antiFas-associated death domain-like interleukin-1 beta-converting enzyme-i

178 s due to the high levels of c-Fas-associated death domain-like interleukin-1-converting enzyme inhibi

179 ng protein (RIP) and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-in

180 tes (PEA-15/PED) and cellular Fas-associated death domain-like interleukin-1beta-converting enzyme-in

181 The latent KSHV protein Fas-associated death domain-like interleukin-1beta-converting enzyme-in

182 We also modelled a newly identified putative death domain, located N-terminal to the caspase-like dom

183 ligomeric nature of the purified recombinant death domain miniprotein.

184 The N1347S mutation prevented the death domain module binding stably to ERK in vitro and i

185 Accordingly, the N1347S death domain module is defective in vivo in the formatio

186 ession of a dominant-negative Fas-associated death domain mutant or silencing of DR5 expression using

187 ther the death domain adaptor Fas-associated death domain nor the apoptosis-initiating protease caspa

188 ovel mutation (N1347S) was identified in the death domain of DAPK-1.

189 pport mouse development, indicating that the death domain of FADD has an additional function required

190 dentified through its ability to bind to the death domain of Fas (CD95).

191 Our data show that CaM binds to the death domain of Fas (FasDD) with an apparent dissociatio

192 mapped to the B-box domain of PML moiety and death domain of Fas.

193 We now provide evidence that the death domain of MALT1 and the CARD of Bcl10 also contrib

194 itation, FRET data strongly suggest that the death domain of MALT1 contributes significantly to the a

195 We have solved the crystal structure for the death domain of Mus musculus IRAK-4 to 1.7 A resolution.

196 nction for the COOH-terminal leucine repeats/death domain of Par-4 in mediating apoptosis.

197 ng a fetal brain two-hybrid library with the death domain of the p75 neurotrophin receptor (NTR), we

198 both by pharmacologic inhibition of the cell death domain of the p75 neurotrophin receptor (TAT-Pep5)

199 on constants for the interaction between the death domains of dMyD88 and Tube and of Pelle and a pref

200 otypic protein interactions comprised of the death domains of Fas and FADD is at the centre of DISC f

201 we found no interaction between the isolated death domains of Pelle and dMyD88.

202 ), which contains one of the most potent BH3 death domains of the BCL-2 protein family, to restore BH

203 The MyD88 death domain, on the other hand, was required for NF-kB

204 that Jurkat variants lacking Fas-associated death domain or procaspase-8 undergo tipifarnib-induced

205 It also regulates the associated death domain pathway and caspase 8-mediated events.

206 rotein complex of p53-induced protein with a death domain (PIDD), receptor-interacting protein-associ

207 enes, including p53-inducible protein with a death domain (Pidd).

208 Fas-associated death domain protein (FADD) and caspase-8 (casp8) are vi

209 or combined deficiency of Fas-associated via death domain protein (FADD) and RIPK3 prevented epitheli

210 Knockdown of Fas-associated death domain protein (FADD) by either siRNA or overexpre

211 Fas-associated death domain protein (FADD) constitutes an essential com

212 al defects as T cells lacking Fas-associated death domain protein (FADD) function.

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 TRADD-Fas-associated death domain protein apoptotic pathway.

231 ently induced cytosolic TRADD-Fas-associated death domain protein complex.

232 f dominant-negative mutant of Fas-associated death domain protein or a caspase-8 inhibitor completely

233 Knock down of CD95 or Fas-associated death domain protein suppressed drug combination toxicit

234 formed by Fas receptor, FADD (Fas-associated death domain protein) and caspase 8 is a pivotal trigger

235 ent of large amounts of FADD (FAS-associated death domain protein) and procaspase 8, leading to direc

236 or its adaptor protein FADD (Fas-associated death domain protein) develop a hyperautophagic morpholo

237 ent in the proapoptotic Bid (BH3-interacting death domain protein) gene (Bid KO) resist apoptosis and

238 SseK2 glycosylated the FADD (Fas-associated death domain protein).

239 modest reduction in levels of Fas-associated death domain protein, and procaspase 8 recruited to the

240 death domain protein (TRADD), Fas-associated death domain protein, and receptor-interacting protein k

241 nti-apoptotic isoform (MAP-kinase activating death domain protein, MADD), which effectively redirects

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 ciated factor 1, and cellular Fas-associated death domain protein-like interleukin-1beta-converting e

251 ociated factor-1 (TRAF1), and Fas-associated death domain protein-like interleukin-1beta-converting e

252 RIP1 participates in the Fas-associated death domain protein-mediated recruitment of caspase-8 t

253 y inhibited in caspase-8- and Fas-associated death domain protein-negative Jurkat cells, though apopt

254 However, signaling through death-domain proteins does not explain how TNFR1 induces

255 domain through which it interacts with other death-domain proteins to promote cellular responses.

256 uroblastomas using responses to distinct BH3 death domains providing a BH3 response profile and direc

257 ciated ICH-1/CED-3 homologous protein with a death domain (RAIDD), and procaspase-2.

258 L1A is a TNF-like cytokine that binds to the death-domain receptor (DR)3 and provides costimulatory s

259 cholesterol biosynthesis, and apoptosis via death domain receptors, were overrepresented biological

260 ceptor DR4 thereby preventing Fas-associated death domain recruitment.

261 involved in regulating necroptosis, and the death domain regulates RIP1 recruitment to the intracell

262 r-346 is required for full activity, and the death domain regulates the activation of IRAK4.

263 associated Ich-1/CED homologous protein with death domain) remained susceptible to heat-induced apopt

264 fic interaction module for the alpha-helical death domain signal transduction.

265 This is significant, because death domain signaling is driven by electrostatic contac

266 af-1-like proteins that are each linked to a death domain, suggesting that echinoderms have evolved u

267 cruitment domains (CARDs) are members of the death domain superfamily and contain six antiparallel he

268 that has been observed in DED/DED and other death domain superfamily interactions.

269 Death domain superfamily members typically act as adapto

270 Seven death domain superfamily members were tested for crystal

271 nonical six-helix (H1-H6) bundle fold in the death domain superfamily.

272 contain N-terminal domains belonging to the death domain superfamily.

273 In this paper, we report that the death domain SXXE/D motifs (i.e., S381DHE motif of TNFR1

274 rg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment of F

275 the prostate by virtue of its intracellular death domain that can initiate apoptosis and inhibit gro

276 pro-death function via its alpha-helical BH3 death domain that has the dual capacity to inhibit antia

277 erized by a cytoplasmic region known as the "death domain" that enables the receptors to initiate cyt

278 The type 1 TNFR (TNFR1) contains a death domain through which it interacts with other death

279 tocyte-intrinsic Fas-associated protein with death domain, TNF-related apoptosis-inducing ligand rece

280 r activity induced by TNFR1, TNFR-associated death domain, TNFR-associated factor 2, and IkappaBalpha

281 ical effect of decoy receptors that lack the death domain to trigger apoptosis.

282 l prion-like fibers through their respective death domains to propagate downstream signaling.

283 alpha Greek key protein FADD (Fas-associated death domain) to investigate this question.

284 FR associated factor (TRAF), TNFR associated death domain (TRADD) and Fas-associated death domain (FA

285 TNF receptor-associated death domain (TRADD) is an essential mediator of TNF rec

286 The TNFR-associated death domain (TRADD) protein has been suggested to be a

287 of tumor necrosis factor receptor-associated death domain (TRADD) was reduced in androgen deprivation

288 (TNF-alpha), TNF receptor (TNFR)-associated death domain (TRADD), and caspases.

289 death domain (FADD), TNFRSF1A-associated via death domain (TRADD), and receptor-interacting serine/th

290 was inhibited by DN-TNF receptor-associated death domain (TRADD), DN-TNF receptor-associated factor

291 d binding of RIP1 to TNFRSF1A-associated via death domain (TRADD), two crucial signal adaptors for NF

292 show that TNF receptor 1 (TNFR1)-associated death domain (TRADD)-dependent TNFR1 signaling in epider

293 ty induced by TNFR1, TNF receptor-associated death domain, TRAF2, TAK1, NF-kappaB-inducing kinase, an

294 ace Fas receptor (FAS), FASL, FAS-associated death domain, tumor necrosis factor-related apoptosis-in

295 sic pathway involving Fas and Fas-associated death domain up-regulation, caspase-8 activation, and BI

296 In reporter assays, a death domain variant, S34Y, was found to be inactive.

297 1 protein harboring a N1347S mutation in the death domain was also defective in binding to ERK in cel

298 RIP's death domain was critical for RIP and Fas association to

299 n Fas-associated death domain (FADD) via the death domain, which recruits downstream signaling protei

300 redicted to be exposed on the surface of the death domain, which we termed the WR motif.

301 either to itself or to FADD (Fas-associated death domain), with the large version of E6 able to inhi