ライフサイエンスコーパス: TRAF

1 TRAF degradation occurs in response to signaling by othe

2 TRAF proteins (except for TRAF1) contain an N-terminal R

3 TRAF proteins are intracellular signal transducers for a

4 TRAF-1 and Bcl-x(L) proteins were localized diffusely in

5 TRAF-1, c-FLIP, and to a lesser extent c-IAP2 protein le

6 TRAFs are intracellular co-inducers of downstream signal

7 ion is mediated by TNFR-associated factor-1 (TRAF-1) and TRAF-2 degradation and subsequent activation

8 stimulation induces TNF-associated factor-1 (TRAF-1) that directly binds NF-kappaB-inducing kinase (N

9 sed high levels of TNFR-associated factor-1 (TRAF-1), TRAF-2, and TRAF-3, markers associated with res

10 ), c-IAP2, TNF receptor-associated factor-1 (TRAF-1), TRAF-2, B-cell leukemia/lymphoma-2 (Bcl-2), Bcl

11 eotide or Escherichia coli DNA prevented: 1) TRAF-1/2 downregulation; 2) activation of caspase-8, Bid

12 levels of TNFR-associated factor-1 (TRAF-1), TRAF-2, and TRAF-3, markers associated with resistance t

13 , TNF receptor-associated factor-1 (TRAF-1), TRAF-2, B-cell leukemia/lymphoma-2 (Bcl-2), Bcl-x, A1, a

14 nt IkappaB blocked TNF-alpha-induced TRAF-1, TRAF-2, c-IAP1, c-IAP2, c-FLIP, and A1 gene expression a

15 TNF-alpha upregulated expression of TRAF-1, TRAF-2, c-IAP1, c-IAP2, c-FLIP, and A1.

16 (11) nucleotide-binding NACHT domains; (12) TRAFs; (13) Hsp70-binding BAG domains; (14) endonuclease

17 h domain), TNF receptor-associated factor-2 (TRAF-2), the Ser/Thr kinase RIP (receptor-interacting pr

18 ecrosis factor receptor-associated factor 6 (TRAF 6) binding site.

19 RAIL-R)2, TNFR-related death receptor (DR)6, TRAF interacting protein (I-TRAF), IL-6, MDA7, IL-1B con

20 ction between the TRAF domain of TRAF3 and a TRAF-interaction motif (TIM) within Cardif.

21 These results show a novel link between a TRAF-like gene and reproductive development in plants.

22 proliferation and induce apoptosis through a TRAF-6-dependent but NF-kappaB-independent mechanism.

23 uced effective degradation, if attached to a TRAF domain that binds to the PXQXT motif of CD40.

24 aptors linking TAK1 to the upstream adaptors TRAFs.

25 ding sites, the P227A polymorphism can alter TRAF binding and dramatically changes the role played by

26 ed the TLR-2 downstream mediators IRAK-1 and TRAF-6, as well as the inflammatory factors cyclooxygena

27 ted by TNFR-associated factor-1 (TRAF-1) and TRAF-2 degradation and subsequent activation of caspase-

28 s suggest that cooperation between Bcl-2 and TRAF pathways contributes to the development of this typ

29 MyD88, whereas associations with IRAK-2 and TRAF-6 were not affected.

30 lular inhibitor of apoptosis-1), cIAP-2, and TRAF-2 (TNF receptor-associated factor-2)) in an NF-kapp

31 FR-associated factor-1 (TRAF-1), TRAF-2, and TRAF-3, markers associated with resistance to apoptosis.

32 ults revealed that TRAF binding affinity and TRAF binding site sequence dictate a distinct subset of

33 demonstrated that C-terminal coiled-coil and TRAF-C domains of TRAF6, unable to mediate NFkappaB acti

34 -TRAF, protease-epidermal growth factor, and TRAF-TRAF interactions.

35 Fbxo3 and TRAF protein in circulation positively correlated with c

36 ner, whereas c-IAP1, survivin, Bcl-x(L), and TRAF-2 protein levels were not influenced by TNF-alpha t

37 rs, mediated by Math-BTB/POZ (for Meprin and TRAF [tumor necrosis factor receptor associated factor]

38 subset of BTB proteins containing Meprin and TRAF homology (MATH) substrate recognition sites was evi

39 s linear motifs through its MATH (meprin and TRAF homology) domain and forms higher-order oligomers t

40 ction of competitive displacement of NIK and TRAF degradation halted NIK turnover, and promoted its a

41 tics to predict interactions between NLR and TRAF proteins, including interactions of TRAF with NLRC3

42 as significant implications for receptor and TRAF-targeted therapies.

43 trigger the degradation of MAVS, TRAF3, and TRAF 6.

44 ch as IAP-1, IAP-2, XIAP, Bcl-2, Bcl-xL, and TRAF-1.

45 In this study, interactions between LMP1 and TRAFs and the activation of PI3K/Akt, JNK, p38, and NF-k

46 n this study for the first time that another TRAF family member, TRAF5, is a negative regulator of TL

47 known for its role in signal transduction as TRAF and TNF receptor-associated protein (TTRAP) and ETS

48 Both TRAF and SF-PTK signal transductions induced by STP-A we

49 MP1 in vivo effects can be mediated via both TRAF binding-dependent and -independent pathways.

50 ovel USP7 substrate that interacts with both TRAF and UBL1-2.

51 e B cell lines lacking TRAF1, TRAF2, or both TRAFs.

52 aB revealed that some events are dictated by TRAF binding site sequences, others are partially regula

53 nal tail of CD40 in the absence of canonical TRAF-binding sites is capable of signaling through an al

54 activation of JNK and p38, and its carboxyl TRAF homology domain physically interacts with TGF-beta

55 ired by the disruption of previously defined TRAF binding sites.

56 stand the mechanisms underlying differential TRAF degradation, mixed protein domain TRAF chimeras wer

57 A seed-sterile mutant with a disrupted TRAF-like gene (At5g26290) exhibiting aberrant gametogen

58 uman CD40, or with CD40 containing disrupted TRAF binding sites.

59 ng TRAF2, TRAF5, and TRAF6, through distinct TRAF-binding motifs.

60 ntial TRAF degradation, mixed protein domain TRAF chimeras were analyzed in murine B cells.

61 IP, and A1 gene expression and downregulated TRAF-1 protein levels.

62 greater loss of function than that of either TRAF alone.

63 In contrast, LMP1 did not require either TRAFs 1 or 2 to induce activation.

64 oma (BCL) 3, TNF receptor-associated factor (TRAF) 1, and TNFAIP3-interacting protein (TNIP) 3.

65 sis factor (TNF) receptor-associated factor (TRAF) 2 and interferes with phosphorylation of transform

66 gradation of TNF receptor-associated factor (TRAF) 2 and TRAF6, which are adaptor molecules that coup

67 g vesicles recruited TNFR-associated factor (TRAF) 2 and were decorated with K63 polyubiquitins.

68 ression with TNF receptor-associated factor (TRAF) 2, and this is achieved by inhibition of the E3 ub

69 sis factor (TNF) receptor-associated factor (TRAF) 2, TRAF6, and NEMO (NF-kappaB essential modulator,

70 ptor protein TNF receptor associated factor (TRAF) 3 is required for effective TCR signaling and norm

71 tion of the upstream TNFR-associated factor (TRAF) 3/TANK-binding kinase (TBK) 1 complex was compromi

72 duced stimulation of TNFR-associated factor (TRAF) 5-deficient T cells resulted in decreased activati

73 ntrinsic deletion of TNFR-associated factor (TRAF) 6 (TRAF6DeltaT) in mice results in diminished peri

74 phosphorylation and TNFR-associated factor (TRAF) 6 ubiquitination in BMMCs pretreated with morphine

75 K) 4, IRAK1, TNF receptor-associated factor (TRAF) 6, TGF-beta-activated kinase (TAK) 1, and IkappaB

76 the BCR, employs the TNFR-associated factor (TRAF) adapter proteins in signaling.

77 necrosis factor receptor-associated factor (TRAF) adaptor proteins for signaling.

78 necrosis factor receptor-associated factor (TRAF) adaptor proteins to induce signaling.

79 40 and LMP1 both use TNFR-associated factor (TRAF) adaptor proteins, but in distinct ways.

80 mbers of the TNF receptor-associated factor (TRAF) and the inhibitor of apoptosis (IAP) families, res

81 tor (TNF) receptor (TNFR)-associated factor (TRAF) family in T cell immunity are not well understood.

82 cal tumor necrosis factor-associated factor (TRAF) family member, TRAF4, as a key negative regulator

83 address the role of TNFR-associated factor (TRAF) family members in facilitating this signaling path

84 The TNF receptor-associated factor (TRAF) family of molecules acts as adapter proteins for s

85 is factor receptor (TNFR)-associated factor (TRAF) family of six adaptor proteins (TRAF1-6) links the

86 veral members of the TNFR-associated factor (TRAF) family, which link CD40 to intracellular signaling

87 Tumor-necrosis-associated factor (TRAF) homologs trf-1 and trf-2 and the p38 mitogen-activ

88 TNFR family recruits TNFR-associated factor (TRAF) molecules leading to IKKalpha/beta/gamma activatio

89 ls are transduced by TNFR-associated factor (TRAF) molecules.

90 necrosis factor receptor-associated factor (TRAF) protein family members are critically involved in

91 The TNFR-associated factor (TRAF) proteins have a vital role in innate immunity by c

92 necrosis factor receptor-associated factor (TRAF) proteins may result in profound tissue injury by l

93 sis factor (TNF)-receptor-associated factor (TRAF) proteins, but the molecular mechanism of its actio

94 ng molecules such as TNFR associated factor (TRAF), TNFR associated death domain (TRADD) and Fas-asso

95 necrosis factor receptor-associated factor (TRAF)-2 and TRAF3 in the CD40-signaling pathway together

96 1 and X-IAP, TNF receptor-associated factor (TRAF)-2, and factors OX40 and 4-1BB.

97 ceptor (TNFR)-1 with TNFR-associated factor (TRAF)-2.

98 necrosis factor receptor-associated factor (TRAF)-6 and is important for signaling.

99 constrained TNF receptor-associated factor (TRAF)-dependent innate immune responses invoked by IL-1b

100 itination of TNF receptor-associated factor (TRAF)-family adapter proteins involved in TLR and TNFR p

101 itination of TNF receptor-associated factor (TRAF)-family adapter proteins involved in Toll-like rece

102 log of human TNF receptor associated factor (TRAF)-interacting protein (TRIP), which has been implica

103 necrosis factor receptor-associated factor (TRAF)-mediated signaling and associated polyubiquitinati

104 TNFR-associated factor (TRAF)1 is an intracellular adaptor molecule important fo

105 cytoplasmic pool of TNFR-associated factor (TRAF)2 and cellular inhibitors of apoptosis (cIAPs) anta

106 normal CD40-mediated TNFR-associated factor (TRAF)2 and TRAF3 degradation.

107 The TNFR-associated factor (TRAF)2 and TRAF6 adaptor proteins are positive regulator

108 ciate with tumor necrosis-associated factor (TRAF)2 and TRAF6.

109 necrosis factor receptor-associated factor (TRAF)2 is a key adaptor molecule that is known to mediat

110 r Bcl-2 or a TNF receptor-associated factor (TRAF)2 mutant lacking the N-terminal RING and zinc finge

111 (TRADD), DN-TNF receptor-associated factor (TRAF)2, DN-receptor-interacting protein (RIP), DN-transf

112 mic adaptor proteins TNFR-associated factor (TRAF)3 and TRAF6 are important mediators of TLR signalin

113 cently reported that TNFR-associated factor (TRAF)3, a ubiquitously expressed adaptor protein, promot

114 TNFR-associated factor (TRAF)3, an adaptor protein that binds the cytoplasmic do

115 examined the role of TNFR-associated factor (TRAF)4 in IL-17 signaling and Th17-mediated autoimmune e

116 a complex containing TNFR-associated factor (TRAF)6.

117 necrosis factor receptor-associated factors (TRAF) in living cells.

118 ing through TNF receptor-associated factors (TRAF), including the TRAF1/TRAF2 positive regulators and

119 mprised of subunits TNFR-associated factors (TRAF)3, TRAF2, and cellular inhibitor of apoptosis (cIAP

120 necrosis factor receptor-associated factors (TRAFs) 1, 2, 3, 5, and 6 to the CD40 cytoplasmic tail up

121 uces the binding of TNFR-associated factors (TRAFs) 1, 2, 3, and 6, followed by the rapid degradation

122 and -2, that engage TNFR-associated factors (TRAFs) and the TNFR-associated death domain protein, res

123 factor-receptor (TNF-R)-associated factors (TRAFs) and TNF-R1-associated death domain protein (TRADD

124 is factor (TNF) receptor-associated factors (TRAFs) are critical signaling adaptors downstream of man

125 is factor (TNF) receptor-associated factors (TRAFs) are cytoplasmic adapter proteins that link a wide

126 necrosis factor receptor-associated factors (TRAFs) are key facilitators of intracellular signaling w

127 TNFR-associated factors (TRAFs) are pivotal adapter proteins involved in signal t

128 TNF receptor-associated factors (TRAFs) are recruited to many TNF-R superfamily members a

129 necrosis factor receptor-associated factors (TRAFs) belong to a family of adapter proteins that are i

130 mber of the TNF receptor-associated factors (TRAFs) family of proteins, is essential for activation o

131 s factor receptor (TNFR)-associated factors (TRAFs) form a family of proteins that are best known as

132 necrosis factor receptor-associated factors (TRAFs) have identified positive roles for TRAF2, TRAF5,

133 eins called TNF receptor associated factors (TRAFs) plays key roles in mediating CD40L-CD40 signaling

134 necrosis factor receptor-associated factors (TRAFs), during signaling.

135 ermediates, TNF receptor-associated factors (TRAFs), in diet-induced obesity (DIO).

136 is factor (TNF) receptor-associated factors (TRAFs), which also mediate NF-kappaB activation from LTb

137 tumor necrosis receptor-associated factors (TRAFs).

138 necrosis factor receptor-associated factors (TRAFs).

139 tumor necrosis receptor-associated factors (TRAFs).

140 ds to intracellular TNFR-associated factors (TRAFs).

141 tor proteins called TNFR-associated factors (TRAFs).

142 necrosis factor receptor-associated factors (TRAFs).

143 necrosis factor receptor-associated factors (TRAFs).

144 Mutation of the Fn14-TRAF domain site or depletion of TNF receptor-associated

145 The overlapping binding site for TRAFs 1, 2, and 3 on many TNFR superfamily molecules, to

146 d a novel NIK interacting protein, TNAP (for TRAFs and NIK-associated protein).

147 se cells requires the presence of functional TRAF.

148 used somatic cell gene targeting to generate TRAF-deficient mouse B cell lines.

149 However, TRAFs 1 and 6 are not degraded in response to CD40 engag

150 However, TRAFs can also contribute to signaling in the absence of

151 receptor (DR)6, TRAF interacting protein (I-TRAF), IL-6, MDA7, IL-1B convertase (ICE)-gamma, delta a

152 AF6 but also by TRAF7, a recently identified TRAF family member.

153 AF3, implicating TRAF2 as a key E3 ligase in TRAF turnover.

154 Studies in TRAF-deficient B cell lines revealed that hCD40-P227A us

155 ith the early lethality of mice deficient in TRAFs 2 and 3, has complicated the quest for a clear und

156 The contribution of the different domains in TRAFs to their respective functions remains unclear.

157 Characterizing roles of individual TRAFs has been hampered by limitations of available expe

158 while retaining CD40 binding, did not induce TRAF degradation, nor could they inhibit CD154-stimulate

159 LMP1 doesn't induce TRAF degradation, and employs TRAF3 as a positive mediat

160 of mutant IkappaB blocked TNF-alpha-induced TRAF-1, TRAF-2, c-IAP1, c-IAP2, c-FLIP, and A1 gene expr

161 n this study, we found that receptor-induced TRAF degradation limits TRAF2-dependent CD40 signals to

162 r proteins, and USP25 regulates inflammatory TRAF signaling.

163 hibiting MAP kinase signaling and inhibiting TRAF-2 interaction with TNFR-1.

164 nding is independent of the MAVS-interactive TRAF-C domain (residues 415 to 568).

165 ty-one SNPs in nine genes (CD14, TLR4, IRF3, TRAF-6, TIRAP, TRIF, IKK-1, ST-2, SOCS1) were found to m

166 SP7 directly interacts with Axin through its TRAF domain, and promotes deubiquitination and stabiliza

167 rray of protein-protein interactions via its TRAF domain and a RING finger domain that possesses non-

168 ctor 3 (IRF3) phosphorylation by IFN kinases TRAF family member-associated NFkb activator (TANK) bind

169 nteraction between V and the IRF3/7 kinases, TRAF family member-associated NFkappaB activator (TANK)-

170 Although located outside of any known TRAF binding sites, the P227A polymorphism can alter TRA

171 re located on the USP7 N-terminal TRAF-like (TRAF) domain and the first and second UBL domains (UBL1-

172 We show in this study that the LMP1 TRAF binding site was required for LMP1-mediated autoant

173 Moreover, the LMP1 TRAF-binding site preferentially caused RelB nuclear acc

174 Furthermore, the LMP1 TRAF-binding site was required for p100 processing and p

175 tivation is principally mediated by the LMP1 TRAF-binding site.

176 inal arm and intermolecular contacts mediate TRAF recognition.

177 mental models and the poor viability of most TRAF-deficient mice.

178 rs838133 in FGF21 (19q13.33), rs197273 near TRAF family member-associated NF-kappa-B activator (TANK

179 " pathway of p100 processing mediated by NIK/TRAF.

180 Furthermore, prevalent NLR-TRAF interactions suggest the formation of a 'TRAFasome'

181 Our studies identified a novel TRAF family member that is involved in MEKK3 signaling a

182 ytokine secretion and impaired activation of TRAF-dependent signal transduction pathways (NF-kappaB,

183 Examination of TRAF binding, degradation, cytokine production, IgM secr

184 TNF-alpha upregulated expression of TRAF-1, TRAF-2, c-IAP1, c-IAP2, c-FLIP, and A1.

185 n this study, we examined the interaction of TRAF proteins with the type I IFN receptor.

186 and TRAF proteins, including interactions of TRAF with NLRC3.

187 n in muscle cells through the recruitment of TRAF-2, Fas-associated protein with death domain, and TN

188 signaling pathways, BCR signal regulation of TRAF function was examined.

189 that TRAF2 serves as the master regulator of TRAF degradation in response to CD40 signaling, and this

190 In plants, the role of TRAF-like proteins with meprin and the TRAF homology (MA

191 n, it is not clear whether simple binding of TRAFs explains why they are such strong activators of NF

192 2 is needed for CD40-mediated degradation of TRAFs 2 and 3.

193 and 6, followed by the rapid degradation of TRAFs 2 and 3.

194 gnaling and associated polyubiquitination of TRAFs 3 and 6, specifically, were regulated negatively b

195 It has been shown that the recruitment of TRAFs to the CD40 cytoplasmic tail is essential for CD40

196 main that are mostly conserved with those of TRAFs.

197 an activate NF-kappaB via an oligomerization/TRAF binding-independent mechanism.

198 However, BAFF-R binds only one TRAF adaptor, TRAF3, and this interaction negatively reg

199 cal within its family because it is the only TRAF family member to negatively regulate innate immune

200 level by overexpression of MyD88, IRAK-2, or TRAF-6.

201 ted protein with death domain but not NIK or TRAF-6 proteins.

202 ns are not sufficient for oligomerization or TRAF binding.

203 ge in TRAF4 that is not present in the other TRAF proteins, and phosphorylation of this site provides

204 Unlike other TRAF family members, which mediate signal transduction b

205 In contrast, expression of other TRAFs (TRAF2, 3 and 4) was minimally altered by PMA.

206 Unlike other TRAFs, TRAF6 is also involved in Toll-like/interleukin (

207 these genes suggests that they (particularly TRAF-2 and cIAP-2) contribute to the protection against

208 including prosequence-prosequence, protease-TRAF, protease-epidermal growth factor, and TRAF-TRAF in

209 ified that muXg elevated the adaptor protein TRAF-6 and fusion genes OC-STAMP and DC-STAMP expression

210 he translocation of the scaffolding protein, TRAF-2, to the endoplasmic reticulum.

211 on of Act1 on Ser311, adjacent to a putative TRAF-binding motif.

212 K13 contains a putative TRAF-interacting motif, which is reportedly required for

213 ANK(369-373) is the only one of six putative TRAF binding motifs sufficient to generate actin rings a

214 ng and report that mutations in the putative TRAF-interacting motif of K13 have no deleterious effect

215 Mutation of this putative TRAF-binding motif within BAFFR abolishes its interactio

216 hosphorylation of Id proteins and recruiting TRAF-6.

217 l-molecule Fbxo3 inhibitors that by reducing TRAF protein levels, potently inhibited cytokine release

218 QET motif in CD40 and PIQCT in the regulator TRAF-associated NF-kappaB activator (TANK), recognition

219 nt receptor functions may not always require TRAF-receptor binding.

220 LMP1 functions require TRAFs 3, 5, and 6, which interact with LMP1.

221 0), and atopy (CD14-rs2915863 and rs2569192, TRAF-6-rs5030411, and IKK-1-rs2230804).

222 we found that TRAF4 and TRAF6 used the same TRAF binding sites on Act1, allowing the competition of

223 flammatory cells by destabilizing a sentinel TRAF inhibitor, Fbxl2.

224 e we show that MAVS polymers recruit several TRAF proteins, including TRAF2, TRAF5, and TRAF6, throug

225 show that 14-3-3zeta interacts with several TRAF proteins; in particular, its interaction with TRAF5

226 Platelets express several TRAFs.

227 LMP1 uses specific TRAFs differently than CD40, resulting in amplified and

228 chondrial depolarization through stabilizing TRAF-1/2 expression and sequential inhibition of caspase

229 f interferon genes (STING), leading to TANK (TRAF family member-associated NF-kappaB activator)-bindi

230 basis for therapeutic intervention targeting TRAF protein abundance.

231 The C-terminal TRAF domain facilitates oligomerization and sequence-spe

232 Both the C-terminal TRAF domain of human TRAF6, which directly interacts wit

233 e N-terminal domains, but not the C-terminal TRAF domain, of the highly homologous TRAF5 can function

234 YOD1 binds to the C-terminal TRAF homology domain of TRAF6 that also serves as the in

235 These are located on the USP7 N-terminal TRAF-like (TRAF) domain and the first and second UBL dom

236 ted that p53 and Mdm2 bind to the N-terminal TRAF-like domain of HAUSP in a mutually exclusive manner

237 TRAF domain of TRAF4 bound to the N-terminal TRAF-like region of the deubiquitinase HAUSP (herpesviru

238 equences were swapped were examined, testing TRAF binding and degradation, and induction of B cell ac

239 evious findings, these results indicate that TRAF-dependent receptor functions may not always require

240 Results revealed that TRAF binding affinity and TRAF binding site sequence dic

241 These data suggest that TRAF-mediated signaling pathways, such as those of LMP1,

242 However, emerging evidence suggests that TRAF proteins, particularly TRAF2 and TRAF3, also regula

243 Results indicate that TRAFs 1 and 2 cooperate in CD40-mediated activation of t

244 The TRAF-C domain of TRAF3 was necessary and sufficient to l

245 ociated factor 1 (TRAF1) is unique among the TRAF family, lacking most zinc-binding features, and sho

246 in the region between zinc finger 5 and the TRAF domains.

247 le of TRAF-like proteins with meprin and the TRAF homology (MATH) domain is far from clear.

248 ed the TRAF-C domain of TRAF3 as well as the TRAF-N domain and zinc fingers 4 and 5 of TRAF2.

249 urs through a direct interaction between the TRAF domain of TRAF3 and a TRAF-interaction motif (TIM)

250 direct and specific interaction between the TRAF domain of TRAF3 and the TIM of Cardif is required f

251 MEKK4 binds the TRAF domain of TRAF4 and MEKK4/TRAF4 activation of JNK i

252 and this function is dependent upon both the TRAF Zn domains and receptor binding position.

253 ng pathway that is uniquely activated by the TRAF-binding domain of LMP1 and is required for transfor

254 ate ERK-MAPK mapped to its CTAR1 domain, the TRAF binding domain previously implicated in PI 3-kinase

255 rosine phosphatase mu) domain and one in the TRAF (tumor necrosis factor receptor-associated factor)

256 by mutating two critical amino acids in the TRAF domain also abolishes TRAF3-dependent IFN productio

257 NF-kappaB activation pathways, including the TRAF (TNF receptor-associated factor) proteins, IKK, NF-

258 terotypic interaction minimally involved the TRAF-C domain of TRAF3 as well as the TRAF-N domain and

259 TRAF4 is a member the TRAF family of adaptor proteins that mediate cellular si

260 ted, and still others are independent of the TRAF binding site sequence.

261 is distinction is due to an inability of the TRAF domain of TRAF5 to bind the TIM of Cardif.

262 ain activity and the specific binding of the TRAF domain to NIK are two critical components of TRAF3

263 ion of JNK is inhibited by expression of the TRAF domain.

264 ation in response to CD40, regardless of the TRAF domains to which they were attached.

265 TRAF1 is a member of the TRAF family, which plays important roles in signal trans

266 nding of BAFF-R solely to this member of the TRAF family.

267 ry cells by mediating the degradation of the TRAF inhibitory protein, Fbxl2.

268 TRAF1 is a member of the TRAF protein family, which regulates the canonical and n

269 is essential for Thr9 phosphorylation of the TRAF-interacting protein TIFA, triggering activation of

270 Here, we demonstrate that the TRAF (tumor necrosis factor receptor-associated factor)

271 determine the mechanism, we showed that the TRAF domain of TRAF4 bound to the N-terminal TRAF-like r

272 1 bears a motif (PQQAT) that conforms to the TRAF recognition motif PVQET in CD40.

273 ion of cell cycle markers were mapped to the TRAF-binding domain within CTAR1 and to the residues bet

274 nce motif, PVPAT, which is homologous to the TRAF-binding site (PVQET) present in CD40, a TNFR known

275 ally interchangeable with that of TRAF5, the TRAF domain of TRAF3 was not.

276 ects of other viral proteins, "usurping" the TRAF/NIK/I-kappaB kinase pathway, and reinforce the noti

277 CD40 and LMP1 mutants in which the TRAF binding site sequences were swapped were examined,

278 y functions by directly interacting with the TRAF-C domain of TNF receptor-associated factor 6 (TRAF6

279 that GnTs bind TRAF3 via residues within the TRAF-N domain (residues 392 to 415) and that binding is

280 We have re-examined the role of the TRAFs in K13 signaling and report that mutations in the

281 These TRAF proteins promoted ubiquitination reactions that rec

282 ubiquitinase, associated activation of these TRAFs by vIRF-2, and activities of vIRF-2 and vIRF-2-USP

283 Here, we present evidence that TIFA (TRAF-interacting protein with a forkhead-associated doma

284 s and selective protein interactions in TNFR-TRAF interactions.

285 ivated by TNF or by overexpression of TNFR1, TRAF 2, NIK, and p65 subunit of NF-kappaB.

286 pathogen Pyrenophora tritici-repentis and to TRAF proteins.

287 these motifs that disrupted MAVS binding to TRAFs abrogated its ability to activate IRF3.

288 TNFR1 recruited the adaptor proteins TRADD, TRAF-2, and RIP into lipid rafts and activated RhoA, NF-

289 Although the TRAF2 TRAF domain binds ASK1, GCK, and the highly related kina

290 ication of the PVPAT sequence to the typical TRAF-binding sequence, PVQET, is sufficient to render th

291 as an allosteric regulator of the ubiquitin:TRAF E3 ligase.

292 have previously shown that LMP1 and CD40 use TRAFs 1, 2, 3, and 5 differently.

293 he disparate ways in which CD40 and LMP1 use TRAFs 2 and 3, and their distinct signaling characterist

294 7 interaction, the latter competing for USP7-TRAF association.

295 we observed that 14-3-3zeta interaction with TRAF proteins is required for the IL-17A-induced IL-6 le

296 Third, StpC physically interacts with TRAF in epithelial cells, and the effect of StpC on NF-k

297 LMP1 co-immunoprecipitated with TRAFs 1, 2, and 3.

298 kappaB-inducible protein that interacts with TRAFs and functions in a negative feedback mechanism dow

299 (including NF-kappaB, Bcl-2, Bcl-x(L), XIAP, TRAF-2, or FLIP).

300 a cells with plasmids expressing CFP- or YFP-TRAF fusion proteins, constitutive homotypic association