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 tivates the JNK/AP1 pathway and does so in a TRAF-dependent fashion.

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

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

25 aptors linking TAK1 to the upstream adaptors TRAFs.

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

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

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

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

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

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

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

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

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

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

36 Fbxo3 and TRAF protein in circulation positively correlated with c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 e selectively incapable of binding different TRAF proteins revealed that TRAF pathways downstream of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 sis factor (TNF) receptor-associated factor (TRAF) adapter proteins, which play important roles in si

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

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

81 40 and LMP1 both use TNFR-associated factor (TRAF) adaptor proteins, but in distinct ways.

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

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

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

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

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

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

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

89 tor (TNF) receptor (TNFR)-associated factor (TRAF) family.

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

91 of tumor necrosis factor-associated factor (TRAF) molecules in CD40-mediated NF-kappaB activation wi

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

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

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

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

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

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

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

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

100 1 and X-IAP, TNF receptor-associated factor (TRAF)-2, and factors OX40 and 4-1BB.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 tumor necrosis receptor-associated factors (TRAFs).

141 necrosis factor receptor-associated factors (TRAFs).

142 tumor necrosis receptor-associated factors (TRAFs).

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

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

145 necrosis factor receptor-associated factors (TRAFs).

146 necrosis factor receptor-associated factors (TRAFs).

147 necrosis factor receptor-associated factors (TRAFs).

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

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

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

151 se cells requires the presence of functional TRAF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 inal arm and intermolecular contacts mediate TRAF recognition.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 2 is needed for CD40-mediated degradation of TRAFs 2 and 3.

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

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 ptor-associated factor 6 (TRAF6) is the only TRAF family member that participates in signal transduct

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

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

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

203 ns are not sufficient for oligomerization or TRAF binding.

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

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

206 ween receptor recognition by TRAF6 and other TRAFs.

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

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

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

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

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

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

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

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

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

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

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

218 hosphorylation of Id proteins and recruiting TRAF-6.

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

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

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

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

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

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

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

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

227 Platelets express several TRAFs.

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

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

230 Here we identify TANK (TRAF family member-associated NF-kappa B activator) as a

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

232 basis for therapeutic intervention targeting TRAF protein abundance.

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

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

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

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

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

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

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

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

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

242 inding different TRAF proteins revealed that TRAF pathways downstream of RANK that affect osteoclast

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 this study we demonstrate the ability of the TRAF-binding domain of LMP1 to signal on the JNK/AP-1 ax

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

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

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

275 1 bears a motif (PQQAT) that conforms to the TRAF recognition motif PVQET in CD40.

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

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

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

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

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

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

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

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

284 These TRAF proteins promoted ubiquitination reactions that rec

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

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

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

288 pathogen Pyrenophora tritici-repentis and to TRAF proteins.

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

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

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

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

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

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

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

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