ライフサイエンスコーパス: TRAF1

1 TRAF1 (TNFR-associated factor 1), TRAF2, and the inhibit

2 TRAF1 and TRAF2 form an oligomeric complex that associat

3 TRAF1 and TRAF2 preferentially form the TRAF1: (TRAF2)(2

4 TRAF1 cleavage was markedly reduced in cells that contai

5 TRAF1 expression negatively correlates with programmed d

6 TRAF1 has been linked to heightened risk to inflammatory

7 TRAF1 is a member of the TRAF family, which plays import

8 TRAF1 is a member of the TRAF protein family, which regu

9 TRAF1 protein levels were also elevated in circulating B

10 TRAF1 reduces linear ubiquitination and subsequent oligo

11 TRAF1 was also highly inducible by CD40 ligand in cultur

12 TRAF1(-/-) dendritic cells show attenuated responses to

13 TRAF1(-/-) mice are viable and have normal lymphocyte de

14 TRAF1(-/-) T cells exhibit stronger than wild-type (WT)

15 TRAF1, a prosurvival signaling adaptor required for 4-1B

16 TRAF1, TRAF2, and TRAF3 appear to associate independentl

17 TRAF1, TRAF2, and TRAF3 bind to a single site in the LMP

18 TRAF1, TRAF2, and TRAF3 interacted with the same region.

19 TRAF1, TRAF2, TRAF3, and TRAF6, but not TRAF4 or TRAF5,

20 TRAF1/2 and cIAP1/2 are members of the TNF receptor-asso

21 TRAF1/C5 rs3761847 GG homozygote status was associated w

22 TRAF1/C5 rs3761847 was identified using real-time polyme

23 ecrosis factor receptor associated factor 1 (TRAF1) and defender-against cell death (DAD-1) is regula

24 factor receptor (TNFR) associated factor 1 (TRAF1) and TRAF3.

25 ecrosis factor receptor-associated factor 1 (TRAF1) has been implicated in the regulation of antiapop

26 s factor (TNF) receptor-associated factor 1 (TRAF1) is a member of the recently defined TRAF family.

27 TNF receptor-associated factor 1 (TRAF1) is a unique TRAF protein because it lacks a RING

28 signaling adaptor TNFR-associated factor 1 (TRAF1) is specifically lost from virus-specific CD8 T ce

29 TNFR-associated factor 1 (TRAF1) is unique among the TRAF family, lacking most zin

30 proteins, TNF receptor-associated factor 1 (TRAF1), is highly regulated in pulmonary cells.

31 Bfl-1/A1, TNF receptor-associated factor-1 (TRAF1), and Fas-associated death domain protein-like int

32 mbers, and TNF receptor-associated factor-1 (TRAF1).

33 crosis factor receptor-associated protein 1 (TRAF1), interleukin-1alpha (IL-1alpha), MCP-2, N-cadheri

34 e data point to an important role for 4-1BB, TRAF1, and mTOR in the persistence of CD8 effector T cel

35 factor receptor-associated factors 1 and 2 (TRAF1 and TRAF2).

36 r interacts with FADD, caspase-8, caspase-3, TRAF1, and TRAF2 through distinct domains.

37 genes such as those encoding interleukin-8, TRAF1, and c-IAP2.

38 expands T cells and reduces viral load in a TRAF1-dependent manner.

39 iapoptosis (IAP1, Bcl-2, Bcl-X(L), Bfl-1/A1, TRAF1 and cFLIP), and invasion (MMP-9) were also downreg

40 , IAP1, IAP2, XIAP, Bcl-2, Bcl-xL, Bfl-1/A1, TRAF1 and FLIP, were all downregulated by zerumbone.

41 survivin, IAP 1, IAP 2, Bcl-x(L), Bfl-1/A1, TRAF1, and FLIP in wild-type mouse embryonic fibroblasts

42 survivin, IAP1, IAP2, XIAP, Bcl-2, Bfl-1/A1, TRAF1, and FLIP were all down-regulated by SCH 66336, wh

43 IAP2, Bcl-xL, Bcl-2, cFLIP, XIAP, Bfl-1/A1, TRAF1, and Survivin), proliferation (cyclin D1, COX2, an

44 Although aberrant TRAF1 expression in tumors has been reported, the role o

45 Activated TRAF1(-/-) T cells, but not TRAF1(+/+) T cells, responde

46 nds the TRAF1 promoter in vivo and activates TRAF1 transcription.

47 n, and is dependent on the signaling adaptor TRAF1.

48 rmal tissues and provide evidence of altered TRAF1 expression in lymphoid malignancies.

49 Although TRAF1 can displace TRAF2 and CD40 from raft fractions, i

50 n blot analysis confirmed that IL-1alpha and TRAF1 mRNA levels resulted in increased protein expressi

51 apoptosis (IAP1, Bfl-1/A1, Bcl-2, cFLIP, and TRAF1), proliferation (cyclin D1 and c-Myc), and angioge

52 ic upregulation of IL-1alpha (21.5-fold) and TRAF1 (27.5-fold) gene expression in tissues of Johne's

53 n of the antiapoptotic genes A1, c-IAP2, and TRAF1; inhibition of caspase 3; and protection from apop

54 optosis (IAP1 and IAP2, Bcl-2, Bcl-x(L), and TRAF1), proliferation (cyclin D1 and c-Myc), invasion (C

55 ates the antiapoptotic activity of p80HT and TRAF1 deficiency reestablishes B cell homeostasis in p80

56 was to delineate the signaling pathways and TRAF1 promoter elements responsible for phorbol ester-me

57 Increased expression of STAT1 and TRAF1 in MLBCL was confirmed by immunohistochemistry.

58 he evidence for association of the STAT4 and TRAF1/C5 loci with RA using imputed data from the Wellco

59 Bcl-2, Bcl-xL, IAP1,(2) MCl-1, survivin, and TRAF1), apoptosis (Bax, Bid), inflammation (COX-2), prol

60 cIAP-1/2, Bcl-2, Bcl-xL, XIAP, Survivin, and TRAF1), proliferation (cyclin D1, c-Myc, COX-2), invasio

61 TNFR1 and TRAF1 were polyubiquitinated in lipid rafts after TBI.

62 Although c-IAP1 bound TRAF2 and TRAF1 in vitro, it ubiquitinated only TRAF2.

63 While 4-1BB bound TRAF2 and TRAF1, Ox40 interacted with TRAF3 and TRAF2.

64 ntiapoptosis (IAP1, IAP2, Bcl-2, Bcl-xL, and TRAF1), proliferation (cyclin D1 and c-Myc), and invasio

65 31)-mediated NF-kappaB activation as well as TRAF1 coactivation, and 30% of TRAF2 is associated with

66 Because TRAF1 is a transcriptional target gene of NF-kappaB, I3C

67 Because TRAF1 is upregulated by many stimuli, it may modulate th

68 We also show that while both TRAF1 and cIAP1 have non-redundant roles in suppressing

69 n by LMP1(1-231) is likely to be mediated by TRAF1/TRAF2 heteroaggregates since TRAF1 is unique among

70 o to the upregulation of genes such as CD40, TRAF1, and IRF5, which encode proteins that promote B ce

71 thritis susceptibility genes including CD40, TRAF1, TNFAIP3 and PRKCQ.

72 siRNA we show that in activated CD8 T cells TRAF1 is also involved in this process and that constitu

73 hway downstream of 4-1BB in primary T cells, TRAF1 also restricts the constitutive activation of NIK

74 c-Myc), cell survival (Bcl-2, Bcl-xL, cFLIP, TRAF1, IAP1, IAP2, and survivin), invasion (matrix metal

75 r newly defined CD40-responsive genes cIAP2, TRAF1, TRAF4/CART and DR3 were unaffected.

76 In contrast, there was a high and consistent TRAF1 overexpression in EBV-induced lymphoproliferations

77 In contrast, TRAF1 alone interacts very weakly with cIAP2.

78 In contrast, TRAF1 is maintained at higher levels in virus-specific T

79 tified proapoptotic fragments Cys-RIPK1, Cys-TRAF1, Asp-BRCA1, Leu-LIMK1, Tyr-NEDD9, Arg-BID, Asp-BCL

80 ffect of reduced pulmonary TRAF1 expression, TRAF1-null (-/-) and control, BALB/c (wild-type), mice w

81 in associating with TNFR-associated factors TRAF1 and TRAF2, and the second site is similar to TNFRI

82 is factor receptor (TNFR)-associated factors TRAF1, TRAF2, TRAF3, and TRAF5 and the TNFR-associated d

83 n NF-kappaB-regulated antiapoptotic factors, TRAF1, TRAF2, c-IAP1, and c-IAP2, is most pronounced in

84 f endogenous NF-kappaB target genes (c-FLIP, TRAF1), and resistance to apoptosis.

85 TRAF proteins (except for TRAF1) contain an N-terminal RING finger domain that is

86 in vivo and suggest a molecular pathway for TRAF1 activation in the pathogenesis of lymphomas.

87 the strongest predictors of death in RA (for TRAF1/C5 GG versus AA, hazard ratio 3.85 [95% confidence

88 s used by LMP1 and identify a novel role for TRAF1 as a modulator of oncogenic signals.

89 naling and identify a physiological role for TRAF1 as a regulator of the subcellular localization of

90 The core binding site for TRAF1, TRAF2, and TRAF3 in CD40 could be minimally subst

91 TRADD is specific for TRAF1 and TRAF2, which ensures the recruitment of clAPs

92 uction but also NIK stabilization by forming TRAF1.NIK complex.

93 Furthermore, skin from TRAF1(-/-) mice was hypersensitive to TNF-induced necros

94 lucidate the function of TRAF1, we generated TRAF1-deficient mice.

95 imeric CD40 was found to be TRAF2 > TRAF3 >> TRAF1 and TRAF6.

96 ge B-cell lymphoma showed a moderate to high TRAF1 signal.

97 However, TRAF1 is absent in many established epithelial cell line

98 However, TRAF1/2-binding mutants of c-IAP2.MALT1 still oligomeriz

99 resent study, we demonstrated that the human TRAF1 mRNA has an unusually long 5'-UTR that contains in

100 1 can also self-associate and binds to human TRAF1, TRAF2, and TRAF4.

101 s of TNF-induced TRAF1 expression identified TRAF1.NIK as a central complex linking canonical and non

102 ome-wide association studies have identified TRAF1/C5 as a rheumatoid arthritis (RA) susceptibility l

103 In summary, this study identifies TRAF1 as a key regulator of IL-1beta production and a po

104 These data identify TRAF1 as a specific target of caspases activated during

105 These findings identify TRAF1 as a potential biomarker of HIV-specific CD8 T cel

106 Variants in IL2RA, TRAF1/C5, and RSBN1 were not associated with JIA.

107 Mice deficient in TRAF1 (TRAF1(-/-)) and wild-type (WT) control animals we

108 Thus, expression of this LMP1 domain in TRAF1-positive lymphoma cells promotes significant JNK a

109 TNF-alpha levels were strikingly elevated in TRAF1-/- mice.

110 omoter activity indicating a role for ERK in TRAF1 induction.

111 The risk of death in RA is increased in TRAF1/C5 rs3761847 GG homozygotes and appears to be inde

112 liferation and excess cytokine production in TRAF1-deficient CD8 T cells compared with WT CD8 T cells

113 ms (e.g., PKCalpha and betaI) play a role in TRAF1 regulation.

114 e 13-acetate (PMA) and bryostatin I, induced TRAF1 mRNA expression; pretreatment with actinomycin D b

115 tational-experimental studies of TNF-induced TRAF1 expression identified TRAF1.NIK as a central compl

116 two genes relevant to chronic inflammation: TRAF1 (encoding tumor necrosis factor receptor-associate

117 t and dependent on the presence of an intact TRAF1/2/3 binding site.

118 e- dependent manner that critically involves TRAF1 and TRAF2.

119 re Toll-like receptor 1 (TLR1), TLR2, IRAK3, TRAF1, IRG1, PTGS2, MMP9, IFI44, IFIT1, and CD40.

120 the endoplasmic reticulum stress-induced JNK/TRAF1 axis as well as the APAF-1/caspase-9 axis, activat

121 2, X chromosome-linked IAP, Bcl-2, Bcl-x(L), TRAF1, FLIP, and survivin), proliferative (cyclin D1, cy

122 T cells lacking TRAF1 hyperproliferate in response to T cell receptor si

123 otein 1 (LMP1) in mouse B cell lines lacking TRAF1, TRAF2, or both TRAFs.

124 1) were for CREB1, FGG, MAP3K5, RIPK3, LSP1, TRAF1, DUSP2, and ITGB3.

125 ments responsible for phorbol ester-mediated TRAF1 induction in human colon cancers.

126 ment with actinomycin D blocked PMA-mediated TRAF1 expression suggesting induction at the transcripti

127 rm-selective inhibitors blocked PMA-mediated TRAF1 mRNA and promoter stimulation; rottlerin, a select

128 In contrast to WT mice, TRAF1(-/-) recipients failed to display goblet cell hype

129 inus of the molecule (TRAF2DN), which mimics TRAF1, developed lymphadenopathy and splenomegaly due to

130 ptides with progressive deletions, a minimal TRAF1, TRAF2, and TRAF3 binding region was mapped to the

131 2/p100 processing, we mathematically modeled TRAF1.NIK as a coupling signaling complex and validated

132 Moreover, TRAF1 knockdown abrogates the antiapoptotic activity of

133 Cs, including CD71, FSCN1, IRF4, NMES1, MX1, TRAF1.

134 Although purified myeloid TRAF1(-/-) dendritic cells (DCs) exhibited normal Ag-pre

135 TNFR-associated factor (TRAF) family, namely TRAF1, TRAF2, TRAF3, and TRAF5, but not to TRAF6.

136 Along with other associations near TRAF1 and TNFAIP3, this implies a central role for the C

137 ly all non-Hodgkin's lymphoma show low or no TRAF1 expression.

138 Activated TRAF1(-/-) T cells, but not TRAF1(+/+) T cells, responded to TNF by proliferation an

139 Moreover, transfer of TRAF1(+) but not TRAF1(-) memory T cells at the chronic stage of infectio

140 Transient overexpression of TRAF2, but not TRAF1, induced NF-kappaB activation and HIV-1-long termi

141 The ability of TRAF1, TRAF2, and CRAF1 to associate with CD30 was confi

142 In the absence of TRAF1, an increased amount of TRAF2 was recruited to lip

143 ruitment and DC activation in the airways of TRAF1(-/-) mice, suggesting that the expression of TRAF1

144 n vivo, CD11c(+)CD11b(+) DCs from airways of TRAF1(-/-) recipients were not activated, and purified d

145 erved, as well as heterotypic association of TRAF1-TRAF2 and TRAF3-TRAF5.

146 The association of TRAF1/C5 rs3761847 alleles with the risk of death was as

147 ntrast to TRAF2 and TRAF3, direct binding of TRAF1, TRAF4, TRAF5, or TRAF6 to CD40 was not detected.

148 UV irradiation did not result in cleavage of TRAF1, and overexpression of the C-terminal TRAF1 fragme

149 carcinogenesis study showed that deletion of TRAF1 in mice results in a significant inhibition of ski

150 ive mutants consisting of the TRAF domain of TRAF1 and TRAF2 inhibited CD30 induction of NF-kappaB ac

151 with the conserved C-terminal TRAF domain of TRAF1 and TRAF2.

152 l analyses demonstrated that TRAF domains of TRAF1, TRAF2, TRAF3, and TRAF6 formed homo-trimers in so

153 -/-) mice, suggesting that the expression of TRAF1 in resident lung cells is required for the develop

154 For example, expression of TRAF1 was highly restricted, with B cell lymphomas consi

155 l-length TRAF3 or dominant negative forms of TRAF1 or TRAF2.

156 , we also observed an increased frequency of TRAF1(+) HIV-specific CD8 T cells 10 wk after completion

157 To elucidate the function of TRAF1, we generated TRAF1-deficient mice.

158 or a clear understanding of the functions of TRAF1.

159 Here we investigated the importance of TRAF1 and TRAF2 for c-IAP2.MALT1-stimulated NF-kappaB ac

160 LMP1 signal on the JNK axis independently of TRAF1 status.

161 r results demonstrate selective induction of TRAF1 in human colon cancer cells through a Ca(2+)-depen

162 To further examine the interactions of TRAF1 and NIK with NF-kappaB2/p100 processing, we mathem

163 h 1 expression and HIV load and knockdown of TRAF1 in CD8 T cells from viral controllers results in d

164 In addition, enhanced levels of TRAF1 could result in cells within the lesions of Johne'

165 ignaling and suggest that cellular levels of TRAF1 may play an important role in modulating the degra

166 cells from p80HT mice express high levels of TRAF1, an antiapoptotic protein also implicated in lymph

167 rked increases in the steady-state levels of TRAF1, TRAF2, TRAF5, and TRAF6.

168 The in vivo locations of TRAF1, TRAF2, TRAF5, and TRAF6 were determined in human

169 GFbeta induces the posttranslational loss of TRAF1, whereas IL-7 restores TRAF1 levels.

170 IL-5, IL-13, or TNF occurred in the lungs of TRAF1(-/-) mice.

171 hat in EBV-transformed B lymphocytes most of TRAF1 or TRAF3 and 5% of TRAF2 are associated with LMP1

172 ain of LMP1 depends on the reconstitution of TRAF1 expression.

173 region appears to inhibit the recruitment of TRAF1 and TRAF2 to membrane rafts by the CTAR1 region.

174 ing to OX40 likely results in recruitment of TRAF1 for downstream signalling.

175 tion of TRAF2 or combined down-regulation of TRAF1 and TRAF2 did not affect c-IAP2.MALT1-stimulated s

176 In this study, we investigated the role of TRAF1 in an adoptive transfer model of allergic lung inf

177 The critical role of TRAF1 in the regulation of TRAF2-dependent JNK signaling

178 ion in tumors has been reported, the role of TRAF1 remains elusive.

179 cIAP1/2, which explains regulatory roles of TRAF1 in TNF signaling.

180 Moreover, transfer of TRAF1(+) but not TRAF1(-) memory T cells at the chronic

181 tribute to the IRES-dependent translation of TRAF1 during vincristine treatment.

182 ulation of the IRES-dependent translation of TRAF1 may be involved in effecting the cancer cell respo

183 h Ras inhibitors had minimal to no effect on TRAF1 induction suggesting dependence on Raf, but not Ra

184 pathway activation is dependent not only on TRAF1 induction but also NIK stabilization by forming TR

185 Moreover, transfer of WT or TRAF1(-/-) DCs failed to restore T cell recruitment and

186 an chronic lymphocytic leukemias overexpress TRAF1 and Bcl-2, our findings suggest that cooperation b

187 epletion of TRAF2 and the associated protein TRAF1 by proteolysis.

188 r kinase RIP (receptor-interacting protein), TRAF1, and cIAP-1 (cellular inhibitor of apoptosis prote

189 actor (TRAF) family of six adaptor proteins (TRAF1-6) links the TNFR superfamily to the nuclear facto

190 RT-1, RIP), TRAF domain containing proteins (TRAF1-6) as well as new members and adaptor proteins suc

191 previously identified TRAF family proteins (TRAF1, TRAF2, TRAF3, TRAF4, TRAF5, and TRAF6), whereas t

192 associated factor (TRAF) family of proteins, TRAF1 and TRAF2, independently bind to the intracellular

193 were genotyped for 5 variants in the PTPN22, TRAF1/C5, STAT4, and TNFAIP3 loci.

194 To determine the effect of reduced pulmonary TRAF1 expression, TRAF1-null (-/-) and control, BALB/c (

195 -kappaB pathway downstream of 4-1BB requires TRAF1, whereas cIAP1 plays a redundant role with cIAP2.

196 on in genes associated with immune response (TRAF1, RIPK3, BAT2, and TLR6), mitogen-activated protein

197 revious results showed that IL-7 can restore TRAF1 expression in virus-specific CD8 T cells in mice,

198 ational loss of TRAF1, whereas IL-7 restores TRAF1 levels.

199 alysis of 232 non-Hodgkin lymphomas revealed TRAF1 overexpression in 112 (48%) cases.

200 diated by TRAF1/TRAF2 heteroaggregates since TRAF1 is unique among the TRAFs in coactivating NF-kappa

201 ssociated factor (TRAF) family, specifically TRAF1, TRAF5, and TRAF6, but not with TRAF2, TRAF3, or T

202 PD98059 and UO126, suppressed PMA-stimulated TRAF1 promoter activity indicating a role for ERK in TRA

203 Raf-C4) significantly reduced PMA-stimulated TRAF1 promoter activity whereas transfection of dominant

204 in which TRAF1 is active in vivo, we studied TRAF1 transcripts in normal lymphoid tissue, in Epstein-

205 his finding is replicated in future studies, TRAF1/C5 genotyping could identify patients at increased

206 Surprisingly, TRAF1 and one chain of TRAF2 in the TRAF1: (TRAF2)(2): c

207 Surprisingly, TRAF1, -2, or -3 does not interact with the terminal LMP

208 Targeting TRAF1 function might lead to strategies for preventing a

209 TRAF1, and overexpression of the C-terminal TRAF1 fragment did not enhance cell death in these cases

210 observed when overexpressing the C-terminal TRAF1 fragment in HEK293T and HT1080 cells.

211 These data confirm that TRAF1 is an inducible molecule and indicates its deregul

212 Collectively these results demonstrate that TRAF1 plays a critical role in regulating T cell activat

213 Taken together, our findings indicate that TRAF1 and TRAF2 cooperate in CD40 but not LMP1 signaling

214 These results indicate that TRAF1 and/or TRAF2 play an important role in cell death

215 These results indicate that TRAF1 translation is initiated via the IRES and regulate

216 In vivo studies indicated that TRAF1 expression levels in mouse skin are induced by sho

217 It is known that TRAF1 transcription is inducible by various cytokines, b

218 Here, we report that TRAF1 is required for solar UV-induced skin carcinogenes

219 However, the biological roles that TRAF1 plays in immune cell signaling have been elusive,

220 Here we show that TRAF1 (but not TRAF2-6) is cleaved by certain caspases i

221 Here we show that TRAF1 and TRAF2 interact with A20, a zinc finger protein

222 We show that TRAF1 depletion prevents TNF-induced NIK stabilization a

223 Moreover, we show that TRAF1 is required for solar UV-induced extracellular sig

224 In this article, we show that TRAF1 negatively regulates inflammasome activation to li

225 Mechanistic studies showed that TRAF1 expression enhances the ubiquitination of ERK5 on

226 Immunohistochemical analysis showed that TRAF1 expression is up-regulated in human actinic kerato

227 These findings suggest that TRAF1 is a negative regulator of TNF signaling.

228 Overall, our results suggest that TRAF1 mediates ERK5 activity by regulating the upstream

229 These studies suggest that TRAF1 provides negative feedback for TNF-alpha synthesis

230 apping TRAF binding regions and suggest that TRAF1, TRAF2, and TRAF3 could bind competitively to one

231 We confirm association of the STAT4 and the TRAF1/C5 loci with RA bringing to 5 the number of confir

232 B1, PTPN22, STAT4, a region in 6q23, and the TRAF1/C5 locus.

233 ystal structures of the TRAF2: cIAP2 and the TRAF1: TRAF2: cIAP2 complexes.

234 A common genetic variant at the TRAF1-C5 locus on chromosome 9 is associated with an inc

235 p80HT binds the TRAF1 promoter in vivo and activates TRAF1 transcription

236 TRAF1 and TRAF2 preferentially form the TRAF1: (TRAF2)(2) heterotrimer, which interacts with cIA

237 Given the TRAF1 expression and known link to nuclear factor-kappa

238 (particularly the most proximal site) in the TRAF1 promoter significantly decreased PMA-mediated prom

239 6736 in the C12orf30 locus, rs3761847 in the TRAF1/C5 locus, rs2104286 in the IL2RA locus, rs7574865

240 isingly, TRAF1 and one chain of TRAF2 in the TRAF1: (TRAF2)(2): cIAP2 ternary complex mediate interac

241 tor-associated factors (TRAF), including the TRAF1/TRAF2 positive regulators and TRAF3 negative regul

242 Consistent with the desensitization of the TRAF1-binding co-stimulatory receptor 4-1BB, 4-1BBL-defi

243 Given the association of the TRAF1/C5 locus in two previous large case-control series

244 study was to examine the association of the TRAF1/C5 locus with death in patients with RA.

245 ing peptide-based mutational analyses of the TRAF1/TRAF2/TRAF3 and TRAF6 binding sequences in CD40 to

246 Interestingly, we found that the TRAF1 expression is induced in cancer cells by chemother

247 e for association of variants mapping to the TRAF1/C5 gene was detected in the 1860 RA cases and 2930

248 ruited to the LMP1 signaling complex via the TRAF1/2/3/5 binding site within the cytoplasmic domain o

249 In normal lymphoid tissue, TRAF1 message proved to be absent from all resting B and

250 L), ice, TNF-alpha, TNF-beta, TNFR1, TNFR2, TRAF1, TRAF2, TRAF3, cIAP2, and tradd at the level of mR

251 of TNF depends on the activity of the TNFR2/TRAF1 pathway that is regulated by MAVS signaling.

252 interaction and established that binding to TRAF1 and TRAF2 is not required for c-IAP2.MALT1-stimula

253 any reports assigning contradictory roles to TRAF1.

254 Mice deficient in TRAF1 (TRAF1(-/-)) and wild-type (WT) control animals were adop

255 inding domain that recruits A20 to the TRAF2-TRAF1 complex and a C-terminal domain that mediates inhi

256 e TNF receptor associated factors 2/1 (TRAF2/TRAF1) heterocomplex, which mediates the recruitment of

257 nally, we demonstrate that T cell-transfused TRAF1(-/-) recipient mice demonstrated impaired up-regul

258 lung injury, intratracheal TNF-alpha-treated TRAF1-/- mice exhibited marked liver injury with an appr

259 alveolar lavage from intratracheally treated TRAF1-/- mice produced more TNF-alpha than cells from tr

260 cell line transduces signals that upregulate TRAF1 levels but does not alter JAK3 levels or activatio

261 which contained the sequence PEQET, whereas TRAF1 and TRAF2 were capable of binding to either the PE

262 To identify the cells in which TRAF1 is active in vivo, we studied TRAF1 transcripts in

263 e resolve this paradox by showing that while TRAF1 is required for maximal activation of the classica

264 ivation, and 30% of TRAF2 is associated with TRAF1 in EBV-transformed B cells.

265 MP1 and that most of LMP1 is associated with TRAF1 or TRAF3.

266 AITR associates with TRAF1 (TNF receptor-associated factor 1), TRAF2, and TRA

267 c-IAP2.MALT1 fusion protein associates with TRAF1 and TRAF2 using the same binding site.

268 etail a region of LMP-1 that associates with TRAF1, TRAF2, and TRAF3.

269 milar in their constitutive association with TRAF1, TRAF2, TRAF3, TRADD, and RIP.

270 Coexpression of CD30 with TRAF1 or TRAF2 but not TRAF3 augmented NF-kappaB activat

271 proach those of TRAF2 upon coexpression with TRAF1 and/or TRAF2, indicating that TRAF2A stability is

272 the EGFR either alone or in combination with TRAF1 and TRAF3.

273 with LMP-1 most avidly and can compete with TRAF1 and TRAF2 for binding to LMP-1.

274 crucial for their physical interaction with TRAF1 and TRAF2.

275 of EGFR expression requires interaction with TRAF1, -2, and -3.

276 AF3 were stronger than the interactions with TRAF1 and TRAF6.

277 etween the cytoplasmic tail of TRANCE-R with TRAF1, TRAF2, TRAF3, TRAF5, and TRAF6.

278 whereas the TD of SPOP interacts weakly with TRAF1 and TRAF6 only.

279 entified as the caspase cleavage site within TRAF1, generating two distinct fragments.