ライフサイエンスコーパス: TRAF2

1 ATM, CCND1, UBR5, TP53, BIRC3, NOTCH1/2 and TRAF2.

2 nt but delayed virus entry in the absence of TRAF2.

3 e endosomal route of entry in the absence of TRAF2.

4 s recruited to the Fn14 cytoplasmic tail via TRAF2.

5 xpression for survival are also dependent on TRAF2.

6 ace that supports binding to both TNF-R1 and TRAF2.

7 nism of interaction among TRUSS, TNF-R1, and TRAF2.

8 F1 and TRAF2 preferentially form the TRAF1: (TRAF2)(2) heterotrimer, which interacts with cIAP2 more

9 TRAF1 and one chain of TRAF2 in the TRAF1: (TRAF2)(2): cIAP2 ternary complex mediate interaction wit

10 factor receptor-associated factors 2 and 3 (TRAF2/3).

11 Mice with deficient CD40-TRAF2/3/5 signaling in MHCII(+) cells exhibited a simila

12 Our study reveals that the CD40-TRAF2/3/5 signaling pathway in MHCII(+) cells protects a

13 mechanism of MAVS signaling and reveal that TRAF2, 5, and 6, which are normally associated with NF-k

14 tivation was also abolished in cells lacking TRAF2, 5, and 6.

15 dition, stable expression of TRAF2-DeltaR in TRAF2/5 DKO cells efficiently inhibited the TNFalpha-ind

16 reover, stable expression of TRAF2-DeltaR in TRAF2/5 DKO cells failed to suppress constitutive p100 p

17 poptotic proteins in TRAF2-DeltaR-expressing TRAF2/5 DKO cells was normal, the cells remained sensiti

18 al level in TRAF2 and TRAF5 double knockout (TRAF2/5 DKO) cells almost completely restores normal TNF

19 s with the TNF receptor-associated factor 2 (TRAF2), a protein required for TNF-alpha-mediated NF-kap

20 ecrosis factor receptor-associated factor 2 (TRAF2), a scaffold protein and E3 ubiquitin ligase impor

21 In this regard we show that TRAF2, a RING finger protein implicated in ubiquitylatio

22 MC159 also interacts with TRAF2, a signaling molecule involved in NF-kappaB activa

23 TNF treatment transcriptionally upregulates TRAF2 abundance in the mitochondrial subfraction.

24 TRAF2 abundance increases in the mitochondrial subfracti

25 promoted the formation of complexes of TRAF5-TRAF2, Act1 and SF2 (ASF).

26 In contrast, NO-mediated TRAF2 activation in the more aggressive MDA-MB-231 cells

27 COX2 induction by NO involved TRAF2 activation that occurred in a TNFalpha-dependent m

28 Modulation of TRAF2 activity by ubiquitination is well studied; howeve

29 TNFR1 signaling where TTP, in alliance with TRAF2, acts as a balancer of JNK-mediated cell survival

30 We also found that TRAF2 affects RSK2 activity through RSK2 ubiquitination.

31 hich interacts with cIAP2 more strongly than TRAF2 alone.

32 TRAF2 also colocalizes and interacts with PARKIN, a prev

33 We further show that TRAF2 also regulates inflammatory cytokine production in

34 Cancer cells that are dependent on TRAF2 also require NF-kappaB for survival.

35 tein, and small interfering RNA targeting of TRAF2 also selectively inhibits SAPK activation.

36 l for the survival of cancer cells harboring TRAF2 amplification.

37 TNF-receptor-associated factor 2 (TRAF2), an E3 ubiquitin ligase, coordinates cytoprotecti

38 Moreover, FKBP51 also interacts with TRAF2, an upstream mediator of IKK activation.

39 gions of TRUSS that interact with TNF-R1 and TRAF2 and (ii) the ability of TRUSS to self-associate to

40 ce with cardiac-restricted overexpression of TRAF2 and characterized the phenotype of mice with highe

41 and that in the absence of RIP1 expression, TRAF2 and cIAP1 cooperatively induce delayed IKK activat

42 otably, depletion of the cytoplasmic pool of TRAF2 and cIAP1 in lymphomas by CD40 ligation inhibits b

43 We also demonstrate that TRAF2 and cIAP1 together, but not either one alone, dire

44 ted scaffolding protein, also interacts with TRAF2 and IKK and contributes to TNF-alpha-induced nucle

45 d depletion of TRAF3 promoted recruitment of TRAF2 and IKK1 to activated LTBR, enabling LTBR-inducibl

46 omains are required for its interaction with TRAF2 and IKKgamma, whereas only the TPR domain is invol

47 Traf2 and NcK interacting kinase (TNiK) contains serine-

48 cells and that this effect requires both the TRAF2 and p53 cellular proteins.

49 does not affect K63-linked ubiquitination of TRAF2 and recruitment of TAK1 to TNFR1, suggesting that

50 The deubiquitinating enzyme USP48 stabilizes TRAF2 and reduces E-cadherin-mediated adherens junctions

51 8 increases K48-linked polyubiquitination of TRAF2 and reduces TRAF2 protein levels.

52 interaction is mediated by an LxxLL motif in TRAF2 and results not only in the inhibition of TRAF2 ub

53 Although both TRAF2 and RIP1 interact with the API2 moiety of API2-MAL

54 an unexpected anti-inflammatory function of TRAF2 and suggest a proteasome-dependent mechanism that

55 biting the ubiquitin ligase (E3) activity of TRAF2 and suppressing TNF-alpha-induced JNK activation.

56 onstrated that expression of both endogenous TRAF2 and tg TRAF2DN was negligible in Traf2DN-tg B cell

57 Further analysis of the expression of TRAF2 and TRAF2DN in purified B cells demonstrated that

58 lex that contained decreased amounts of both TRAF2 and TRAF3 and TRAF2-associated signaling proteins.

59 TRAF2 and TRAF3 form a complex with the E3 ubiquitin lig

60 A well-recognized function of TRAF2 and TRAF3 in this aspect is to mediate ubiquitin-d

61 ce suggests that TRAF proteins, particularly TRAF2 and TRAF3, also regulate signal transduction by co

62 appaB pathway is differentially regulated by TRAF2 and TRAF3, and that distinct interactions of LMP1

63 abolished the association of TBK1 with ICOS, TRAF2 and TRAF3, which identified a TBK1-binding consens

64 is-factor receptor (TNFR)-associated factors TRAF2 and TRAF3.

65 of TRAF2-DeltaR at a physiological level in TRAF2 and TRAF5 double knockout (TRAF2/5 DKO) cells almo

66 TRAF2 and TRAF5 were necessary for IL-17 to signal the s

67 tion of the complex of Act1 and the adaptors TRAF2 and TRAF5, activation of mitogen-activated protein

68 matory programs are selectively activated by TRAF2 and TRAF6 association with RET/PTC oncoproteins.

69 e apoptotic pathway required the presence of TRAF2 and TRAF6 in addition.

70 resence of TNF receptor-associated factor 2 (TRAF2) and intracellular isoform of osteopontin (iOPN) w

71 s factor (TNF) receptor-associated factor 2 (TRAF2) and receptor-interacting protein 1 (RIP1) play cr

72 (FADD), caspase-8, TNFR-associated factor 2 (TRAF2), and receptor-interacting protein (RIP).

73 ignaling complexes, decreased recruitment of TRAF2, and attenuated phosphorylation of IkappaB alpha a

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

75 ining its cognate receptor FN14, the adaptor TRAF2, and cellular inhibitor of apoptosis protein 1 (cI

76 inhibited the E3 ligase activities of TRAF6, TRAF2, and cIAP1 by antagonizing interactions with the E

77 Furthermore, p43FLIP associates with Raf1, TRAF2, and RIPK1, which augments ERK and NF-kappaB activ

78 XC2) with apoptotic dysregulation (LCK, TNF, TRAF2, and SFN) and decreased expression of hair follicl

79 ons were also observed recurrently in MEF2B, TRAF2, and TET2.

80 ls during insulitis, and Arl6ip5, Tnfrsf10b, Traf2, and Ubc are key executioners of this program.

81 ys) revealed that CEBPA, ARL6IP5, TNFRSF10B, TRAF2, and UBC are the top five central nodes.

82 aB activation has been believed to depend on TRAF2- and cIAP1-mediated RIP1 ubiquitination.

83 family of MAP4 kinases consisting of MAP4K4, Traf2- and Nck-interacting kinase (TNIK or MAP4K7), and

84 pen-like kinase 1 (MINK1 or MAP4K6) and TNIK Traf2- and Nck-interacting kinase (TNIK or MAP4K7), as u

85 TRAF2- and NCK-interacting kinase (TNIK) represents one

86 lear localization of active beta-catenin and TRAF2- and NCK-interacting kinase (TNIK).

87 Together, these observations identify TRAF2 as a frequently amplified oncogene.

88 main of TRAF2, but not of TRAF3, implicating TRAF2 as a key E3 ligase in TRAF turnover.

89 Recent studies identified TRAF2 as a sphingosine 1-phosphate target, implicating S

90 rification strategy and LC-MS, we identified TRAF2 as the predominant protein that interacts with WT

91 In silico analysis further suggests TRAF2 as trait d'union node between CEBPA and the NFkB p

92 ecreased amounts of both TRAF2 and TRAF3 and TRAF2-associated signaling proteins.

93 The phosphorylation of TRAF2 at serine 11 is essential for the survival of canc

94 S1P specifically binds to TRAF2 at the amino-terminal RING domain and stimulates i

95 AP1 recruitment and maintenance of recruited TRAF2 at the TNF receptor.

96 ecrosis factor receptor-associated factor 2 (TRAF2) at Ser11 in vitro and in vivo.

97 nation-dependent route, and CD137-associated TRAF2 becomes K63 polyubiquitinated.

98 erface for TNF-R1 is closely linked with the TRAF2 binding interface, and (iii) the assembly of homom

99 TRAF2 binds to sphingosine kinase 1 (SphK1), one of the

100 Knockdown of TRAF2 blocked EGF-induced AP-1 activity and anchorage- i

101 Exogenous expression of TRAF2, but not its E3 ligase-deficient mutants, is suffi

102 ia/reperfusion-modeled hearts; and exogenous TRAF2, but not its E3 ligase-deficient mutants, reduces

103 adation of TRAF3 required the RING domain of TRAF2, but not of TRAF3, implicating TRAF2 as a key E3 l

104 Keratinocyte-specific deletion of Traf2, but not Sphk1 deficiency, disrupted TNF mediated

105 Thus, destabilization of TRAF2 by miR-17 reduced the ability of TRAF2 to associat

106 ed morphologic map of gene function revealed TRAF2/c-REL negative regulation of YAP1/WWTR1-responsive

107 dihydro-S1P, markedly increased recombinant TRAF2-catalysed lysine-63-linked, but not lysine-48-link

108 omain ubiquitin ligase, direct evidence that TRAF2 catalyses the ubiquitination of RIP1 is lacking.

109 These results suggest that the hepatic TRAF2 cell autonomously promotes hepatic gluconeogenesis

110 creased the K48-linked polyubiquitination of TRAF2, cIAP1, and cIAP2 in TNF-alpha-stimulated RA SFs.

111 ern blot analysis confirmed the reduction in TRAF2, cIAP1, cIAP2, USP2, and PSMD13 expression by miR-

112 with caspase-8 but not formation of the FN14-TRAF2-cIAP1 complex and inhibited apoptosis activation.

113 to reduced activity of the TNFR1-associated TRAF2-cIAP1/2 ubiquitinase complex and did not affect th

114 of RIP1, and the delayed phase, activated by TRAF2/cIAP1-dependent recruitment of LUBAC.

115 activation: the immediate phase, induced by TRAF2/cIAP1-mediated ubiquitination of RIP1, and the del

116 and non-canonical pathways by disrupting the TRAF2-cIAP2 ubiquitin ligase complex.

117 gradation by disrupting its interaction with TRAF2.cIAP2 ubiquitin ligase complex.

118 ere, we report the crystal structures of the TRAF2: cIAP2 and the TRAF1: TRAF2: cIAP2 complexes.

119 tructures of the TRAF2: cIAP2 and the TRAF1: TRAF2: cIAP2 complexes.

120 TRAF2 colocalizes with ubiquitin, p62 adaptor protein, a

121 Traf3DE8 disrupts the NIK-Traf3-Traf2 complex and allows accumulation of NIK to initiate

122 factor 3 (Traf3) as formation of a NIK-Traf3-Traf2 complex targets NIK for degradation.

123 TCR-related intracellular molecules into the TRAF2 complex, OX40 provides the T cell with a high leve

124 Interestingly, TRAF2 controls the fate of c-Rel and IRF5 via a proteaso

125 ppression of TRAF2 in cancer cells harboring TRAF2 copy number gain inhibits proliferation, NF-kappaB

126 Mechanistically, Traf2 critically regulates receptor-interacting proteins

127 Altogether, our results suggest that TRAF2 deficiency cooperates with BCL-2 in promoting chro

128 TRAF2 deficiency does not enhance upstream signalling ev

129 In contrast, TRAF2 deficiency had no effect on CD40-mediated p38 MAPK

130 TRAF2 deficient mice die around birth, therefore its rol

131 n, and rendered TRAF2DN B cells as bona fide TRAF2-deficient B cells.

132 Interestingly, traf2-deficient macrophages produced reduced levels of i

133 or alpha level was significantly elevated in Traf2-deficient mice, and genetic ablation of TNFR1 larg

134 Similar to B cells with targeted Traf2 deletion, Traf2DN-tg mice show expanded marginal z

135 y rescued the cardiac phenotype triggered by Traf2 deletion, validating a critical role of necroptosi

136 c remodeling and dysfunction associated with Traf2 deletion.

137 Here, we report that stable expression of TRAF2-DeltaR at a physiological level in TRAF2 and TRAF5

138 In addition, stable expression of TRAF2-DeltaR in TRAF2/5 DKO cells efficiently inhibited

139 Moreover, stable expression of TRAF2-DeltaR in TRAF2/5 DKO cells failed to suppress con

140 tivation, and the RING-domain-deleted TRAF2 (TRAF2-DeltaR) has been widely used as a dominant negativ

141 ble expression of anti-apoptotic proteins in TRAF2-DeltaR-expressing TRAF2/5 DKO cells was normal, th

142 erminal protein kinase (JNK) activation in a TRAF2-dependent manner, and that a JNK inhibitor abolish

143 monstrate that TTP interacts with TNFR1 in a TRAF2-dependent manner, thereby initiating the MEKK1/MKK

144 and subsequent proteasomal degradation in a TRAF2-dependent manner.

145 TRAF2 depletion lowers the signal threshold for DR-media

146 TRAF2 directly mediates RING-dependent, K48-linked polyu

147 1P, and that S1P is the missing cofactor for TRAF2 E3 ubiquitin ligase activity, indicating a new par

148 Mechanistically, the TRAF2 E3 ubiquitin ligase promotes K63-linked polyubiqui

149 thin LC3-bound autophagosomes; and exogenous TRAF2 enhances autophagic removal of mitochondria.

150 Loss of TRAF2 expression, either through small interfering RNA t

151 pletion of TNF receptor-associated factor 2 (TRAF2) expression by siRNA oligonucleotides blocked SGEF

152 nuclear p50 were expressed at high levels in TRAF2(-/-) fibroblasts and were not induced by CTAR1.

153 -mediated GAPDH O-GlcNAcylation disrupts the TRAF2-GAPDH interaction to suppress TRAF2 polyubiquitina

154 homozygous mutant mouse ES cell line in the Traf2 gene that is known to play a role in tumour necros

155 show that myeloid cell-specific ablation of TRAF2 greatly promotes TLR-stimulated proinflammatory cy

156 TRAF2 has an important function in mediating the TNF-R s

157 e significantly upregulated genes in the MHC-TRAF2(HC) hearts contained kappaB elements in their prom

158 As the MHC-TRAF2(HC) mice aged, there was a significant decrease in

159 nal kinases activation at 4 weeks in the MHC-TRAF2(HC) mice.

160 MHC-TRAF2(HC) transgenic mice developed a time-dependent inc

161 on levels of TRAF2 (myosin heavy chain [MHC]-TRAF2(HC)).

162 ecrosis factor receptor-associated factor 2 (TRAF2); however, virtually nothing is known about TRAF2

163 Thus, HGK deficiency induces TRAF2/IL-6 upregulation, leading to IL-6/leptin-induced

164 Suppression of TRAF2 in cancer cells harboring TRAF2 copy number gain i

165 ly, stable expression of phospho-null mutant TRAF2 in cancer cells leads to an increase in the basal

166 Consistent with a role for TRAF2 in CD137 signaling, transgenic mice functionally d

167 assay, we demonstrate that Na interacts with TRAF2 in cells.

168 r, these data indicate an essential role for TRAF2 in concert with PARKIN as a mitophagy effector, wh

169 entified DUB to deubiquitinate and stabilize TRAF2 in epithelial cells.

170 hydrazone, suggesting an essential role for TRAF2 in homeostatic and stress-induced mitochondrial au

171 Cardiac-specific deletion of Traf2 in mice triggered necroptotic cardiac cell death,

172 We identified a critical role for Traf2 in myocardial survival and homeostasis by suppress

173 Second, we confirm the critical role of TRAF2 in regulating NIK degradation, whereas TRAF3 enhan

174 zed with the TRADD, FADD, the caspase-8, and TRAF2 in the cytosolic fraction, TNFR1 in the mitochondr

175 Here we reveal a novel function of TRAF2 in the epidermal growth factor (EGF) signaling pat

176 We examined the role of hepatic TRAF2 in the regulation of insulin sensitivity and gluco

177 Surprisingly, TRAF1 and one chain of TRAF2 in the TRAF1: (TRAF2)(2): cIAP2 ternary complex me

178 ecrosis factor receptor-associated factor 2 (TRAF2) in a yeast two-hybrid assay, we demonstrate that

179 ators of autophagy (eg, CDKN2A, PPP2R2C, and TRAF2) in HCC as compared with normal liver.

180 ecrosis factor receptor-associated factor 2 (Traf2) in regulating myocardial necroptosis and remodeli

181 s a mitophagy effector, which contributes to TRAF2-induced cytoprotective signaling.

182 erations to cell morphology, indicating that TRAF2 influences early stages of virus replication.

183 A homologous mutation in TRAF2 inhibited cIAP interaction and blocked NIK degrada

184 Gene knockout studies have revealed that TRAF2 inhibits TNF-alpha-induced cell death but promotes

185 ine with this, signaling by the CD40-related TRAF2-interacting receptor TNFR2 was also attenuated but

186 failed to reveal a correlation between MC159-TRAF2 interactions and MC159's inhibitory function.

187 bust cycling of HSCs lacking functional CYLD-TRAF2 interactions was not elicited by increased NF-kapp

188 e that MC159-IKK interactions, but not MC159-TRAF2 interactions, are responsible for inhibiting NF-ka

189 ecrosis factor receptor-associated factor 2 (TRAF2) interacts with caspase-8 at the DISC, downstream

190 TRAF2 is a component of TNF superfamily signalling compl

191 Our data show that TRAF2 is a novel intracellular target of S1P, and that S

192 Thus, TRAF2 is a proviral factor for VACV that plays a role in

193 We have discovered that TRAF2 is a proviral factor in vaccinia virus replication

194 Although TRAF2 is a RING domain ubiquitin ligase, direct evidence

195 Genetic evidence indicates that TRAF2 is necessary for the polyubiquitination of recepto

196 In addition, TRAF2 is overexpressed in colon cancer and required for

197 Noting that TRAF2 is recruited to mitochondria, and that autophagic

198 Furthermore, we show that TRAF2 is required for Na induction of lytic gene express

199 e first time that targeted overexpression of TRAF2 is sufficient to mediate adverse cardiac remodelin

200 s factor (TNF) receptor-associated factor 2 (TRAF2) is a key component in NF-kappaB signalling trigge

201 factor receptor (TNFR)-associated factor 2 (TRAF2) is a pivotal intracellular mediator of signaling

202 ecrosis factor receptor-associated factor 2 (TRAF2) is a second messenger adaptor protein that plays

203 Inhibition of TRAF2/JNK pathway increases E (epithelial)-cadherin expr

204 ivation and cell death through inhibition of TRAF2 K63-polyubiquitination in a transcription-independ

205 JNK activation and cell death by suppressing TRAF2 K63-polyubiquitination; upon TNF stimulation, the

206 TRAF2 knockdown with adenoviral shRNA transduction induc

207 Hepatocyte-specific TRAF2 knockout (HKO) mice exhibited normal body weight,

208 HGK directly phosphorylates TRAF2, leading to its lysosomal degradation and subseque

209 igase reaction to polyubiquitinate TRAF3 and TRAF2, leading to their proteosomal degradation.

210 TRAF2 localizes to the mitochondria in neonatal rat card

211 These results identify an important Traf2-mediated, NFkappaB-independent, prosurvival pathwa

212 ytoprotective, we tested the hypothesis that TRAF2 mediates mitochondrial autophagy.

213 idification greatly reduced virus entry into TRAF2(-/-) MEFs, suggesting that VACV is reliant on the

214 NK) signaling were apparent in VACV-infected TRAF2(-/-) MEFs, treatment of wild-type cells with a JNK

215 or colon cancer development, suggesting that TRAF2 might be a potential molecular target for cancer p

216 s both BCL-2 and a TNFR-associated factor 2 (TRAF2) mutant lacking the really interesting new gene an

217 ype of mice with higher expression levels of TRAF2 (myosin heavy chain [MHC]-TRAF2(HC)).

218 s)-related kinase (MINK) and closely related TRAF2/Nck-interacting kinase (TNIK) are proteins that sp

219 em effector protein VceC into host cells, is TRAF2, NOD1/2 and RIP2-dependent and can be reduced by t

220 s with MCL identified recurrent mutations in TRAF2 or BIRC3 in 15% of these individuals.

221 F-kappaB activation induced by overexpressed TRAF2 or IkappaB kinase 2.

222 that involved the adaptor Act1, the adaptors TRAF2 or TRAF5 and the splicing factor SF2 (also known a

223 In addition, TRAF2 overexpression significantly increased the ability

224 phenotype of CYLD loss, identifying the CYLD-TRAF2-p38MAPK pathway as a novel important regulator of

225 TNFalpha-induced IKK activation modulated by TRAF2 phosphorylation and suggest that TRAF2 phosphoryla

226 t TNF-alpha and oxidative stress both induce TRAF2 phosphorylation at serines 11 and 55 and that this

227 On the other hand, TRAF2 phosphorylation in response to oxidative stress si

228 These results suggest that TRAF2 phosphorylation is essential for cell survival und

229 ed by TRAF2 phosphorylation and suggest that TRAF2 phosphorylation is one of the events that are resp

230 This work defines TRAF2 phosphorylation to be one key effector of IKKepsil

231 ugh the formation of a signalosome involving TRAF2/PKC- leading to NF-kB activation.

232 It has been shown that TRAF2 plays a role in CD40L-mediated platelet activation

233 upts the TRAF2-GAPDH interaction to suppress TRAF2 polyubiquitination and NF-kappaB activation.

234 mediated NF-kappaB activation, and regulates TRAF2 polyubiquitination.

235 sociated factors (TRAF), including the TRAF1/TRAF2 positive regulators and TRAF3 negative regulator o

236 TRAF1 and TRAF2 preferentially form the TRAF1: (TRAF2)(2) heterotr

237 nked polyubiquitination of TRAF2 and reduces TRAF2 protein levels.

238 fication of Thr-61 as a critical residue for TRAF2 recruitment and canonical NFkappaB signaling by CD

239 found that TNF receptor-associated factor 2 (TRAF2) recruitment is required for API2-MALT1 to induce

240 he c-IAPs through a TRAF2-TRAF3 bridge where TRAF2 recruits c-IAP1/2 and TRAF3 binds to NIK.

241 Ligated LTbetaR complexed with TRAF3 and TRAF2 redirected the specificity of the ubiquitin ligase

242 studies to elucidate the mechanisms by which Traf2 regulates necroptosis signaling.

243 ha (TNF-alpha) receptor-associated factor 2 (TRAF2) regulates activation of the c-Jun N-terminal kina

244 Interestingly, USP48 only targets the TRAF2 related to JNK pathway, not the TRAF2 related to N

245 ts the TRAF2 related to JNK pathway, not the TRAF2 related to NF-kappaB and p38 pathways.

246 that (i) the interaction between TNF-R1 and TRAF2 requires sequences located in the entire N-termina

247 It has been claimed that the atypical TRAF2 RING cannot function as a ubiquitin E3 ligase but

248 These data suggest that (i) the TRAF2 RING domain plays a critical role in inhibiting ce

249 The TRAF2 RING domain-mediated polyubiquitination of RIP1 is

250 Furthermore, the role of the TRAF2 RING is controversial.

251 ubiquitin E3 ligase but counterclaimed that TRAF2 RING requires a co-factor, sphingosine-1-phosphate

252 bles a unique complex that not only contains TRAF2, RIP, and IKKalpha/beta/gamma but also CARMA1, MAL

253 97) did not directly interact with TNF-R1 or TRAF2, sequences located in this region were capable of

254 Thus, TRAF2 sets a critical barrier for cell-extrinsic apoptos

255 g, transgenic mice functionally deficient in TRAF2 showed delayed immunotherapeutic activity of anti-

256 intact catalytic domain, but unable to bind TRAF2, showed the same HSC phenotype.

257 These data identify GAPDH as a TRAF2 signaling cofactor and reveal a virulence strategy

258 ); however, virtually nothing is known about TRAF2 signaling in the adult mammalian heart.

259 lammatory responses induced by the IRE1alpha/TRAF2 signalling pathway provides a novel link between i

260 In contrast, TRAF2 siRNA knockdown, targeting receptor-mediated NF-ka

261 ubiquitinating enzyme (DUB), which regulates TRAF2 stability, has not been identified.

262 pithelial barrier integrity through reducing TRAF2 stability.

263 tinated by TNF receptor-associated factor 2 (TRAF2), suggesting a regulatory role in TNFR signaling.

264 e 2 (RSK2) ubiquitination, and knocking down TRAF2 suppresses ubiquitination of RSK2 induced by EGF.

265 ermore, we reveal a new biologic function of TRAF2 that contributes to epithelial barrier dysfunction

266 enzyme Ubc13, TNF receptor-associated factor TRAF2, the protein kinase TAK1, and the IkappaB kinase (

267 domain of TNF-receptor associated factor 2 (TRAF2), thereby inhibiting the ubiquitin ligase (E3) act

268 TRAF2 therefore has essential tissue specific functions

269 TNF-alpha induced the ubiquitination of TRAF2 (TNF receptor-associated factor 2), which interact

270 owever, both knockdowns reduce expression of TRAF2 (TNF receptor-associated factor-2) protein, and sm

271 on of TRAF2 by miR-17 reduced the ability of TRAF2 to associate with cIAP2, resulting in the downregu

272 sure of cells expressing phospho-null mutant TRAF2 to sublethal oxidative stress results in a rapid d

273 Once activated, IRE1alpha recruits TRAF2 to the ER membrane to initiate inflammatory respon

274 Furthermore, the recruitment of TRAF3 and TRAF2 to the ligated LTbetaR competitively displaced NIK

275 IKK activation, and the RING-domain-deleted TRAF2 (TRAF2-DeltaR) has been widely used as a dominant

276 This correlates with increased TRAF2, TRAF3, and TRAF6 recruitment to His159Tyr BAFF-R.

277 ubiquitin moieties from proteins, including TRAF2, TRAF3, and TRAF6.

278 NF-kappaB-inducing kinase (NIK) levels (NIK, TRAF2, TRAF3, cIAP1&2, and CD40) activate the alternativ

279 R)-associated signaling complexes, including TRAF2, TRAF3, NIK, IKK1, and IKK2 have been shown to par

280 into close proximity to the c-IAPs through a TRAF2-TRAF3 bridge where TRAF2 recruits c-IAP1/2 and TRA

281 Recent evidence suggests that the cIAP-TRAF2-TRAF3 E3 complex also targets additional signaling

282 estricted in unstimulated cells by a cIAP1/2:TRAF2:TRAF3:NIK complex.

283 ers recruit several TRAF proteins, including TRAF2, TRAF5, and TRAF6, through distinct TRAF-binding m

284 ation of selected mRNA species through Act1, TRAF2-TRAF5 and the RNA-binding protein SF2 (ASF).

285 ith alanine impaired the IL-17-mediated Act1-TRAF2-TRAF5 interaction and gene expression.

286 Two chains of the TRAF2 trimer directly contact cIAP2, and key residues at

287 A TRAF2 trimer interacts with one cIAP2 both in the crysta

288 lines, we identify the NF-kappaB regulator, TRAF2 (tumor necrosis factor (TNF) receptor-associated f

289 interactions between CYLD and its substrate TRAF2 (tumor necrosis factor-associated factor 2).

290 quitylation and JNK activation by inhibiting TRAF2/Ubc13 enzymatic activity.

291 This activity promotes Lys63-linked TRAF2 ubiquitination and NF-kappaB activation and is ess

292 F2 and results not only in the inhibition of TRAF2 ubiquitination but also in Lys63-linked Nur77 ubiq

293 TP, which we identified as the corresponding TRAF2 ubiquitination site.

294 TRAF2 was deleted specifically in hepatocytes using the

295 However, TRAF2 was deleterious for BCR-mediated activation of the

296 F-kappaB1 p105/p50, NF-kappaB2 p100/p52, and TRAF2 was increased in UAKD.

297 Finally, we further confirm that TRAF2 was required for CD40-mediated proliferation, but

298 ent with previous results, we also show that TRAF2 was required for efficient JNK and ERK activation

299 ken together, indicate that USP48 stabilizes TRAF2, which is promoted by GSK3beta-mediated phosphoryl

300 stimuli, it may modulate the interaction of TRAF2 with cIAP1/2, which explains regulatory roles of T