ライフサイエンスコーパス: TRAF2

1 TRAF3 but not with TNFR-associated factor 2 (TRAF2).

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

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

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

5 s recruited to the Fn14 cytoplasmic tail via TRAF2.

6 xpression for survival are also dependent on TRAF2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 TRAF2 abundance increases in the mitochondrial subfracti

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

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

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

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

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

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

32 hich interacts with cIAP2 more strongly than TRAF2 alone.

33 wild-type or phosphorylation mutant forms of TRAF2, along with immunoprecipitation, immunoblotting, g

34 TRAF2 also colocalizes and interacts with PARKIN, a prev

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

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

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

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

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

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

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

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

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

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

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 recruitment of ubiquitin ligases, including TRAF2 and TRAF6, to the vacuole membrane, which enhances

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 kinase 1 (TBK1)-mediated phosphorylation of TRAF2 at Ser-11.

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

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

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

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

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

98 and Apt-1 bind to a pocket on the N-terminal TRAF2-binding domain of TRADD (TRADD-N), which interacts

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 ion with OX40, and TNFR-associated factor 2 (TRAF2) bridged these two proteins.

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

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

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

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

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

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

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 inked ubiquitination of beclin 1 mediated by TRAF2, cIAP1 and cIAP2, thereby reducing autophagy.

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

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

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

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

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

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

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

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

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

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

121 TRAF2 colocalizes with ubiquitin, p62 adaptor protein, a

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

123 ospholipids and enabled translocation of the TRAF2 complex from CD40 to the cytoplasm.

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

125 olipids, leading to the translocation of the TRAF2 complex to lipid rafts, resulting in its degradati

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

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

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

129 Mechanistically, Traf2 critically regulates receptor-interacting proteins

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

131 TRAF2 deficiency does not enhance upstream signalling ev

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

133 TRAF2 deficient mice die around birth, therefore its rol

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

135 Here, using four different TRAF2-deficient cell lines (A20.2J, CH12.LX, HAP1, and m

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

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

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

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

140 c remodeling and dysfunction associated with Traf2 deletion.

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

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

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

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

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

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

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

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

149 TRAF2 depletion lowers the signal threshold for DR-media

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 TRAF2 is a component of TNF superfamily signalling compl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 TRAF2 knockdown with adenoviral shRNA transduction induc

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

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

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

212 TRAF2 localizes to the mitochondria in neonatal rat card

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

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

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

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

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

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

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

220 Here, we analyse the role of the TRAF2-/NCK-interacting kinase (TNIK), a signaling molecu

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

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

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

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

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

226 In addition, TRAF2 overexpression significantly increased the ability

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

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

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

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

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

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

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

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

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

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

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

238 nked polyubiquitination of TRAF2 and reduces TRAF2 protein levels.

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

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

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

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

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

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

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

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

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

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

249 n the absence of Ser-11 phosphorylation, the TRAF2 RING domain interacts with phospholipids, leading

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

251 The TRAF2 RING domain-mediated polyubiquitination of RIP1 is

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

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

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

255 tion interfered with the interaction between TRAF2's RING domain and membrane phospholipids and enabl

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

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

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

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

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

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

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

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

264 pithelial barrier integrity through reducing TRAF2 stability.

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

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

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

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

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

270 TRAF2 therefore has essential tissue specific functions

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

272 domain-dependent subcellular localization of TRAF2 to modulate the spatiotemporal activation of the J

273 cts with the C-terminal domain (TRADD-C) and TRAF2 to modulate the ubiquitination of RIPK1 and beclin

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ed by B cell-intrinsic checkpoints TRAF3 and TRAF2, whose deletion in B cells enables the BCR to indu

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