ライフサイエンスコーパス: TRAF6

1 trimeric (i.e., TNFR-associated factor 6 or TRAF6).

2 motif for TNF receptor-associated factor 6 (TRAF6).

3 ase 4, and TNF receptor-associated factor 6 (TRAF6).

4 f tumor necrosis factor-associated factor 6 (TRAF6).

5 AK-1), and TNF receptor-associated factor 6 (TRAF6).

6 ecrosis factor receptor-associated factor 6 (TRAF6).

7 auxiliary splicing factor, as a substrate of TRAF6.

8 on that disrupt the recruitment of MyD88 and TRAF6.

9 IkappaBalpha and a dominant negative form of TRAF6.

10 les of TLR4, including Rho GTPase Cdc 42 and TRAF6.

11 ts receptor, RANK, and the signaling adaptor TRAF6.

12 ng can restore invasion in cells depleted of Traf6.

13 ed muscle atrophy and its regulation through TRAF6.

14 paB or toll-like receptor proteins IRAK1 and TRAF6.

15 vation increased tyrosine phosphorylation of TRAF6.

16 nd to the TLR adaptors and to both TRAF3 and TRAF6.

17 sites, thereby leading to the degradation of TRAF6.

18 h the induction of autophagic degradation of TRAF6.

19 d bind to TRAF6 and its silencing stabilized TRAF6.

20 TNF receptor-associated factor 6 (TRAF6), a verified target of miR-146a, was up-regulated

21 wild-type TLR3, leads to the recruitment of TRAF6, a downstream signal transducer of the MyD88-depen

22 We show that TRIM12c interacts with TRAF6, a key protein in the pathogen recognition recepto

23 This was due to reduced ubiquitination of TRAF6, a key step in signal transduction.

24 TRAF6, a TLR effector with ubiquitin (Ub) ligase activit

25 We identified IL-18 as a TRAF6-activating factor capable of enhancing lymphopenia

26 g of NF-kappaB function was noted to require TRAF6 activation.

27 TRAF6 activity can be impeded by deubiquitinating enzyme

28 sociation of TAB2 with its signaling partner TRAF6 after TLR ligation in B cells.

29 tion of TRAF6 from cytosol to nucleus, where TRAF6 also facilitates the K63-linked ubiquitination of

30 Ablation of TRAF6 also improved the phosphorylation of Akt and FoxO3

31 Ablation of TRAF6 also increases satellite cells proliferation and m

32 Deletion of TRAF6 also inhibited the activity of transcription facto

33 s factor (TNF) receptor-associated factor 6 (TRAF6), an adaptor protein involved in receptor-mediated

34 ates that, TNF receptor-associated factor 6 (TRAF6), an E3 ubiquitin ligase involved in innate immune

35 racts with TNF receptor-associated factor 6 (TRAF6), an E3 ubiquitin ligase that functions as a key m

36 TRAF6, an E3 ubiquitin protein ligase, plays a critical

37 0, a member of the inflammasome pathway, and Traf6, an inflammatory signaling member.

38 Here, we identify an E3 ligase, Traf6 and a de-ubiquitinating enzyme, Cezanne/ZA20D1, as

39 IL-1beta upregulated expression of IRAK and TRAF6 and activated PI 3-kinase; expression of IRAK and

40 tenuate Lys63 (K63)-linked ubiquitination of TRAF6 and activation of NF-kappaB.

41 formation of a molecular complex composed of TRAF6 and beta-arrestin-2.

42 by disrupting RANKL-induced localization of TRAF6 and c-SRC into lipid rafts and preventing nuclear

43 the inhibitory effect of Tbeta4 on IRAK1 and TRAF6 and decreased expression of MBP.

44 imDCs and mDCs was inversely correlated with TRAF6 and IRAK1 expression.

45 binds to the downstream signaling components TRAF6 and IRAK2.

46 for selective autophagy, as it could bind to TRAF6 and its silencing stabilized TRAF6.

47 cells leads to increased NUMBL and decreased TRAF6 and NEMO expression.

48 dies show that NUMBL directly interacts with TRAF6 and NEMO, and induces their K48-poly-ubiquitinatio

49 we demonstrate that GSK3beta interacts with TRAF6 and positively regulates the TLR3-mediated signall

50 DJ-1 suppresses the activation of both RANK-TRAF6 and RANK-FcRgamma/Syk signaling pathways because o

51 pted the TRAF6-ECSIT complex by sequestering TRAF6 and substantially diminished ROS production and en

52 This interaction fosters ubiquitination of TRAF6 and TAK1 and promotes LPS-induced NF-kappaB, JNK,

53 We demonstrate that TRAF6 and TAK1 are required for NF-kappaB and JNK activa

54 However, the role of TRAF6 and TAK1 in C-type lectin receptors (CLRs) in resp

55 K1-deficient mice and determined the role of TRAF6 and TAK1 in CLR-induced signal transduction events

56 Small interfering RNA-mediated silencing of TRAF6 and TAK1, and inhibition of TAK1 blocked CD158d-de

57 In WT osteoclast precursors, Itch bound to TRAF6 and the deubiquitinating enzyme cylindromatosis.

58 s A20, CYLD, and DUBA prevent association of TRAF6 and TRAF3 with their partners, in addition to remo

59 Furthermore, siRNA silencing of TRAF6 and/or IRAK1 in imDCs and mDCs enhanced DC apoptos

60 By contrast, lentivirus overexpression of TRAF6 and/or IRAK1 promoted DC survival.

61 racts with TNF receptor-associated factor 6 (TRAF6) and attenuates IkappaB kinase beta-dependent (IKK

62 racts with TNF receptor associated factor 6 (TRAF6) and is required for mTORC1 translocation to the l

63 ecrosis factor receptor-associated factor 6 (TRAF6) and mammalian target of rapamycin (mTOR), respect

64 ecrosis factor receptor-associated factor 6 (TRAF6) and TGFbeta-activated kinase 1 (TAK1) are conside

65 r (TH9) cells in a TNFR-associated factor 6 (TRAF6)- and NF-kappaB-dependent manner and inhibited the

66 y decay of a "trafasome" comprised of IRAK1, TRAF6, and MAP3K proteins, abrogating downstream activat

67 ally reduced Lys 63-linked ubiquitination of TRAF6, and the deubiquitinating enzyme A20 was found to

68 ciation of USP25 with the adaptors TRAF5 and TRAF6, and USP25 induced removal of Lys63-linked ubiquit

69 BE2R1- (CDC34), UBE2N/UBE2V1- (UBC13/UEV1A), TRAF6- and HOIP-mediated chain assembly is inhibited by

70 stablished that the developmental defects of TRAF6- and integrin alpha3-null mouse kidneys are simila

71 proteins TNFR-associated factor (TRAF)3 and TRAF6 are important mediators of TLR signaling.

72 demonstrate that the levels and activity of TRAF6 are increased in skeletal muscle of mdx (a mouse m

73 abases further indicates that MUC1, TAK1 and TRAF6 are upregulated in tumors associated with decrease

74 We undertook to study the role of TRAF6 as a candidate gene for SLE, since it plays a majo

75 Together, our study identifies TRAF6 as a critical gatekeeper to restrict p53 mitochond

76 We identified the ubiquitin-modifying enzyme TRAF6 as an interactor with the integrin beta1 subunit a

77 promote tumorigenesis and suggest DCBLD2 and TRAF6 as potential therapeutic targets for human cancers

78 restored the Lys 63-linked ubiquitination of TRAF6 as well as IL-12 and TNF-alpha levels with a conco

79 We show that YOD1 competes with p62 for TRAF6 association and abolishes the sequestration of TRA

80 ced NF-kappaB activation and IL-8 secretion, TRAF6 association with CD158d, and TRAF6 recruitment to

81 g NK cells with soluble Ab to CD158d induced TRAF6 association with CD158d, induced TAK1 phosphorylat

82 19A to catalyze K48-linked ubiquitination of TRAF6 at multiple sites, thereby leading to the degradat

83 ound that miR-146a and miR-146b targeting of Traf6 attenuates TCR signaling in the thymus and inhibit

84 antagomiR restores expressions of IRAK1 and TRAF6, augments IFNbeta production, inhibits viral propa

85 n IL-1beta stimulation, thereby facilitating TRAF6 auto-ubiquitination as well as NEMO/IKKgamma subst

86 LPS increased TRAF6 autoubiquitination and binding to IRAK1.

87 cific protease 20 (USP20), which can reverse TRAF6 autoubiquitination, and by association with the mu

88 not a mutant defective in p38 activation and TRAF6 binding (F154A), caused TRAF6 oligomerization and

89 al TRAF6-binding motif that is essential for TRAF6 binding and p38 activation but dispensable for NFk

90 TRAF6 (pro-inflammatory) suggest that TRAF3/TRAF6 binding sites on MyD88 DD partially overlap, as do

91 tified a conserved TNFR-associated factor 6 (TRAF6) binding motif, which was required for CD158d-indu

92 ice expressing the TNFR-associated factor 6 (TRAF6) binding-defective mutant IRAK2[E525A] or the cata

93 Here, we show that A52 has a non-canonical TRAF6-binding motif that is essential for TRAF6 binding

94 nked ubiquitination of MLK3 via a conserved, TRAF6-binding peptapeptide motif in the catalytic domain

95 The E3 ligase TRAF6 binds to DCP1a and indirectly regulates DCP1a phos

96 Knockdown of RIP2 and TRAF6 by RNA interference and neutralization of interleu

97 Reversible arginine methylation of TRAF6 by the opposing effects of PRMT1 and JMJD6 is, the

98 Moreover, TRAF6/c-JUN signaling repressed the levels of the microR

99 Furthermore, the catalytically dead mutant TRAF6 C70A abolished the TRAF6-mediated polyubiquitinati

100 Traf6 can promote the formation of Cdc42-dependent F-act

101 During the TRAF6-SFK association, TRAF6 catalyzed Lys(63)-linked ubiquitination of c-Src a

102 tion of mTORC1 to the lysosomes and that the TRAF6-catalyzed K63 ubiquitination of mTOR regulates mTO

103 ine-rich motif reduced SFK binding to WT GST-TRAF6 compared with the Pro --> Ala-substituted peptide.

104 tion involves the formation of a CARD9/BCL10/TRAF6 complex as a proximal signal to sequentially stimu

105 owed by assembling of the CARMA1/BCL10/MALT1/TRAF6 complex to SMO.

106 ates with the formation of a beta-arrestin-2/TRAF6 complex.

107 condary to aberrant assembly of a raptor-p62-TRAF6 complex.

108 Silencing of IRAK1 or TRAF6, confirmed targets of miR-146a, resulted in a 3-fo

109 The TRAF6 decoy peptide blocked both LPS-induced SFK ubiquit

110 incubation of HMVEC-Ls with a cell-permeable TRAF6 decoy peptide decreased both LPS-induced SFK activ

111 In contrast, myeloid cell-specific TRAF6 deficiency caused exacerbated atherosclerosis, wit

112 Endothelial TRAF6 deficiency reduced atherosclerosis in female ApoE(

113 TRAF6-deficient macrophages showed impaired expression o

114 ecrosis factor receptor-associated factor 6 (TRAF6)-dependent signaling, involved the mitogen-activat

115 at IL-18 synergizes with high-dose IL-7 in a TRAF6-dependent manner to induce slow, LIP/homeostatic-l

116 IN85 in response to TGFbeta stimulation in a TRAF6-dependent manner.

117 ls promoted osteoclastogenesis by activating TRAF6-dependent signaling pathways in osteoclast progeni

118 eceptor-dependent IL-10 induction, which was TRAF6-dependent, but the manner in which A52 manipulates

119 20 association and subsequent USP20-mediated TRAF6 deubiquitination were beta-arrestin2-dependent.

120 nd delayed TNF receptor-associated factor 6 (TRAF6) deubiquitination.

121 Silencing of TRAF6, TRAF6-dominant-negative overexpression, or preincubation

122 Here, we report that TRAF6 E3 ligase activity contributes to but is not essen

123 Here, we show that TRAF6 E3 ligase is a crucial factor to restrict mitochon

124 The TRAF6 E3 ligase orchestrates IGF-1-mediated Akt ubiquiti

125 2 Y750 recruited TRAF6, leading to increased TRAF6 E3 ubiquitin ligase activity and subsequent activa

126 g the human Rac2(D57N) mutant, disrupted the TRAF6-ECSIT complex by sequestering TRAF6 and substantia

127 ike receptor (TLR)-triggered assembly of the TRAF6-ECSIT complex that is required for the recruitment

128 Intriguingly, ablation of TRAF6 exacerbates muscle injury and increases fibrosis i

129 ned that satellite cell-specific deletion of Traf6 exaggerates the dystrophic phenotype in the mdx (a

130 2 and accounted for hematopoietic defects in TRAF6-expressing HSPCs.

131 TEC depletion due to conditional deletion of Traf6 expression in murine thymic epithelial cells (Traf

132 n and an important signaling network of SKP2-TRAF6-EZH2/H3K27me3, and targeting SKP2-EZH2 pathway may

133 Therefore, TLR/MyD88-dependent, TRAF6-facilitated CREBH activation represents a mammalia

134 hage-specific deletion of TRAF6 (LysM(C)(re) Traf6 (fl/fl) ) or mTOR (LysM(C)(re) Mtor(fl/fl) ) did n

135 ic rejection in CTLA4-Ig-treated LysM(C)(re) Traf6 (fl/fl) mice was similar to that of CTLA4-Ig-treat

136 n, whereas the similarly treated LysM(C)(re) Traf6 (fl/fl) recipients developed severe transplant vas

137 c gene, inhibits TLR signalling by targeting TRAF6 for degradation.

138 nism by which the NLRP11-RNF19A axis targets TRAF6 for degradation.

139 0 phosphorylation-dependent translocation of TRAF6 from cytosol to nucleus, where TRAF6 also facilita

140 trated that hepatitis C virus (HCV) depleted TRAF6 from its host cells through a posttranslational me

141 In multiple cellular contexts, TRAF6 function is essential not only for proper activati

142 complex in vitro with similar efficiently to TRAF6-generated K63-Ub chains.

143 The adaptor protein TRAF6 has a central function in Toll-like receptor (TLR)

144 Furthermore, Traf6 has a key role in autocrine interleukin-1beta sign

145 tor (IL-1R)-mediated activation of NFkappaB, TRAF6 has since been identified as an actor downstream o

146 In conclusion, Traf6 has two important roles in SCC invasion: it promot

147 Targeted deletion of TRAF6 improves muscle strength and reduces fiber necrosi

148 study suggests that while the inhibition of TRAF6 improves muscle structure and function in young md

149 GSK3beta physically associates with TRAF6 in a TLR3 ligand poly I:C-dependent manner.

150 Collectively, our findings reveal a role for TRAF6 in directing DC maintenance of intestinal immune t

151 enzyme YOD1 (OTUD2) as a novel interactor of TRAF6 in human cells.

152 Skeletal muscle-specific depletion of TRAF6 in mice (TRAF6(mko)) improved regeneration of myof

153 therapeutic potential of inhibition of CD40-TRAF6 in obesity, DIO mice were treated with a small-mol

154 However, the role of TRAF6 in pathogenesis of DMD remains unknown.

155 Selective deletion of Traf6 in satellite cells of adult mice led to profound m

156 ely, our study reveals an essential role for TRAF6 in satellite stem cell function.

157 Because TAK1 activation is mediated through TRAF6 in the interleukin 1 receptor (IL-1R) and toll-lik

158 complex, thus inhibiting the recruitment of TRAF6 in TLR2 signaling.

159 YOD1 associates with TRAF6 in unstimulated cells but is released upon IL-1bet

160 s widely accepted that the essential role of TRAF6 in vivo is to generate the Lys63-linked ubiquitin

161 signaling activated the E3 ubiquitin ligase TRAF6, increasing K63-linked ubiquitination and enhancin

162 TRAF6 inhibition reduces the markers of autophagy and Ak

163 domain of NOSTRIN is involved in the NOSTRIN-TRAF6 interaction and is required for NOSTRIN-induced do

164 Loss of the IRAK2-TRAF6 interaction had little effect on the MyD88-depende

165 duction in BMDM and pDCs, and that the IRAK2-TRAF6 interaction is needed to sustain IkappaB-inducing

166 Our results establish that the IRAK2-TRAF6 interaction is rate limiting for the late, but not

167 Interfering with the p62-TRAF6 interaction serves to modulate autophagy and nutri

168 naling pathway was used instead of the IRAK2-TRAF6 interaction to sustain late-phase mRNA production.

169 arrow-derived macrophages (BMDMs), the IRAK2-TRAF6 interaction was required for the late (2-8 h) but

170 ivation of p62-associated mitophagy, and p62-TRAF6 interaction.

171 cations associated with obesity whereas CD40-TRAF6 interactions in MHCII(+) cells aggravate these com

172 that we designed to specifically block CD40-TRAF6 interactions; this compound improved insulin sensi

173 -rich Src homology 3 domain-binding motif in TRAF6 interacts directly with activated SFKs to couple L

174 pregulates miR-146a, which targets IRAK1 and TRAF6 involved in TLR signalling and type I interferon p

175 ify mechanisms of contextual specificity for TRAF6, involving both regulatory protein interactions, a

176 feedback mechanism involving the miR-146a/b-TRAF6/IRAK1-NF-kappaB axis in promoting DC apoptosis.

177 The ubiquitin ligase TRAF6 is a key regulator of canonical IkappaB kinase (IK

178 TRAF6 is also an E3 ubiquitin ligase and an important re

179 TRAF6 is an important signaling molecule that mediates a

180 TRAF6 is critical for the production of inflammatory cyt

181 The intracellular signaling molecule TRAF6 is critical for Toll-like receptor (TLR)-mediated

182 In response to toll-like receptor ligands, TRAF6 is demethylated by the Jumonji domain protein JMJD

183 TRAF6 is determined to be a direct E3 ligase for GSK3bet

184 yubiquitination of the novel LUBAC substrate TRAF6 is essential for NFkappaB signaling.

185 We also demonstrate that TRAF6 is involved in the SopB/SopE2-induced phosphorylat

186 The adaptor TRAF6 is known to couple proximal signals from receptors

187 Under basal conditions, TRAF6 is methylated by the methyltransferase PRMT1, and

188 We also show that TRAF6 is necessary for the translocation of mTORC1 to th

189 Here we show that TRAF6 is recruited to and activates mTORC1 through p62 i

190 we describe herein novel mechanisms by which TRAF6 is regulated through bortezomib/autophagy-mediated

191 factor receptor (TNFR)-associated factor 6 (TRAF6) is an adapter protein that mediates a wide array

192 TNF receptor-associated factor 6 (TRAF6) is an adaptor protein and an E3 ubiquitin ligase

193 TNF receptor-associated factor 6 (TRAF6) is an adaptor protein which acts as a signaling i

194 factor receptor (TNFR)-associated factor 6 (TRAF6) is an important adaptor molecule that mediates th

195 TNF receptor-associated factor 6 (TRAF6) is identified as a direct E3 ligase for PSD-95, w

196 biquitin-conjugating enzyme that facilitates TRAF6 K63-linked ubiquitination and NF-kappaB activation

197 y, we have utilized macrophages derived from TRAF6 knock-out mice and myeloid-specific TAK1-deficient

198 In contrast, TRAF6 knockdown resulted in a reduced EZH2 ubiquitinatio

199 mutants partially restored IL-1 signaling in TRAF6 KO cells, but not in TRAF6/Pellino1/Pellino2 tripl

200 h of the TRAF6[L74H] mice was normal, unlike TRAF6 KO mice.

201 lino2 triple-knockout (KO) cells, but not in TRAF6 KO or Pellino1/2 double-KO cells.

202 of bone marrow to osteoclasts was similar in TRAF6[L74H] and wild-type cells, explaining why the bone

203 ning why the bone structure and teeth of the TRAF6[L74H] mice was normal, unlike TRAF6 KO mice.

204 ockin mice expressing the E3 ligase-inactive TRAF6[L74H] mutant, but the late-phase production of IL-

205 ectly with TNF receptor-associated factor 6 (TRAF6), leading to the suppression of NFkappaB activity

206 ly, phosphorylation of DCBLD2 Y750 recruited TRAF6, leading to increased TRAF6 E3 ubiquitin ligase ac

207 ulator of donor T cells in GVHD by targeting TRAF6, leading to reduced TNF transcription.

208 reductions in IL-1R-associated kinase 1 and TRAF6 levels following LOS retreatment of cells.

209 Higher TRAF6 levels translated into increased nuclear factor-ka

210 showed that macrophage-specific deletion of TRAF6 (LysM(C)(re) Traf6 (fl/fl) ) or mTOR (LysM(C)(re)

211 In addition to NFkappaB, TRAF6 may also direct activation of mitogen-activated pr

212 of Lys63-linked ubiquitination in TRAF5 and TRAF6 mediated by the adaptor Act1.

213 atively regulated TNF receptor associated 6 (TRAF6)-mediated ubiquitination and stabilization of hypo

214 s in human PCa cells through upregulation of TRAF6-mediated and lysine(K) 63-linked ubiquitination of

215 d to be a direct E3 ligase for GSK3beta, and TRAF6-mediated GSK3beta ubiquitination is essential for

216 e discovered a novel regulatory axis through TRAF6-mediated IRE1alpha ubiquitination in regulating TL

217 tically dead mutant TRAF6 C70A abolished the TRAF6-mediated polyubiquitination of recombinant human E

218 Here, we demonstrated that TRAF6-mediated signaling is critical for homeostasis of

219 In the context of the immune system, TRAF6-mediated signals have proven critical for the deve

220 TRAF6-mediated ubiquitination was required for dissociat

221 Further analysis demonstrated that TRAF6 mediates K63-linked ubiquitination of CREBH to fac

222 Specifically, TRAF6 mediates lysine-63 ubiquitination within the Src h

223 MT1/JMJD6 ratio significantly correlate with TRAF6 methylation, basal activation of NF-kappaB, and ma

224 muscle-specific depletion of TRAF6 in mice (TRAF6(mko)) improved regeneration of myofibers upon inju

225 The reexpression of E3 ligase-inactive TRAF6 mutants partially restored IL-1 signaling in TRAF6

226 aling in cells expressing E3 ligase-inactive TRAF6 mutants.

227 ctive removal of Lys63-linked ubiquitin from TRAF6, NEMO and RIP1 after stimulation with tumor necros

228 and osteoclastogenesis by targeting the TAK1-TRAF6-NEMO axis.

229 phai and Galpha12 to activate PKCbeta/CARMA1/TRAF6/NEMO signaling axis followed by assembling of the

230 nd increased apoptosis, which coincided with TRAF6/NF-kappaB inhibition.

231 activation and TRAF6 binding (F154A), caused TRAF6 oligomerization and subsequent TRAF6-TAK1 associat

232 We found that TRAF6 overexpression in mouse HSPC results in impaired h

233 ectal cancer samples with WT p53 reveal that TRAF6 overexpression negatively correlates with apoptosi

234 Hence, our data define that YOD1 antagonizes TRAF6/p62-dependent IL-1 signaling to NF-kappaB.

235 of IRAK1, IRAK4, and MyD88 was abolished in TRAF6/Pellino1/Pellino2 triple-knockout (KO) cells, but

236 IL-1 signaling in TRAF6 KO cells, but not in TRAF6/Pellino1/Pellino2 triple-KO cells.

237 se (IRAK), TNF receptor-associated factor 6 (TRAF6), phosphatidylinositol 3-kinase (PI 3-kinase), Ika

238 cked both LPS-induced SFK ubiquitination and TRAF6 phosphorylation.

239 s factor (TNF) receptor-associated factor 6 (TRAF6) plays a key role in TLR-mediated IRE1alpha activa

240 ith TRAF3 (anti-viral/anti-inflammatory) and TRAF6 (pro-inflammatory) suggest that TRAF3/TRAF6 bindin

241 Ectopic expression of TRAF6 promoted the K63-linked ubiquitination of EZH2 to

242 es proteasome-independent degradation of the TRAF6 protein, but not mRNA, in myelodysplastic syndrome

243 ctivated PI 3-kinase; expression of IRAK and TRAF6 reached maximum within 60 minutes, after which the

244 ecretion, TRAF6 association with CD158d, and TRAF6 recruitment to CD158d(+) endosomes in transfected

245 However, it is poorly understood how TRAF6 regulates TLR3 responses.

246 Lys-63-linked ubiquitination and identified TRAF6-related NF-kappaB activation as a novel pathway in

247 el, XN disrupted the association of RANK and TRAF6, resulted in the inhibition of NF-kappaB and Ca(2+

248 cting with TRAF6, was unable to cause either TRAF6 self-association, induce the TRAF6-TAK1 associatio

249 The results suggest that an A52 dimer causes TRAF6 self-association, leading to TAK1 recruitment and

250 During the TRAF6-SFK association, TRAF6 catalyzed Lys(63)-linked ub

251 Inhibition of CD40-TRAF6 signaling by our compound may provide a therapeuti

252 In contrast, mice with deficient CD40-TRAF6 signaling in MHCII(+) cells displayed no insulin r

253 of PCBs and suggest that targeting the TLR4/TRAF6 signaling may protect against these effects.

254 astogenesis and bone resorption through RANK/TRAF6 signaling pathways.

255 ory protein (IL1RAP) SNP (rs10513854), and 1 TRAF6 SNP (rs5030411).

256 Although beta-arrestin2 effects on TRAF6 suggest an anti-inflammatory role, physiologic bet

257 The depletion of TRAF6 suppressed activation of NF-kappaB and induction o

258 In contrast, the overexpression of TRAF6 suppressed HCV replication.

259 Targeted ablation of TRAF6 suppresses the expression of key regulators of atr

260 as a scaffold molecule to independently bind TRAF6, TAK1, IkappaB kinase alpha, and IkappaB kinase be

261 se either TRAF6 self-association, induce the TRAF6-TAK1 association, or activate p38 MAPK.

262 caused TRAF6 oligomerization and subsequent TRAF6-TAK1 association.

263 betaRI/TbetaRIII-mediated, SMAD-independent, TRAF6/TAK1/p38 signaling pathway; and defective cell pro

264 tivation pathway facilitated through a STING-TRAF6-TBK1 axis and suggest a target for therapeutic int

265 ds to the C-terminal TRAF homology domain of TRAF6 that also serves as the interaction surface for th

266 We identify two essential roles of TRAF6 that are independent of its E3 ligase activity.

267 l TRAF proteins, including TRAF2, TRAF5, and TRAF6, through distinct TRAF-binding motifs.

268 TRAF6, through its interaction with p62 and activation o

269 zyme and is required for deubiquitination of TRAF6, thus limiting RANKL-induced osteoclast formation.

270 ine kinase) and subsequently integrates with TRAF6 (TNF receptor-associated factor 6) and/or c-fos si

271 interleukin-1 receptor-associated kinase)1/4-TRAF6 (TNF receptor-associated factor 6), leading to int

272 ed of TAK1, TAB1 (TAK1 binding protein), and TRAF6 (TNF receptor-associated factor 6).

273 ular mechanism whereby poxviruses manipulate TRAF6 to activate MAPKs (which can be proviral) without

274 y interacting with the TLR signaling adaptor TRAF6 to attenuate Lys63 (K63)-linked ubiquitination of

275 sociation and abolishes the sequestration of TRAF6 to cytosolic p62 aggregates by a non-catalytic mec

276 d CD40 signaling complexes failed to recruit TRAF6 to detergent-insoluble membrane fractions.

277 s a scaffold protein by recruiting E3 ligase TRAF6 to IKK complex to activate NF-kappaB in response t

278 ent, but the manner in which A52 manipulates TRAF6 to stimulate p38 activation was unclear.

279 Silencing of TRAF6, TRAF6-dominant-negative overexpression, or preinc

280 We now report that DC-specific deletion of TRAF6 (TRAF6DeltaDC) resulted, unexpectedly, in loss of

281 is consisting of miR-146a, signaling protein TRAF6, transcriptional factor NF-kappaB, and cytokine IL

282 appaB signaling through the ubiquitin ligase TRAF6 (tumor necrosis factor receptor-associated factor

283 ecrosis factor receptor-associated factor 6 (TRAF6), two proinflammatory cytokines of the TLR signali

284 ed by the IRAK2 variant was due to increased TRAF6 ubiquitination and faster IkappaBalpha degradation

285 This TRAF6 ubiquitination is triggered by the Salmonella path

286 TRAF6 ubiquitination of hnRNPA1 regulated alternative sp

287 TRAF6 ubiquitination participates in STAT3 phosphorylati

288 our protein interaction studies showed that TRAF6/USP20 association and subsequent USP20-mediated TR

289 n, these results suggested that HCV depleted TRAF6 via autophagy.

290 The degradation of TRAF6 was apparently mediated by the p62 sequestosome pr

291 f this finding was not clear until 2000 when TRAF6 was found to be a ubiquitin E3 ligase that catalyz

292 TRAF6 was required for the activation of MAPKs ERK1/2 an

293 52-M65E although capable of interacting with TRAF6, was unable to cause either TRAF6 self-association

294 ingle-nucleotide polymorphisms (SNPs) across TRAF6 were evaluated in 7,490 SLE patients and 6,780 con

295 und miR-146a target genes, such as IRAK1 and TRAF6, were manifestly downregulated.

296 s factor (TNF) receptor-associated factor 6 (TRAF6), which are known target genes of miR-146a, leadin

297 AK1 and confers the association of TAK1 with TRAF6, which is necessary for TAK1-mediated activation o

298 K48-linked ubiquitination and degradation of TRAF6, which promotes activation of NF-kappaB and MAPK s

299 ilomycin A1, which led to the association of TRAF6 with autophagosomes.

300 data indicate the presence of association of TRAF6 with SLE, consistent with the previous report of a

301 y be due to impairment of the association of TRAF6 with the TAK-TAB complex, thus inhibiting the recr