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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 sites, thereby leading to the degradation of TRAF6.
8 h the induction of autophagic degradation of TRAF6.
9 d bind to TRAF6 and its silencing stabilized TRAF6.
10 on that disrupt the recruitment of MyD88 and TRAF6.
11 IkappaBalpha and a dominant negative form of TRAF6.
12 les of TLR4, including Rho GTPase Cdc 42 and TRAF6.
13 ts receptor, RANK, and the signaling adaptor TRAF6.
14 tion at lysine 262 mediated by the E3 ligase TRAF6.
15 e association of viperin with both IRAK1 and TRAF6.
16 nd inhibiting its association with TRAF3 and TRAF6.
17 auxiliary splicing factor, as a substrate of TRAF6.
18 ha-THP (15 mg/kg, IP) administration reduced TRAF6 (~20%), CRF (~30%), and MCP-1 (~20%) levels, as we
20 wild-type TLR3, leads to the recruitment of TRAF6, a downstream signal transducer of the MyD88-depen
24 by Muto et al., MDS stem cells sparked with TRAF6-activated innate immune signaling were found to ou
30 tion of TRAF6 from cytosol to nucleus, where TRAF6 also facilitates the K63-linked ubiquitination of
32 ates that, TNF receptor-associated factor 6 (TRAF6), an E3 ubiquitin ligase involved in innate immune
33 racts with TNF receptor-associated factor 6 (TRAF6), an E3 ubiquitin ligase that functions as a key m
38 by disrupting RANKL-induced localization of TRAF6 and c-SRC into lipid rafts and preventing nuclear
42 IC3 loop, respectively, can directly recruit TRAF6 and its negative regulator ARRB2 to form a multi-p
45 dies show that NUMBL directly interacts with TRAF6 and NEMO, and induces their K48-poly-ubiquitinatio
46 s modulated by the Gln-dependent activity of TRAF6 and p62 in the migrating front, and depletion of t
47 we demonstrate that GSK3beta interacts with TRAF6 and positively regulates the TLR3-mediated signall
48 DJ-1 suppresses the activation of both RANK-TRAF6 and RANK-FcRgamma/Syk signaling pathways because o
49 g Akt K64 methylation and recruits E3 ligase TRAF6 and Skp2-SCF to the Akt complex, independently of
50 pted the TRAF6-ECSIT complex by sequestering TRAF6 and substantially diminished ROS production and en
51 This interaction fosters ubiquitination of TRAF6 and TAK1 and promotes LPS-induced NF-kappaB, JNK,
52 Small interfering RNA-mediated silencing of TRAF6 and TAK1, and inhibition of TAK1 blocked CD158d-de
53 tion induces a signalling cascade recruiting TRAF6 and TBK-1, while TBK-1 phosphorylates STAT3 on S72
54 omplex with the RING-finger ubiquitin ligase TRAF6 and the downstream NF-kappaB inflammatory response
55 s A20, CYLD, and DUBA prevent association of TRAF6 and TRAF3 with their partners, in addition to remo
58 racts with TNF receptor-associated factor 6 (TRAF6) and attenuates IkappaB kinase beta-dependent (IKK
59 racts with TNF receptor associated factor 6 (TRAF6) and is required for mTORC1 translocation to the l
60 ecrosis factor receptor-associated factor 6 (TRAF6) and mammalian target of rapamycin (mTOR), respect
61 ike (Mal), TNF receptor-associated factor 6 (TRAF6), and IkappaB kinase (IKK)-related kinases, but no
62 r (TH9) cells in a TNFR-associated factor 6 (TRAF6)- and NF-kappaB-dependent manner and inhibited the
63 y decay of a "trafasome" comprised of IRAK1, TRAF6, and MAP3K proteins, abrogating downstream activat
64 h innate immune signaling proteins TRAF3 and TRAF6, and that vIRF-2 targeting of USP7 regulates HHV-8
65 BE2R1- (CDC34), UBE2N/UBE2V1- (UBC13/UEV1A), TRAF6- and HOIP-mediated chain assembly is inhibited by
66 stablished that the developmental defects of TRAF6- and integrin alpha3-null mouse kidneys are simila
67 -17A signal transduction triggers two broad, TRAF6- and TRAF5-dependent, intracellular signaling path
69 demonstrate that the levels and activity of TRAF6 are increased in skeletal muscle of mdx (a mouse m
70 abases further indicates that MUC1, TAK1 and TRAF6 are upregulated in tumors associated with decrease
73 We identified the ubiquitin-modifying enzyme TRAF6 as an interactor with the integrin beta1 subunit a
74 promote tumorigenesis and suggest DCBLD2 and TRAF6 as potential therapeutic targets for human cancers
75 tin ligase TNF receptor-associated factor 6 (TRAF6) as a SOD1 interactor, and we determined that expo
76 ecrosis factor receptor-associated factor 6 (TRAF6) as part of the Toll-like receptor-7 and -9 (TLR7/
78 ced NF-kappaB activation and IL-8 secretion, TRAF6 association with CD158d, and TRAF6 recruitment to
79 g NK cells with soluble Ab to CD158d induced TRAF6 association with CD158d, induced TAK1 phosphorylat
80 19A to catalyze K48-linked ubiquitination of TRAF6 at multiple sites, thereby leading to the degradat
81 ound that miR-146a and miR-146b targeting of Traf6 attenuates TCR signaling in the thymus and inhibit
82 antagomiR restores expressions of IRAK1 and TRAF6, augments IFNbeta production, inhibits viral propa
83 n IL-1beta stimulation, thereby facilitating TRAF6 auto-ubiquitination as well as NEMO/IKKgamma subst
84 cific protease 20 (USP20), which can reverse TRAF6 autoubiquitination, and by association with the mu
85 TRAF6 (pro-inflammatory) suggest that TRAF3/TRAF6 binding sites on MyD88 DD partially overlap, as do
86 tified a conserved TNFR-associated factor 6 (TRAF6) binding motif, which was required for CD158d-indu
87 ice expressing the TNFR-associated factor 6 (TRAF6) binding-defective mutant IRAK2[E525A] or the cata
93 the interactions between viperin, IRAK1, and TRAF6 by transiently expressing these enzymes in HEK 293
95 Furthermore, the catalytically dead mutant TRAF6 C70A abolished the TRAF6-mediated polyubiquitinati
97 tion of mTORC1 to the lysosomes and that the TRAF6-catalyzed K63 ubiquitination of mTOR regulates mTO
101 ecrosis factor receptor-associated factor 6 (TRAF6)-dependent signaling, involved the mitogen-activat
102 at IL-18 synergizes with high-dose IL-7 in a TRAF6-dependent manner to induce slow, LIP/homeostatic-l
104 ls promoted osteoclastogenesis by activating TRAF6-dependent signaling pathways in osteoclast progeni
105 eceptor-dependent IL-10 induction, which was TRAF6-dependent, but the manner in which A52 manipulates
106 20 association and subsequent USP20-mediated TRAF6 deubiquitination were beta-arrestin2-dependent.
110 2 Y750 recruited TRAF6, leading to increased TRAF6 E3 ubiquitin ligase activity and subsequent activa
112 ture endosomes, RAB7 directly interacts with TRAF6 E3 ubiquitin ligase, which catalyzes K63 polyubiqu
113 g the human Rac2(D57N) mutant, disrupted the TRAF6-ECSIT complex by sequestering TRAF6 and substantia
114 ike receptor (TLR)-triggered assembly of the TRAF6-ECSIT complex that is required for the recruitment
115 regulates K63 polyubiquitination activity of TRAF6, enhances NF-kappaB activation and activation-indu
118 ned that satellite cell-specific deletion of Traf6 exaggerates the dystrophic phenotype in the mdx (a
121 TEC depletion due to conditional deletion of Traf6 expression in murine thymic epithelial cells (Traf
122 n and an important signaling network of SKP2-TRAF6-EZH2/H3K27me3, and targeting SKP2-EZH2 pathway may
124 hage-specific deletion of TRAF6 (LysM(C)(re) Traf6 (fl/fl) ) or mTOR (LysM(C)(re) Mtor(fl/fl) ) did n
125 ic rejection in CTLA4-Ig-treated LysM(C)(re) Traf6 (fl/fl) mice was similar to that of CTLA4-Ig-treat
126 n, whereas the similarly treated LysM(C)(re) Traf6 (fl/fl) recipients developed severe transplant vas
129 n machinery, likely through interaction with TRAF6 for the assembly of "intracellular membrane signal
130 0 phosphorylation-dependent translocation of TRAF6 from cytosol to nucleus, where TRAF6 also facilita
131 trated that hepatitis C virus (HCV) depleted TRAF6 from its host cells through a posttranslational me
137 tor (IL-1R)-mediated activation of NFkappaB, TRAF6 has since been identified as an actor downstream o
139 study suggests that while the inhibition of TRAF6 improves muscle structure and function in young md
141 Collectively, our findings reveal a role for TRAF6 in directing DC maintenance of intestinal immune t
145 therapeutic potential of inhibition of CD40-TRAF6 in obesity, DIO mice were treated with a small-mol
147 ing the expression of the signaling mediator Traf6 in RLR deficient embryos restored HSPC numbers.
150 extensive interaction between tRXRalpha and TRAF6 in the cytoplasm of macrophages, leading to TRAF6
152 s widely accepted that the essential role of TRAF6 in vivo is to generate the Lys63-linked ubiquitin
154 signaling activated the E3 ubiquitin ligase TRAF6, increasing K63-linked ubiquitination and enhancin
156 lled by all SOD1 variants and differentiated TRAF6 interacting from TRAF6 noninteracting SOD1 variant
157 domain of NOSTRIN is involved in the NOSTRIN-TRAF6 interaction and is required for NOSTRIN-induced do
158 duction in BMDM and pDCs, and that the IRAK2-TRAF6 interaction is needed to sustain IkappaB-inducing
161 naling pathway was used instead of the IRAK2-TRAF6 interaction to sustain late-phase mRNA production.
162 arrow-derived macrophages (BMDMs), the IRAK2-TRAF6 interaction was required for the late (2-8 h) but
164 cations associated with obesity whereas CD40-TRAF6 interactions in MHCII(+) cells aggravate these com
165 that we designed to specifically block CD40-TRAF6 interactions; this compound improved insulin sensi
166 pregulates miR-146a, which targets IRAK1 and TRAF6 involved in TLR signalling and type I interferon p
167 ify mechanisms of contextual specificity for TRAF6, involving both regulatory protein interactions, a
168 ion, senescence, and apoptosis controlled by TRAF6/IRAK-dependent activation of AP1 and TP53 mediated
169 feedback mechanism involving the miR-146a/b-TRAF6/IRAK1-NF-kappaB axis in promoting DC apoptosis.
170 Taken together, our results support that TRAF6 is a key molecule that mediates the interaction be
172 lls and stromal fibroblasts, suggesting that TRAF6 is a potentially promising target in melanoma ther
177 In response to toll-like receptor ligands, TRAF6 is demethylated by the Jumonji domain protein JMJD
185 athways, the poly-ubiquitination of IRAK1 by TRAF6 is necessary to activate IRAK1, which then phospho
187 factor receptor (TNFR)-associated factor 6 (TRAF6) is an adapter protein that mediates a wide array
190 factor receptor (TNFR)-associated factor 6 (TRAF6) is an important adaptor molecule that mediates th
192 biquitin-conjugating enzyme that facilitates TRAF6 K63-linked ubiquitination and NF-kappaB activation
194 mutants partially restored IL-1 signaling in TRAF6 KO cells, but not in TRAF6/Pellino1/Pellino2 tripl
197 of bone marrow to osteoclasts was similar in TRAF6[L74H] and wild-type cells, explaining why the bone
199 ockin mice expressing the E3 ligase-inactive TRAF6[L74H] mutant, but the late-phase production of IL-
200 ectly with TNF receptor-associated factor 6 (TRAF6), leading to the suppression of NFkappaB activity
201 ly, phosphorylation of DCBLD2 Y750 recruited TRAF6, leading to increased TRAF6 E3 ubiquitin ligase ac
205 showed that macrophage-specific deletion of TRAF6 (LysM(C)(re) Traf6 (fl/fl) ) or mTOR (LysM(C)(re)
208 atively regulated TNF receptor associated 6 (TRAF6)-mediated ubiquitination and stabilization of hypo
210 , such as TAK1, IKKs, and PP2A, that impairs TRAF6-mediated activation of NF-kappaB and expression of
211 s in human PCa cells through upregulation of TRAF6-mediated and lysine(K) 63-linked ubiquitination of
212 d to be a direct E3 ligase for GSK3beta, and TRAF6-mediated GSK3beta ubiquitination is essential for
213 n of hDNA2 localization and establishes that TRAF6-mediated hDNA2 ubiquitination activates DNA repair
214 e discovered a novel regulatory axis through TRAF6-mediated IRE1alpha ubiquitination in regulating TL
216 dispensable for the latter, indicating that TRAF6-mediated polyubiquitination and aggregation of the
217 tically dead mutant TRAF6 C70A abolished the TRAF6-mediated polyubiquitination of recombinant human E
224 MT1/JMJD6 ratio significantly correlate with TRAF6 methylation, basal activation of NF-kappaB, and ma
227 ctive removal of Lys63-linked ubiquitin from TRAF6, NEMO and RIP1 after stimulation with tumor necros
229 as evidenced by increased levels of p-TAK1, TRAF6, NF-kappaB p50, phospho-NF-kappaB- p65, pCREB, HMG
232 by addition of IL-1beta or overexpression of TRAF6 or IKKbeta, the kinase needed for IkappaBalpha pho
234 ectal cancer samples with WT p53 reveal that TRAF6 overexpression negatively correlates with apoptosi
236 of IRAK1, IRAK4, and MyD88 was abolished in TRAF6/Pellino1/Pellino2 triple-knockout (KO) cells, but
239 ith TRAF3 (anti-viral/anti-inflammatory) and TRAF6 (pro-inflammatory) suggest that TRAF3/TRAF6 bindin
244 ecretion, TRAF6 association with CD158d, and TRAF6 recruitment to CD158d(+) endosomes in transfected
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 n inhibits the interaction between UBC13 and TRAF6 RING-domain (TRAF6(RING)) by perturbing both the n
250 raction between UBC13 and TRAF6 RING-domain (TRAF6(RING)) by perturbing both the native and transient
251 cting with TRAF6, was unable to cause either TRAF6 self-association, induce the TRAF6-TAK1 associatio
260 as a scaffold molecule to independently bind TRAF6, TAK1, IkappaB kinase alpha, and IkappaB kinase be
262 tivation pathway facilitated through a STING-TRAF6-TBK1 axis and suggest a target for therapeutic int
263 ds to the C-terminal TRAF homology domain of TRAF6 that also serves as the interaction surface for th
265 ssion of classic miR-146a targets (IRAK1 and TRAF6), thereby blocking activation of NF-kappaB in targ
266 d that FGF19 was a key cytokine regulated by TRAF6 through NF-kappaB1 using luciferase assay and chro
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
273 ular mechanism whereby poxviruses manipulate TRAF6 to activate MAPKs (which can be proviral) without
274 sociation and abolishes the sequestration of TRAF6 to cytosolic p62 aggregates by a non-catalytic mec
276 s a scaffold protein by recruiting E3 ligase TRAF6 to IKK complex to activate NF-kappaB in response t
278 nt of ubiquitin ligases, including TRAF2 and TRAF6, to the vacuole membrane, which enhances recruitme
279 We now report that DC-specific deletion of TRAF6 (TRAF6DeltaDC) resulted, unexpectedly, in loss of
280 is consisting of miR-146a, signaling protein TRAF6, transcriptional factor NF-kappaB, and cytokine IL
281 appaB signaling through the ubiquitin ligase TRAF6 (tumor necrosis factor receptor-associated factor
282 ecrosis factor receptor-associated factor 6 (TRAF6), two proinflammatory cytokines of the TLR signali
283 ed by the IRAK2 variant was due to increased TRAF6 ubiquitination and faster IkappaBalpha degradation
284 in the cytoplasm of macrophages, leading to TRAF6 ubiquitination and subsequent activation of the NF
288 our protein interaction studies showed that TRAF6/USP20 association and subsequent USP20-mediated TR
293 52-M65E although capable of interacting with TRAF6, was unable to cause either TRAF6 self-association
295 vivo; mice with Treg-restricted deletion of TRAF6 were resistant to implanted tumors and displayed e
297 s factor (TNF) receptor-associated factor 6 (TRAF6), which are known target genes of miR-146a, leadin
298 AK1 and confers the association of TAK1 with TRAF6, which is necessary for TAK1-mediated activation o
299 K48-linked ubiquitination and degradation of TRAF6, which promotes activation of NF-kappaB and MAPK s