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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
19            TNF receptor-associated factor 6 (TRAF6), a verified target of miR-146a, was up-regulated
20  wild-type TLR3, leads to the recruitment of TRAF6, a downstream signal transducer of the MyD88-depen
21          We show that TRIM12c interacts with TRAF6, a key protein in the pathogen recognition recepto
22    This was due to reduced ubiquitination of TRAF6, a key step in signal transduction.
23                                              TRAF6, a TLR effector with ubiquitin (Ub) ligase activit
24  by Muto et al., MDS stem cells sparked with TRAF6-activated innate immune signaling were found to ou
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                            In the absence of TRAF6 activity or upon mutation of the ubiquitination si
29 sociation of TAB2 with its signaling partner TRAF6 after TLR ligation in B cells.
30 tion of TRAF6 from cytosol to nucleus, where TRAF6 also facilitates the K63-linked ubiquitination of
31                                  Ablation of TRAF6 also increases satellite cells proliferation and m
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
34                                              TRAF6, an E3 ubiquitin protein ligase, plays a critical
35 0, a member of the inflammasome pathway, and Traf6, an inflammatory signaling member.
36              Here, we identify an E3 ligase, Traf6 and a de-ubiquitinating enzyme, Cezanne/ZA20D1, as
37 formation of a molecular complex composed of TRAF6 and beta-arrestin-2.
38  by disrupting RANKL-induced localization of TRAF6 and c-SRC into lipid rafts and preventing nuclear
39 the inhibitory effect of Tbeta4 on IRAK1 and TRAF6 and decreased expression of MBP.
40 imDCs and mDCs was inversely correlated with TRAF6 and IRAK1 expression.
41 binds to the downstream signaling components TRAF6 and IRAK2.
42 IC3 loop, respectively, can directly recruit TRAF6 and its negative regulator ARRB2 to form a multi-p
43 for selective autophagy, as it could bind to TRAF6 and its silencing stabilized TRAF6.
44 cells leads to increased NUMBL and decreased TRAF6 and NEMO expression.
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
56              Furthermore, siRNA silencing of TRAF6 and/or IRAK1 in imDCs and mDCs enhanced DC apoptos
57    By contrast, lentivirus overexpression of TRAF6 and/or IRAK1 promoted DC survival.
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
68  proteins TNFR-associated factor (TRAF)3 and TRAF6 are important mediators of TLR signaling.
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
71               Together, our study identifies TRAF6 as a critical gatekeeper to restrict p53 mitochond
72                      These results implicate TRAF6 as a key posttranslational, Treg-stabilizing regul
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/
77      We show that YOD1 competes with p62 for TRAF6 association and abolishes the sequestration of TRA
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
88           Here, we report that the E3 ligase TRAF6 binds to and mediates the K63-linked polyubiquitin
89                                The E3 ligase TRAF6 binds to DCP1a and indirectly regulates DCP1a phos
90 drives R-RT in a pathway involving IRAK4 and TRAF6 but not the IL-1R/TLR-IRAK adaptor MyD88.
91                        Knockdown of RIP2 and TRAF6 by RNA interference and neutralization of interleu
92           Reversible arginine methylation of TRAF6 by the opposing effects of PRMT1 and JMJD6 is, the
93 the interactions between viperin, IRAK1, and TRAF6 by transiently expressing these enzymes in HEK 293
94                                    Moreover, TRAF6/c-JUN signaling repressed the levels of the microR
95   Furthermore, the catalytically dead mutant TRAF6 C70A abolished the TRAF6-mediated polyubiquitinati
96                                              Traf6 can promote the formation of Cdc42-dependent F-act
97 tion of mTORC1 to the lysosomes and that the TRAF6-catalyzed K63 ubiquitination of mTOR regulates mTO
98 e role of deamidation in silencing the UBC13/TRAF6 complex is unknown.
99 condary to aberrant assembly of a raptor-p62-TRAF6 complex.
100                          Here, we found that TRAF6-deficient Tregs were dysfunctional in vivo; mice w
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
103 IN85 in response to TGFbeta stimulation in a TRAF6-dependent manner.
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.
107 nd delayed TNF receptor-associated factor 6 (TRAF6) deubiquitination.
108                         Here, we report that TRAF6 E3 ligase activity contributes to but is not essen
109                           Here, we show that TRAF6 E3 ligase is a crucial factor to restrict mitochon
110 2 Y750 recruited TRAF6, leading to increased TRAF6 E3 ubiquitin ligase activity and subsequent activa
111                                              TRAF6 E3 ubiquitin ligase activity was required for the
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
116           Thus, K63-linked ubiquitination by TRAF6 ensures proper localization of FOXP3 and facilitat
117                    Intriguingly, ablation of TRAF6 exacerbates muscle injury and increases fibrosis i
118 ned that satellite cell-specific deletion of Traf6 exaggerates the dystrophic phenotype in the mdx (a
119 2 and accounted for hematopoietic defects in TRAF6-expressing HSPCs.
120               Meanwhile, the intervention of TRAF6 expression in melanoma cells affected the activati
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
123              Therefore, TLR/MyD88-dependent, TRAF6-facilitated CREBH activation represents a mammalia
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
127 c gene, inhibits TLR signalling by targeting TRAF6 for degradation.
128 nism by which the NLRP11-RNF19A axis targets TRAF6 for degradation.
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
132 he release of the essential ubiquitin ligase TRAF6 from the complex.
133               In multiple cellular contexts, TRAF6 function is essential not only for proper activati
134 complex in vitro with similar efficiently to TRAF6-generated K63-Ub chains.
135                          The adaptor protein TRAF6 has a central function in Toll-like receptor (TLR)
136                                 Furthermore, Traf6 has a key role in autocrine interleukin-1beta sign
137 tor (IL-1R)-mediated activation of NFkappaB, TRAF6 has since been identified as an actor downstream o
138                         Targeted deletion of TRAF6 improves muscle strength and reduces fiber necrosi
139  study suggests that while the inhibition of TRAF6 improves muscle structure and function in young md
140          GSK3beta physically associates with TRAF6 in a TLR3 ligand poly I:C-dependent manner.
141 Collectively, our findings reveal a role for TRAF6 in directing DC maintenance of intestinal immune t
142                  Moreover, the expression of TRAF6 in fibroblasts promoted the malignant phenotype of
143 enzyme YOD1 (OTUD2) as a novel interactor of TRAF6 in human cells.
144                         However, the role of TRAF6 in melanoma CAFs remains unclear.
145  therapeutic potential of inhibition of CD40-TRAF6 in obesity, DIO mice were treated with a small-mol
146                         However, the role of TRAF6 in pathogenesis of DMD remains unknown.
147 ing the expression of the signaling mediator Traf6 in RLR deficient embryos restored HSPC numbers.
148                        Selective deletion of Traf6 in satellite cells of adult mice led to profound m
149 ely, our study reveals an essential role for TRAF6 in satellite stem cell function.
150  extensive interaction between tRXRalpha and TRAF6 in the cytoplasm of macrophages, leading to TRAF6
151                         YOD1 associates with TRAF6 in unstimulated cells but is released upon IL-1bet
152 s widely accepted that the essential role of TRAF6 in vivo is to generate the Lys63-linked ubiquitin
153                       We show that IRAK1 and TRAF6 increase viperin activity ~10-fold to efficiently
154  signaling activated the E3 ubiquitin ligase TRAF6, increasing K63-linked ubiquitination and enhancin
155                                              TRAF6 inhibition reduces the markers of autophagy and Ak
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
159         Our results establish that the IRAK2-TRAF6 interaction is rate limiting for the late, but not
160                     Interfering with the p62-TRAF6 interaction serves to modulate autophagy and nutri
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
163 ivation of p62-associated mitophagy, and p62-TRAF6 interaction.
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
171                         The ubiquitin ligase TRAF6 is a key regulator of canonical IkappaB kinase (IK
172 lls and stromal fibroblasts, suggesting that TRAF6 is a potentially promising target in melanoma ther
173                                              TRAF6 is also an E3 ubiquitin ligase and an important re
174                                              TRAF6 is an important signaling molecule that mediates a
175                                              TRAF6 is critical for the production of inflammatory cyt
176         The intracellular signaling molecule TRAF6 is critical for Toll-like receptor (TLR)-mediated
177   In response to toll-like receptor ligands, TRAF6 is demethylated by the Jumonji domain protein JMJD
178                                              TRAF6 is determined to be a direct E3 ligase for GSK3bet
179 yubiquitination of the novel LUBAC substrate TRAF6 is essential for NFkappaB signaling.
180 n particular, its interaction with TRAF5 and TRAF6 is increased in the presence of IL-17A.
181                     We also demonstrate that TRAF6 is involved in the SopB/SopE2-induced phosphorylat
182                                  The adaptor TRAF6 is known to couple proximal signals from receptors
183                      Under basal conditions, TRAF6 is methylated by the methyltransferase PRMT1, and
184                            We also show that TRAF6 is necessary for the translocation of mTORC1 to th
185 athways, the poly-ubiquitination of IRAK1 by TRAF6 is necessary to activate IRAK1, which then phospho
186                            Here we show that TRAF6 is recruited to and activates mTORC1 through p62 i
187  factor receptor (TNFR)-associated factor 6 (TRAF6) is an adapter protein that mediates a wide array
188            TNF receptor-associated factor 6 (TRAF6) is an adaptor protein and an E3 ubiquitin ligase
189            TNF receptor-associated factor 6 (TRAF6) is an adaptor protein which acts as a signaling i
190  factor receptor (TNFR)-associated factor 6 (TRAF6) is an important adaptor molecule that mediates th
191            TNF receptor-associated factor 6 (TRAF6) is identified as a direct E3 ligase for PSD-95, w
192 biquitin-conjugating enzyme that facilitates TRAF6 K63-linked ubiquitination and NF-kappaB activation
193                                 In contrast, TRAF6 knockdown resulted in a reduced EZH2 ubiquitinatio
194 mutants partially restored IL-1 signaling in TRAF6 KO cells, but not in TRAF6/Pellino1/Pellino2 tripl
195 h of the TRAF6[L74H] mice was normal, unlike TRAF6 KO mice.
196 lino2 triple-knockout (KO) cells, but not in TRAF6 KO or Pellino1/2 double-KO cells.
197 of bone marrow to osteoclasts was similar in TRAF6[L74H] and wild-type cells, explaining why the bone
198 ning why the bone structure and teeth of the TRAF6[L74H] mice was normal, unlike TRAF6 KO mice.
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
202 ulator of donor T cells in GVHD by targeting TRAF6, leading to reduced TNF transcription.
203  reductions in IL-1R-associated kinase 1 and TRAF6 levels following LOS retreatment of cells.
204                                       Higher TRAF6 levels translated into increased nuclear factor-ka
205  showed that macrophage-specific deletion of TRAF6 (LysM(C)(re) Traf6 (fl/fl) ) or mTOR (LysM(C)(re)
206                     In addition to NFkappaB, TRAF6 may also direct activation of mitogen-activated pr
207 t the interaction between misfolded SOD1 and TRAF6 may be relevant to the etiology of ALS.
208 atively regulated TNF receptor associated 6 (TRAF6)-mediated ubiquitination and stabilization of hypo
209 gnaling, a process that was dependent on TLR-TRAF6-mediated activation of A20.
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
215                                   Inhibiting TRAF6-mediated polyubiquitination abolishes the nuclear
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
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                   Furthermore, we found that TRAF6-mediated ubiquitination of IRAK1 requires the asso
221                                              TRAF6-mediated ubiquitination was required for dissociat
222           Further analysis demonstrated that TRAF6 mediates K63-linked ubiquitination of CREBH to fac
223                                Specifically, TRAF6 mediates lysine-63 ubiquitination within the Src h
224 MT1/JMJD6 ratio significantly correlate with TRAF6 methylation, basal activation of NF-kappaB, and ma
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  as evidenced by increased levels of p-TAK1, TRAF6, NF-kappaB p50, phospho-NF-kappaB- p65, pCREB, HMG
230 nd increased apoptosis, which coincided with TRAF6/NF-kappaB inhibition.
231 ts and differentiated TRAF6 interacting from TRAF6 noninteracting SOD1 variants.
232 by addition of IL-1beta or overexpression of TRAF6 or IKKbeta, the kinase needed for IkappaBalpha pho
233                                We found that TRAF6 overexpression in mouse HSPC results in impaired h
234 ectal cancer samples with WT p53 reveal that TRAF6 overexpression negatively correlates with apoptosi
235 Hence, our data define that YOD1 antagonizes TRAF6/p62-dependent IL-1 signaling to NF-kappaB.
236  of IRAK1, IRAK4, and MyD88 was abolished in TRAF6/Pellino1/Pellino2 triple-knockout (KO) cells, but
237 IL-1 signaling in TRAF6 KO cells, but not in TRAF6/Pellino1/Pellino2 triple-KO cells.
238             The competitive advantage of TLR-TRAF6-primed HSPCs could be restored by deletion of A20
239 ith TRAF3 (anti-viral/anti-inflammatory) and TRAF6 (pro-inflammatory) suggest that TRAF3/TRAF6 bindin
240                Functional assays showed that TRAF6 promoted fibroblast proliferation and migration as
241                        Ectopic expression of TRAF6 promoted the K63-linked ubiquitination of EZH2 to
242           A previous study demonstrated that TRAF6 promotes the malignant phenotype of melanoma cells
243        In murine fibroblasts, GRA15-mediated TRAF6 recruitment mediates the recruitment of immunity-r
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 n inhibits the interaction between UBC13 and TRAF6 RING-domain (TRAF6(RING)) by perturbing both the n
249 termolecular salt-bridge at the native UBC13/TRAF6(RING) interface.
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
252                           Inhibition of CD40-TRAF6 signaling by our compound may provide a therapeuti
253        In contrast, mice with deficient CD40-TRAF6 signaling in MHCII(+) cells displayed no insulin r
254 astogenesis and bone resorption through RANK/TRAF6 signaling pathways.
255 ory protein (IL1RAP) SNP (rs10513854), and 1 TRAF6 SNP (rs5030411).
256                                Functionally, TRAF6 stimulated polyubiquitination and aggregation of t
257           Although beta-arrestin2 effects on TRAF6 suggest an anti-inflammatory role, physiologic bet
258                             The depletion of TRAF6 suppressed activation of NF-kappaB and induction o
259           In contrast, the overexpression of TRAF6 suppressed HCV replication.
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 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
264           We identify two essential roles of TRAF6 that are independent of its E3 ligase activity.
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
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 sociation and abolishes the sequestration of TRAF6 to cytosolic p62 aggregates by a non-catalytic mec
275 d CD40 signaling complexes failed to recruit TRAF6 to detergent-insoluble membrane fractions.
276 s a scaffold protein by recruiting E3 ligase TRAF6 to IKK complex to activate NF-kappaB in response t
277 ent, but the manner in which A52 manipulates TRAF6 to stimulate p38 activation was unclear.
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
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                                              TRAF6 was required for the activation of MAPKs ERK1/2 an
292                 In this study, we found that TRAF6 was significantly upregulated in CAFs adjacent to
293 52-M65E although capable of interacting with TRAF6, was unable to cause either TRAF6 self-association
294                               In contrast to TRAF6, we found TRAF5 to be an endogenous suppressor of
295  vivo; mice with Treg-restricted deletion of TRAF6 were resistant to implanted tumors and displayed e
296 und miR-146a target genes, such as IRAK1 and TRAF6, were manifestly downregulated.
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
300 ilomycin A1, which led to the association of TRAF6 with autophagosomes.

 
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