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Depletion of TRAF2 inhibits gastric cancer cell growth, migration and invasion. The expression of TRAF2 is increased in gastric tumor tissue.
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Results demonstrated that TRAF2 interacts physically with the N-terminal portion of FAK and colocalizes to cell membrane protrusions. This interaction was found to be critical for promoting resistance to cell anoikis. In breast cancer tissues, coamplification of TRAF2 and FAK was found to be predictive value for shorter survival, further supporting a potential role of TRAF2-FAK cooperative signaling in cancer progression.
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Ubiquitin E3 ligase TRAF2 reduces BMAL1 protein level.BMAL1 interacts with the zinc finger domain in TRAF2.TRAF2 promotes BMAL1 ubiquitination and degradation.TRAF2 attenuates the BMAL1 transcriptional activity.
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The authors found that tumor necrosis factor receptor-associated factor 2 (TRAF2), as well as TRAF1 and 3, directly binds to the active caspase-2 dimer.
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The up-regulation of TRAF2 may play an important role in the inhibition of chondrocyte apoptosis of facet joint osteoarthritis (FJOA).
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The TRAIP coiled-coil domain altered its stoichiometry between dimer and trimer in a concentration-dependent manner. Additionally, the TRAIP RING domain induced even higher-ordered assembly, which was necessary for interacting with the TRAF-N domain of TRAF2 but not TRAF1.
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high levels of CASC9.5 expression promote the proliferation, metastasis and metabolism of lung adenocarcinoma cells and might serve as a prognostic indicator.
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down-regulation of USP48 increases E-cadherin expression and epithelial barrier integrity through reducing TRAF2 stability
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DR5-Cbl-b/c-Cbl-TRAF2 complex inhibited TRAIL-induced apoptosis by promoting TRAF2-mediated polyubiquitination of caspase-8 in gastric cancer cells.
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CPNE1 overexpression can upregulate TRAF2 expression in prostate cancer DU-145 cells as determined by Western blotting and immunofluorescence assays.
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TRAF2 functions as an important modulator in tumor metastasis and tumor microenvironment formation and is a novel independent prognostic factor of gastric cancer.
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High expression of TRAF2 can predict poorer prognosis of GBM and was identified as an independent biomarker in GBM prognosis.
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TRAF2 can influence in vitro growth of TRAIL-treated DU-145 cells at least partially via regulating SIRT1 expression.
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Intestinal I/R induced the membrane translocation and phosphorylation of PKCzeta. Pretreatment with the PKCzeta activator phosphatidylcholine remarkably attenuated gut injury by suppressing apoptosis. H/R induced PKCzeta to combine with TRAF2, which was phosphorylated by PKCzeta at Ser(55), but not at Ser(11), under intestinal I/R or H/R conditions
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In conclusion, for the first time, we report that TRADD, TRAF2, RIP1 and TAK1 play a role in the regulating TNF-alpha signalling in human myometrium. These findings are of significance given the central role of TNF-alpha in the processes of human labour and delivery.
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Both S1P and caspase-8 are critical for TRAF2 stabilization, polyubiquitination, subsequent activation of JNK/AP1 signaling and MMP1 expression and final promotion of cell invasion.
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Results showed that high expression of TRAF2 was significantly associated with tumor stage of prostate cancer.
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The addition of nanomolar concentration of TRAF2 in GUVs also seems to exert a mechanical action.
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TRAF2 and OTUD7B govern a ubiquitin-dependent switch that regulates mTORC2 signalling
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destabilization of TRAF2 by miR-17 reduced the ability of TRAF2 to associate with cIAP2, resulting in the downregulation of TNF-alpha-induced NF-kappaBp65, c-Jun, and STAT3 nuclear translocation and the production of IL-6, IL-8, MMP-1, and MMP-13 in human rheumatoid arthritis synovial fibroblasts.