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The overexpression of miR-146a significantly increased the ErbB4 expression, decreased the expression of TRAF6, IRAK1, caspase 3, and the phosphorylation level of NF-kappaB, and also increased the Bcl-2/Bax ratio, suggesting the inhibition of inflammation and apoptosis.
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TRAF6 can promote the proliferation of stromal cells of benign prostatic hyperplasia via Akt/mTOR signaling.
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Study identified IRAK1 and TRAF6 are direct targets of miR-146a in cervical cancer cells. Their expression is downregulated by miR-146a to promote cell viability.
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Immune profiling of human prostate epithelial cells in health and pathology determined by expression of p38/TRAF-6/ERK MAP kinases pathways has been reported.
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Downregulation of miR-124 in human osteosarcoma tissues and cell lines may increase the expression of TRAF6 protein. miR-124 may inhibit cell cycle progression and invasion of osteosarcoma cells, and promote apoptosis by regulating TRAF6.
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Low TRAF6 expression is associated with posterior longitudinal ligament ossification.
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these results suggest that miR-146a-5p affects proliferation and apoptosis in a cellular context-dependent manner and selectively disarms the TRAF6-mediated branch of the TGF-beta signaling in oral squamous cell carcinoma cell lines by sparing Smad4 involvement
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MALT1 and TRAF6 cooperatively interact with CARMA1-BCL10 filaments and form CARMA1-BCL10-MALT1-TRAF6 signalosome.
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our data demonstrated that miR146b5p, as a tumor suppressor, mediated temozolomide resistance in GBM cells through negatively regulating TRAF6 expression, indicating that miR146b5p and its targeted genes would be potential therapeutic targets for glioma therapy.
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genetic association studies in Han population in southern China: Data suggest that, in subjects with type 2 diabetes, an SNP in NLRX1 (rs4245191) is associated with macro-vascular complications and cerebral infarction in the population studied; no such association was found for two other SNPs in NLRX1 (rs10790286, rs561830) or for two SNPs in TRAF6 (rs5030445, rs16928973). (NLRX1 = NLR family member-X1)
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protein-protein interaction studies on TRAF6 and BSG to get molecular level insights of the reactions.
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miR-146a suppresses the inflammatory response in human white adipocytes via targeting the expression of IRAK1 and TRAF6.
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miRNA146a expression was significantly higher in hepatitis C patients with a best cut off value 1.63 to discriminate between hepatitis C patients and healthy controls. Meanwhile, it was negatively correlated to IRAK1 and TRAF6 levels and positively correlated to viral load in hepatitis C patients.
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Suggest role for EBV-EBER1 in the induction of increased TRAF6 expression in the peripheral B cells of Sjogren's patients.
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theses results indicate that miR-146b-5p inhibits tumor growth and metastasis of hepatocellular carcinoma by targeting TRAF6 mediated Akt phosphorylation
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TRAF6 plays direct roles in the pro-inflammatory effects and proliferation of Rheumatoid arthritis (RA) fibroblast-like synoviocytes. TRAF6 may serve as a potential treatment target in RA.
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MiR-146a declined, while TRAF6 increased in lupus nephritis patients compared with healthy controls.
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Epigallocatechin-3-gallate is a novel E3 ubiquitin ligase inhibitor that could be used to target TRAF6 activity in melanoma cells, inhibiting cell proliferation/migration.
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Results identified TRAF6 as a direct target of miR-429, and its downregulation partially attenuates the effect of miR-429 in promoting hepatocellular carcinoma cell proliferation and motility.
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Compared with normal chondrocytes, the expression of miR-146a decreased, while the mRNA and protein expressions of TRAF6 and NF-kappaB increased in osteoarthritis chondrocytes.
