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multiple GPCR agonists utilize non-canonical TAB1-TAB2 and TAB1-TAB3-dependent p38 activation to promote endothelial inflammatory responses.
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TAB3 may play a significant role at the level of T-cell activation and may also be a candidate biomarker for peanut allergy.
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these results demonstrated that TAB3 may be a promising therapeutic target for the treatment of Esophageal squamous cell carcinoma.
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The combination of WES, genomic triangulation, and systems biology has uncovered perturbations in TGF-beta activated kinase 1 signaling as a novel pathogenic substrate for polyvalvular syndrome.
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Our study provides insights into the mechanism of TAB3 regulating activity and suggests its important implications in triple negative breast cancer metastasis.
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Data show that knockdown of transforming growth factor-activated kinase 1 (TAK1)-binding protein 3 (TAB3) inhibited proliferation of non-small cell lung cancer (NSCLC) cells.
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TAB3 regulated ovarian cancer cell bioactivity and chemotherapy performance via the NF-kappaB pathway.
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Upregulation of miR-532-5p and subsequent suppression of the SESTD1 and TAB3 genes represent an antiviral response aimed at limiting West Nile virus infection.
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miR-30a in MSCs may participate in the immune dysregulation of the maternal-fetal interface during PE
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miR-26b suppresses NF-kappaB signaling and sensitizes hepatocellular carcinoma cells to doxorubicin-induced apoptosis by inhibiting the expression of TAK1 and TAB3.
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conclude that TRIM38 negatively regulates TNFalpha- and IL-1beta-induced signaling by mediating lysosome-dependent degradation of TAB2/3, two critical components in TNFalpha- and IL-1beta-induced signaling pathways
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Studies show that three proteins expressed in HEK-293T cells (NAP1, TANK and TBKBP1) interact with TBK1.
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MiR-23b suppresses IL-17-, tumor necrosis factor alpha (TNF-alpha)- or IL-1beta-induced NF-kappaB activation and inflammatory cytokine expression by targeting TAB2, TAB3 and IKK-alpha.
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human TAB2 and TAB3, ubiquitin-chain sensory proteins involved in NF-kappaB signalling, are directly inactivated by enteropathogenic Escherichia coli NleE, a conserved bacterial type-III-secreted effector responsible for blocking host NF-kappaB signalling
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These results point to the existence of an autophagy-stimulatory 'switch' whereby TAB2 and TAB3 abandon inhibitory interactions with Beclin 1 to engage in a stimulatory liaison with TAK1.
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TAB3 is involved in IL-1-induced NF-kappaB activation by physically linking TAK1 to TRAF6.
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Identification of TAB3 as a binding partner of the protein kinase TAK1.
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TAB3 transforming growth factor is a constituent of the NF-kappaB pathway functioning upstream of tumor necrosis factor alpha-associated factor 6/transforming growth factor beta-activated kinase
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Data show that TAB2 and TAB3 are receptors that bind preferentially to polyubiquitin chains through a highly conserved zinc finger (ZnF) domain, and activate NF-kappa B and IKK.
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The TAB2/TAB3 interaction with TAK1 is crucial for the activation of signaling cascades mediated by interleukin-1, tumor necrosis factor, and receptor activator of nuclear factor-kappa B ligand (RANKL).