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anti-Human TAB3 Antibodies:
anti-Mouse (Murine) TAB3 Antibodies:
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Human Polyclonal TAB3 Primary Antibody for IF (p), IHC (p) - ABIN801873
Hussain, Zhao, Shah, Wang, Yue, Liao, Sabir, Yang, Zhou et al.: MicroRNA 27a-3p Regulates Antimicrobial Responses of Murine Macrophages Infected by Mycobacterium avium subspecies paratuberculosis by Targeting Interleukin-10 and TGF-β-Activated Protein Kinase 1 ... in Frontiers in immunology 2017
Show all 2 Pubmed References
Human Polyclonal TAB3 Primary Antibody for ELISA - ABIN548013
Lu, Lin, Huang, Kang, Rich, Lo, Myszka, Han, Wu: XIAP induces NF-kappaB activation via the BIR1/TAB1 interaction and BIR1 dimerization. in Molecular cell 2007
multiple GPCR agonists utilize non-canonical TAB1-TAB2 and TAB1-TAB3-dependent p38 activation to promote endothelial inflammatory responses.
TAB3 may play a significant role at the level of T-cell activation and may also be a candidate biomarker for peanut allergy.
these results demonstrated that TAB3 may be a promising therapeutic target for the treatment of Esophageal squamous cell carcinoma.
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.
Our study provides insights into the mechanism of TAB3 regulating activity and suggests its important implications in triple negative breast cancer metastasis.
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.
TAB3 regulated ovarian cancer cell bioactivity and chemotherapy performance via the NF-kappaB pathway.
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.
miR-30a in MSCs may participate in the immune dysregulation of the maternal-fetal interface during PE
miR-26b suppresses NF-kappaB signaling and sensitizes hepatocellular carcinoma cells to doxorubicin-induced apoptosis by inhibiting the expression of TAK1 and TAB3.
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
Studies show that three proteins expressed in HEK-293T cells (NAP1, TANK and TBKBP1) interact with TBK1.
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.
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
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.
TAB3 is involved in IL-1-induced NF-kappaB activation by physically linking TAK1 to TRAF6.
Identification of TAB3 as a binding partner of the protein kinase TAK1.
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
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.
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).
Findings indicate that the absence of TAB3 plays a harmful role in ischemic heart disease
TAB2 and TAB3 are essential for B cell activation leading to antigen-specific antibody responses, as well as B-1 and marginal zone B cell development.
The product of this gene functions in the NF-kappaB signal transduction pathway. The encoded protein, and the similar and functionally redundant protein MAP3K7IP2/TAB2, forms a ternary complex with the protein kinase MAP3K7/TAK1 and either TRAF2 or TRAF6 in response to stimulation with the pro-inflammatory cytokines TNF or IL-1. Subsequent MAP3K7/TAK1 kinase activity triggers a signaling cascade leading to activation of the NF-kappaB transcription factor. The human genome contains a related pseudogene. Alternatively spliced transcript variants have been described, but their biological validity has not been determined.
NF-kappa-B-activating protein 1
, NFkB activating protein 1
, TAK1-binding protein 3
, TGF-beta-activated kinase 1 and MAP3K7-binding protein 3
, TGF-beta-activated kinase 1-binding protein 3
, mitogen-activated protein kinase kinase kinase 7 interacting protein 3
, mitogen activated protein kinase kinase kinase 7 interacting protein 3
, mitogen-activated protein kinase kinase kinase 7-interacting protein 3
, TGF-beta activated kinase 1/MAP3K7 binding protein 3
, mitogen-activated protein kinase kinase kinase 7-interacting protein 3-like
, mitogen-activated protein kinase kinase kinase 7 interacting protein 3 like
, LOW QUALITY PROTEIN: TGF-beta-activated kinase 1 and MAP3K7-binding protein 3