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抗Human TAB3 抗体:
抗Mouse (Murine) TAB3 抗体:
抗Rat (Rattus) TAB3 抗体:
The combination of WES, genomic triangulation, and systems biology has uncovered perturbations in TGF-beta activated kinase 1 (显示 MAP3K7 抗体) 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 (显示 NFKB1 抗体) pathway.
Upregulation of miR (显示 MLXIP 抗体)-532-5p and subsequent suppression of the SESTD1 (显示 SESTD1 抗体) and TAB3 genes represent an antiviral response aimed at limiting West Nile virus infection.
miR (显示 MLXIP 抗体)-30a in MSCs may participate in the immune dysregulation of the maternal-fetal interface during PE
miR (显示 MLXIP 抗体)-26b suppresses NF-kappaB (显示 NFKB1 抗体) signaling and sensitizes hepatocellular carcinoma cells to doxorubicin-induced apoptosis by inhibiting the expression of TAK1 (显示 MAP3K7 抗体) and TAB3.
conclude that TRIM38 (显示 TRIM38 抗体) negatively regulates TNFalpha (显示 TNF 抗体)- and IL-1beta (显示 IL1B 抗体)-induced signaling by mediating lysosome-dependent degradation of TAB2 (显示 TAB2 抗体)/3, two critical components in TNFalpha (显示 TNF 抗体)- and IL-1beta (显示 IL1B 抗体)-induced signaling pathways
Studies show that three proteins expressed in HEK (显示 EPHA3 抗体)-293T cells (NAP1 (显示 IL8 抗体), TANK and TBKBP1 (显示 TBKBP1 抗体)) interact with TBK1 (显示 TBK1 抗体).
MiR (显示 MLXIP 抗体)-23b suppresses IL-17 (显示 IL17A 抗体)-, tumor necrosis factor alpha (TNF-alpha (显示 TNF 抗体))- or IL-1beta (显示 IL1B 抗体)-induced NF-kappaB (显示 NFKB1 抗体) activation and inflammatory cytokine expression by targeting TAB2 (显示 TAB2 抗体), TAB3 and IKK-alpha (显示 CHUK 抗体).
Findings indicate that the absence of TAB3 plays a harmful role in ischemic heart disease
TAB2 (显示 TAB2 抗体) and TAB3 are essential for B cell activation (显示 BLNK 抗体) 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
, TAK-1 binding protein, hypothetical protein Zn finger
, mitogen-activated protein kinase kinase kinase 7 interacting protein 3 like
, LOW QUALITY PROTEIN: TGF-beta-activated kinase 1 and MAP3K7-binding protein 3