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抗Human TAB1 抗体:
抗Mouse (Murine) TAB1 抗体:
抗Rat (Rattus) TAB1 抗体:
we show that IL-1 (显示 IL1A 抗体) induces robust p38a (显示 MAPK14 抗体) activation both in the nucleus and in the cytoplasm/membrane.Following stimulation, p38a (显示 MAPK14 抗体) activity returns to a basal level in absence of receptor degradation. While nuclear pulse is controlled by MKP1 (显示 DUSP1 抗体) through a negative feedback to pp38, its basal activity is controlled by both TAB1 and MKP1 (显示 DUSP1 抗体) through a positive feedback loop.
TAK1 (显示 MAP3K7 抗体)/TAB1 expression in non-small cell lung carcinoma tissue is significantly increased and closely associated with patient clinical prognosis.
miR (显示 MLXIP 抗体)-29a repressed TAB1-mediated TIMP-1 (显示 TIMP1 抗体) production in dermal fibroblasts, demonstrating that miR (显示 MLXIP 抗体)-29a may be a therapeutic target in SSc (显示 CYP11A1 抗体).
Data indicate that mitogen-activated protein kinase (显示 MAPK1 抗体) (MAPK) p38 (显示 MAPK1 抗体) activation is triggered by AMP (显示 APRT 抗体)-activated protein kinases (AMPK (显示 PRKAA1 抗体)) and mediated by TAB1 protein.
The amino acid sequence between positions 373 and 502 of TAB1 is required for TP interaction.
USP18 (显示 USP18 抗体) inhibits NF-kappaB (显示 NFKB1 抗体) and NFAT (显示 NFATC1 抗体) activation during Th17 differentiation by deubiquitinating the TAK1 (显示 MAP3K7 抗体)-TAB1 complex.
We found that endothelial TAK1 (显示 MAP3K7 抗体) and TAB2 (显示 TAB2 抗体), but not TAB1, were critically involved in vascular formation
TAK1 (显示 MAP3K7 抗体) plays a critical role in accentuated epithelial to mesenchymal transition in obliterative bronchiolitis after lung transplantation.
data suggest a complex role of aa 452-457 of TAB1 in controlling p38 MAPK (显示 MAPK14 抗体) activity and subcellular localization and implicate these residues in TAK1 (显示 MAP3K7 抗体)- or p38 MAPK (显示 MAPK14 抗体)-dependent post-transcriptional control of gene expression
Phosphorylation and polyubiquitination of TAK1 (显示 MAP3K7 抗体) are necessary for activation of NF-kappaB (显示 NFKB1 抗体) by the Kaposi's sarcoma-associated herpesvirus vGPCR.
our study uncovers that RNF114 (显示 RNF114 抗体)-mediated ubiquitination and degradation of TAB1 activate the NF-kappaB (显示 NFKB1 抗体) pathway during MZT, and thus directly link maternal clearance to early embryo development.
We confirmed that PGC (显示 PGC 抗体)-1b inhibited downstream inflammatory signals via binding with TAB1 and thus preventing TAB1/TAK1 (显示 NR2C2 抗体) binding and TAK1 (显示 NR2C2 抗体) activation.
The E3 ubiquitin ligase (显示 MUL1 抗体) Itch inhibits p38alpha (显示 MAPK14 抗体) signaling and skin inflammation through the ubiquitylation of Tab1.
TAB1 and TAB2 (显示 TAB2 抗体) are required for activated macrophages, making TAB1 and TAB2 (显示 TAB2 抗体) effective targets to control inflammation by modulating macrophage survival.
Both the MEKK1 (显示 MAP2K1 抗体) PHD (显示 PDC 抗体) and TAB1 are critical for ES-cell differentiation
The enhanced JNK (显示 MAPK8 抗体) and IkappaB kinase (显示 CHUK 抗体) activation in DUSP14 (显示 DUSP14 抗体)-deficient T cells was attenuated by TAB1 short hairpin RNA knockdown.
TAB1 binding stabilizes active p38alpha (显示 MAPK14 抗体) and induces rearrangements within the activation segment by helical extension of the Thr (显示 TRH 抗体)-Gly-Tyr (显示 TYR 抗体) motif, allowing autophosphorylation in cis (显示 CISH 抗体)
We found that endothelial TAK1 (显示 NR2C2 抗体) and TAB2 (显示 TAB2 抗体), but not TAB1, were critically involved in vascular formation
O-GlcNAcylation of TAB1 is required for full TAK1 (显示 NR2C2 抗体) activation upon stimulation with IL-1 (显示 IL1A 抗体)/osmotic stress.
Epithelial TAK1 (显示 NR2C2 抗体) activity is regulated through two unique, TAB1-dependent basal & TAB2 (显示 TAB2 抗体)-mediated stimuli-dependent mechanisms.
The protein encoded by this gene was identified as a regulator of the MAP kinase kinase kinase MAP3K7/TAK1, which is known to mediate various intracellular signaling pathways, such as those induced by TGF beta, interleukin 1, and WNT-1. This protein interacts and thus activates TAK1 kinase. It has been shown that the C-terminal portion of this protein is sufficient for binding and activation of TAK1, while a portion of the N-terminus acts as a dominant-negative inhibitor of TGF beta, suggesting that this protein may function as a mediator between TGF beta receptors and TAK1. This protein can also interact with and activate the mitogen-activated protein kinase 14 (MAPK14/p38alpha), and thus represents an alternative activation pathway, in addition to the MAPKK pathways, which contributes to the biological responses of MAPK14 to various stimuli. Alternatively spliced transcript variants encoding distinct isoforms have been reported.
TAK1-binding protein 1
, TGF-beta-activated kinase 1 and MAP3K7-binding protein 1
, mitogen-activated protein kinase kinase kinase 7-interacting protein 1
, transforming growth factor beta-activated kinase-binding protein 1
, TGF-beta-activated kinase 1-binding protein 1
, Tak1-binding protein 1
, beta activated kinase-1 binding protein-1
, mitogen activated protein kinase kinase kinase 7 interacting protein 1
, mitogen-activated protein kinase kinase kinase 7 interacting protein 1