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TAB1 was identified as a functional target of miR (显示 MLXIP 蛋白)-134, and the expression of TAB1 was increased by the transcription factors of NF-kappaB1 (显示 NFKB1 蛋白), c-Rel (显示 NFkBP65 蛋白), and ELK1 (显示 ELK1 蛋白) via miR (显示 MLXIP 蛋白)-134.
we show that IL-1 (显示 IL1A 蛋白) induces robust p38a (显示 MAPK14 蛋白) activation both in the nucleus and in the cytoplasm/membrane.Following stimulation, p38a (显示 MAPK14 蛋白) activity returns to a basal level in absence of receptor degradation. While nuclear pulse is controlled by MKP1 (显示 DUSP1 蛋白) through a negative feedback to pp38, its basal activity is controlled by both TAB1 and MKP1 (显示 DUSP1 蛋白) through a positive feedback loop.
TAK1 (显示 MAP3K7 蛋白)/TAB1 expression in non-small cell lung carcinoma tissue is significantly increased and closely associated with patient clinical prognosis.
miR (显示 MLXIP 蛋白)-29a repressed TAB1-mediated TIMP-1 (显示 TIMP1 蛋白) production in dermal fibroblasts, demonstrating that miR (显示 MLXIP 蛋白)-29a may be a therapeutic target in SSc (显示 CYP11A1 蛋白).
Data indicate that mitogen-activated protein kinase (显示 MAPK1 蛋白) (MAPK) p38 (显示 MAPK1 蛋白) activation is triggered by AMP (显示 APRT 蛋白)-activated protein kinases (AMPK (显示 PRKAA1 蛋白)) 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 蛋白) inhibits NF-kappaB (显示 NFKB1 蛋白) and NFAT (显示 NFATC1 蛋白) activation during Th17 differentiation by deubiquitinating the TAK1 (显示 MAP3K7 蛋白)-TAB1 complex.
We found that endothelial TAK1 (显示 MAP3K7 蛋白) and TAB2 (显示 TAB2 蛋白), but not TAB1, were critically involved in vascular formation
TAK1 (显示 MAP3K7 蛋白) 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 蛋白) activity and subcellular localization and implicate these residues in TAK1 (显示 MAP3K7 蛋白)- or p38 MAPK (显示 MAPK14 蛋白)-dependent post-transcriptional control of gene expression
our study uncovers that RNF114 (显示 RNF114 蛋白)-mediated ubiquitination and degradation of TAB1 activate the NF-kappaB (显示 NFKB1 蛋白) pathway during MZT, and thus directly link maternal clearance to early embryo development.
We confirmed that PGC (显示 PGC 蛋白)-1b inhibited downstream inflammatory signals via binding with TAB1 and thus preventing TAB1/TAK1 (显示 NR2C2 蛋白) binding and TAK1 (显示 NR2C2 蛋白) activation.
The E3 ubiquitin ligase (显示 MUL1 蛋白) Itch inhibits p38alpha (显示 MAPK14 蛋白) signaling and skin inflammation through the ubiquitylation of Tab1.
TAB1 and TAB2 (显示 TAB2 蛋白) are required for activated macrophages, making TAB1 and TAB2 (显示 TAB2 蛋白) effective targets to control inflammation by modulating macrophage survival.
Both the MEKK1 (显示 MAP2K1 蛋白) PHD (显示 PDC 蛋白) and TAB1 are critical for ES-cell differentiation
The enhanced JNK (显示 MAPK8 蛋白) and IkappaB kinase (显示 CHUK 蛋白) activation in DUSP14 (显示 DUSP14 蛋白)-deficient T cells was attenuated by TAB1 short hairpin RNA knockdown.
TAB1 binding stabilizes active p38alpha (显示 MAPK14 蛋白) and induces rearrangements within the activation segment by helical extension of the Thr (显示 TRH 蛋白)-Gly-Tyr (显示 TYR 蛋白) motif, allowing autophosphorylation in cis (显示 CISH 蛋白)
We found that endothelial TAK1 (显示 NR2C2 蛋白) and TAB2 (显示 TAB2 蛋白), but not TAB1, were critically involved in vascular formation
O-GlcNAcylation of TAB1 is required for full TAK1 (显示 NR2C2 蛋白) activation upon stimulation with IL-1 (显示 IL1A 蛋白)/osmotic stress.
Epithelial TAK1 (显示 NR2C2 蛋白) activity is regulated through two unique, TAB1-dependent basal & TAB2 (显示 TAB2 蛋白)-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