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High TAB1 expression is associated with colorectal cancer.
TAB1 was identified as a functional target of miR (zeige MLXIP Proteine)-134, and the expression of TAB1 was increased by the transcription factors of NF-kappaB1 (zeige NFKB1 Proteine), c-Rel (zeige NFkBP65 Proteine), and ELK1 (zeige ELK1 Proteine) via miR (zeige MLXIP Proteine)-134.
we show that IL-1 (zeige IL1A Proteine) induces robust p38a (zeige MAPK14 Proteine) activation both in the nucleus and in the cytoplasm/membrane.Following stimulation, p38a (zeige MAPK14 Proteine) activity returns to a basal level in absence of receptor degradation. While nuclear pulse is controlled by MKP1 (zeige DUSP1 Proteine) through a negative feedback to pp38, its basal activity is controlled by both TAB1 and MKP1 (zeige DUSP1 Proteine) through a positive feedback loop.
TAK1 (zeige MAP3K7 Proteine)/TAB1 expression in non-small cell lung carcinoma tissue is significantly increased and closely associated with patient clinical prognosis.
miR (zeige MLXIP Proteine)-29a repressed TAB1-mediated TIMP-1 (zeige TIMP1 Proteine) production in dermal fibroblasts, demonstrating that miR (zeige MLXIP Proteine)-29a may be a therapeutic target in SSc (zeige CYP11A1 Proteine).
Data indicate that mitogen-activated protein kinase (zeige MAPK1 Proteine) (MAPK) p38 (zeige MAPK1 Proteine) activation is triggered by AMP (zeige APRT Proteine)-activated protein kinases (AMPK (zeige PRKAA1 Proteine)) and mediated by TAB1 protein.
The amino acid sequence between positions 373 and 502 of TAB1 is required for TP interaction.
USP18 (zeige USP18 Proteine) inhibits NF-kappaB (zeige NFKB1 Proteine) and NFAT (zeige NFATC1 Proteine) activation during Th17 differentiation by deubiquitinating the TAK1 (zeige MAP3K7 Proteine)-TAB1 complex.
We found that endothelial TAK1 (zeige MAP3K7 Proteine) and TAB2 (zeige TAB2 Proteine), but not TAB1, were critically involved in vascular formation
TAK1 (zeige MAP3K7 Proteine) plays a critical role in accentuated epithelial to mesenchymal transition in obliterative bronchiolitis after lung transplantation.
our study uncovers that RNF114 (zeige RNF114 Proteine)-mediated ubiquitination and degradation of TAB1 activate the NF-kappaB (zeige NFKB1 Proteine) pathway during MZT, and thus directly link maternal clearance to early embryo development.
We confirmed that PGC (zeige PGC Proteine)-1b inhibited downstream inflammatory signals via binding with TAB1 and thus preventing TAB1/TAK1 (zeige NR2C2 Proteine) binding and TAK1 (zeige NR2C2 Proteine) activation.
The E3 ubiquitin ligase (zeige MUL1 Proteine) Itch inhibits p38alpha (zeige MAPK14 Proteine) signaling and skin inflammation through the ubiquitylation of Tab1.
TAB1 and TAB2 (zeige TAB2 Proteine) are required for activated macrophages, making TAB1 and TAB2 (zeige TAB2 Proteine) effective targets to control inflammation by modulating macrophage survival.
Both the MEKK1 (zeige MAP2K1 Proteine) PHD (zeige PDC Proteine) and TAB1 are critical for ES-cell differentiation
The enhanced JNK (zeige MAPK8 Proteine) and IkappaB kinase (zeige CHUK Proteine) activation in DUSP14 (zeige DUSP14 Proteine)-deficient T cells was attenuated by TAB1 short hairpin RNA knockdown.
TAB1 binding stabilizes active p38alpha (zeige MAPK14 Proteine) and induces rearrangements within the activation segment by helical extension of the Thr (zeige TRH Proteine)-Gly-Tyr (zeige TYR Proteine) motif, allowing autophosphorylation in cis (zeige CISH Proteine)
We found that endothelial TAK1 (zeige NR2C2 Proteine) and TAB2 (zeige TAB2 Proteine), but not TAB1, were critically involved in vascular formation
O-GlcNAcylation of TAB1 is required for full TAK1 (zeige NR2C2 Proteine) activation upon stimulation with IL-1 (zeige IL1A Proteine)/osmotic stress.
Epithelial TAK1 (zeige NR2C2 Proteine) activity is regulated through two unique, TAB1-dependent basal & TAB2 (zeige TAB2 Proteine)-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