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