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