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TAK1 (show MAP3K7 ELISA Kits)/TAB1 expression in non-small cell lung carcinoma tissue is significantly increased and closely associated with patient clinical prognosis.
miR (show MLXIP ELISA Kits)-29a repressed TAB1-mediated TIMP-1 (show TIMP1 ELISA Kits) production in dermal fibroblasts, demonstrating that miR (show MLXIP ELISA Kits)-29a may be a therapeutic target in SSc (show CYP11A1 ELISA Kits).
Data indicate that mitogen-activated protein kinase (show MAPK1 ELISA Kits) (MAPK) p38 (show MAPK1 ELISA Kits) activation is triggered by AMP (show APRT ELISA Kits)-activated protein kinases (AMPK (show PRKAA1 ELISA Kits)) and mediated by TAB1 protein.
The amino acid sequence between positions 373 and 502 of TAB1 is required for TP interaction.
USP18 (show USP18 ELISA Kits) inhibits NF-kappaB (show NFKB1 ELISA Kits) and NFAT (show NFATC1 ELISA Kits) activation during Th17 differentiation by deubiquitinating the TAK1 (show MAP3K7 ELISA Kits)-TAB1 complex.
We found that endothelial TAK1 (show MAP3K7 ELISA Kits) and TAB2 (show TAB2 ELISA Kits), but not TAB1, were critically involved in vascular formation
TAK1 (show MAP3K7 ELISA Kits) 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 ELISA Kits) activity and subcellular localization and implicate these residues in TAK1 (show MAP3K7 ELISA Kits)- or p38 MAPK (show MAPK14 ELISA Kits)-dependent post-transcriptional control of gene expression
Phosphorylation and polyubiquitination of TAK1 (show MAP3K7 ELISA Kits) are necessary for activation of NF-kappaB (show NFKB1 ELISA Kits) by the Kaposi's sarcoma-associated herpesvirus vGPCR.
Co-expression of TAK1 (show MAP3K7 ELISA Kits) and TAB1 resulted in a functional and active TAK1 (show MAP3K7 ELISA Kits)-TAB1 complex capable of directly activating full-length heterotrimeric mammalian AMP-activated protein kinase (AMPK (show PRKAA2 ELISA Kits)) in vitro.
We confirmed that PGC (show PGC ELISA Kits)-1b inhibited downstream inflammatory signals via binding with TAB1 and thus preventing TAB1/TAK1 (show NR2C2 ELISA Kits) binding and TAK1 (show NR2C2 ELISA Kits) activation.
The E3 ubiquitin ligase Itch inhibits p38alpha (show MAPK14 ELISA Kits) signaling and skin inflammation through the ubiquitylation of Tab1.
TAB1 and TAB2 (show TAB2 ELISA Kits) are required for activated macrophages, making TAB1 and TAB2 (show TAB2 ELISA Kits) effective targets to control inflammation by modulating macrophage survival.
Both the MEKK1 (show MAP2K1 ELISA Kits) PHD (show PDC ELISA Kits) and TAB1 are critical for ES-cell differentiation
The enhanced JNK (show MAPK8 ELISA Kits) and IkappaB kinase (show CHUK ELISA Kits) activation in DUSP14 (show DUSP14 ELISA Kits)-deficient T cells was attenuated by TAB1 short hairpin RNA knockdown.
TAB1 binding stabilizes active p38alpha (show MAPK14 ELISA Kits) and induces rearrangements within the activation segment by helical extension of the Thr (show TRH ELISA Kits)-Gly-Tyr (show TYR ELISA Kits) motif, allowing autophosphorylation in cis (show CISH ELISA Kits)
We found that endothelial TAK1 (show NR2C2 ELISA Kits) and TAB2 (show TAB2 ELISA Kits), but not TAB1, were critically involved in vascular formation
O-GlcNAcylation of TAB1 is required for full TAK1 (show NR2C2 ELISA Kits) activation upon stimulation with IL-1 (show IL1A ELISA Kits)/osmotic stress.
Epithelial TAK1 (show NR2C2 ELISA Kits) activity is regulated through two unique, TAB1-dependent basal & TAB2 (show TAB2 ELISA Kits)-mediated stimuli-dependent mechanisms.
XIAP (show XIAP ELISA Kits)-TAB1-TAK1 (show NR2C2 ELISA Kits) complex is dependent on NRAGE (show MAGED1 ELISA Kits) for IKK-alpha (show CHUK ELISA Kits)/beta phosphorylation and NF-kappaB (show NFKB1 ELISA Kits) activation.
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