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