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