TAB2
Gene Ontology Biological Process
Gene Ontology Molecular Function
MAP3K7
Gene Ontology Biological Process
- I-kappaB phosphorylation [ISO, ISS]
- JNK cascade [ISO]
- MAPK cascade [IDA, ISO]
- activation of MAPK activity [ISO]
- activation of MAPKK activity [IDA, ISO]
- activation of NF-kappaB-inducing kinase activity [ISO]
- angiogenesis [ISO]
- histone H3 acetylation [ISO]
- negative regulation of apoptotic signaling pathway [ISO]
- negative regulation of necroptotic process [ISO]
- negative regulation of reactive oxygen species metabolic process [ISO]
- negative regulation of ripoptosome assembly involved in necroptotic process [ISO]
- neural tube formation [ISO]
- positive regulation of I-kappaB kinase/NF-kappaB signaling [IMP, ISO]
- positive regulation of JNK cascade [ISO]
- positive regulation of JUN kinase activity [ISO, ISS]
- positive regulation of T cell cytokine production [ISO]
- positive regulation of interleukin-2 production [ISO]
- protein phosphorylation [IDA, ISO]
- regulation of reactive oxygen species metabolic process [ISO]
- stress-activated MAPK cascade [ISO]
- transforming growth factor beta receptor signaling pathway [ISO]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Affinity Capture-Western
An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner identified by Western blot with a specific polyclonal antibody or second epitope tag. This category is also used if an interacting protein is visualized directly by dye stain or radioactivity. Note that this differs from any co-purification experiment involving affinity capture in that the co-purification experiment involves at least one extra purification step to get rid of potential contaminating proteins.
Publication
Tripartite motif 38 attenuates cardiac fibrosis after myocardial infarction by suppressing TAK1 activation via TAB2/3 degradation.
The role of tripartite motif (TRIM) 38, a ubiquitin E3 ligase regulating various pathophysiological processes, in cardiac fibrosis remains unclear. Here, a model of angiotensin II and myocardial infarction (MI)-induced fibrosis was established to explore its role in cardiac fibrosis and its underlying mechanisms. Cardiac fibrosis in the mouse MI model was mitigated by TRIM38 overexpression, but aggravated by its ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID