MAPK3
Gene Ontology Biological Process
- BMP signaling pathway [IMP]
- DNA damage induced protein phosphorylation [IDA]
- Fc-epsilon receptor signaling pathway [TAS]
- Fc-gamma receptor signaling pathway involved in phagocytosis [TAS]
- JAK-STAT cascade involved in growth hormone signaling pathway [TAS]
- MAPK cascade [NAS, TAS]
- MyD88-dependent toll-like receptor signaling pathway [TAS]
- MyD88-independent toll-like receptor signaling pathway [TAS]
- Ras protein signal transduction [TAS]
- TRIF-dependent toll-like receptor signaling pathway [TAS]
- activation of MAPK activity [TAS]
- activation of MAPKK activity [TAS]
- axon guidance [TAS]
- blood coagulation [TAS]
- caveolin-mediated endocytosis [TAS]
- cellular response to mechanical stimulus [IEP]
- cytokine-mediated signaling pathway [TAS]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- gene expression [TAS]
- innate immune response [TAS]
- insulin receptor signaling pathway [TAS]
- interleukin-1-mediated signaling pathway [IMP]
- neurotrophin TRK receptor signaling pathway [TAS]
- peptidyl-tyrosine autophosphorylation [IDA]
- phosphorylation [IDA]
- platelet activation [TAS]
- positive regulation of ERK1 and ERK2 cascade [IMP]
- positive regulation of histone acetylation [IMP]
- positive regulation of histone phosphorylation [IMP]
- positive regulation of protein phosphorylation [IMP]
- positive regulation of transcription from RNA polymerase II promoter [IMP]
- protein phosphorylation [IDA]
- regulation of Golgi inheritance [TAS]
- regulation of cytoskeleton organization [TAS]
- regulation of early endosome to late endosome transport [TAS]
- regulation of sequence-specific DNA binding transcription factor activity [TAS]
- regulation of stress-activated MAPK cascade [TAS]
- response to epidermal growth factor [IDA]
- small GTPase mediated signal transduction [TAS]
- stress-activated MAPK cascade [TAS]
- toll-like receptor 10 signaling pathway [TAS]
- toll-like receptor 2 signaling pathway [TAS]
- toll-like receptor 3 signaling pathway [TAS]
- toll-like receptor 4 signaling pathway [TAS]
- toll-like receptor 5 signaling pathway [TAS]
- toll-like receptor 9 signaling pathway [TAS]
- toll-like receptor TLR1:TLR2 signaling pathway [TAS]
- toll-like receptor TLR6:TLR2 signaling pathway [TAS]
- toll-like receptor signaling pathway [TAS]
- transcription from RNA polymerase I promoter [TAS]
- transcription initiation from RNA polymerase I promoter [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
ATP1A1
Gene Ontology Biological Process
- cardiac muscle contraction [TAS]
- cell communication by electrical coupling involved in cardiac conduction [TAS]
- cellular potassium ion homeostasis [IDA]
- cellular response to steroid hormone stimulus [IDA]
- cellular sodium ion homeostasis [IDA]
- ion transmembrane transport [TAS]
- membrane repolarization [IDA]
- membrane repolarization during cardiac muscle cell action potential [IC]
- potassium ion import [IDA]
- regulation of sodium ion transport [ISS]
- relaxation of cardiac muscle [TAS]
- response to glycoside [IDA]
- sodium ion export from cell [IDA]
- transmembrane transport [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Biochemical Activity (Phosphorylation)
An interaction is inferred from the biochemical effect of one protein upon another, for example, GTP-GDP exchange activity or phosphorylation of a substrate by a kinase. The bait protein executes the activity on the substrate hit protein. A Modification value is recorded for interactions of this type with the possible values Phosphorylation, Ubiquitination, Sumoylation, Dephosphorylation, Methylation, Prenylation, Acetylation, Deubiquitination, Proteolytic Processing, Glucosylation, Nedd(Rub1)ylation, Deacetylation, No Modification, Demethylation.
Publication
ERK1/2 mediates insulin stimulation of Na(+),K(+)-ATPase by phosphorylation of the alpha-subunit in human skeletal muscle cells.
Insulin stimulates Na(+),K(+)-ATPase activity and induces translocation of Na(+),K(+)-ATPase molecules to the plasma membrane in skeletal muscle. We determined the molecular mechanism by which insulin regulates Na(+),K(+)-ATPase in differentiated primary human skeletal muscle cells (HSMCs). Insulin action on Na(+),K(+)-ATPase was dependent on ERK1/2 in HSMCs. Sequence analysis of Na(+),K(+)-ATPase alpha-subunits revealed several potential ERK phosphorylation sites. Insulin increased ouabain-sensitive (86)Rb(+) ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID