PRKCB
Gene Ontology Biological Process
- B cell activation [ISS]
- B cell receptor signaling pathway [ISS]
- blood coagulation [TAS]
- histone H3-T6 phosphorylation [IDA]
- lipoprotein transport [TAS]
- negative regulation of glucose transport [ISS]
- negative regulation of insulin receptor signaling pathway [ISS]
- platelet activation [TAS]
- positive regulation of B cell receptor signaling pathway [ISS]
- positive regulation of I-kappaB kinase/NF-kappaB signaling [ISS]
- positive regulation of NF-kappaB transcription factor activity [ISS]
- positive regulation of angiogenesis [ISS]
- positive regulation of vascular endothelial growth factor receptor signaling pathway [ISS]
- protein phosphorylation [TAS]
- regulation of transcription from RNA polymerase II promoter [IMP]
- signal transduction [NAS]
- synaptic transmission [TAS]
Gene Ontology Molecular Function
RGS2
Gene Ontology Biological Process
- negative regulation of G-protein coupled receptor protein signaling pathway [ISS]
- negative regulation of MAP kinase activity [ISS]
- negative regulation of cardiac muscle hypertrophy [ISS]
- negative regulation of phospholipase activity [ISS]
- positive regulation of cardiac muscle contraction [ISS]
- regulation of G-protein coupled receptor protein signaling pathway [TAS]
- regulation of adrenergic receptor signaling pathway [ISS]
- relaxation of cardiac muscle [ISS]
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
Protein kinase C phosphorylates RGS2 and modulates its capacity for negative regulation of Galpha 11 signaling.
RGS proteins (regulators of G protein signaling) attenuate heterotrimeric G protein signaling by functioning as both GTPase-activating proteins (GAPs) and inhibitors of G protein/effector interaction. RGS2 has been shown to regulate Galpha(q)-mediated inositol lipid signaling. Although purified RGS2 blocks PLC-beta activation by the nonhydrolyzable GTP analog guanosine 5'-O-thiophosphate (GTPgammaS), its capacity to regulate inositol lipid signaling under conditions where GTPase-promoted ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID