PRKACA
Gene Ontology Biological Process
- G2/M transition of mitotic cell cycle [TAS]
- activation of phospholipase C activity [TAS]
- activation of protein kinase A activity [TAS]
- blood coagulation [TAS]
- calcium-mediated signaling using intracellular calcium source [TAS]
- carbohydrate metabolic process [TAS]
- cell communication by electrical coupling involved in cardiac conduction [TAS]
- cellular response to epinephrine stimulus [TAS]
- cellular response to glucagon stimulus [TAS]
- cellular response to glucose stimulus [IDA]
- cytosolic calcium ion homeostasis [TAS]
- energy reserve metabolic process [TAS]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- gluconeogenesis [TAS]
- glucose metabolic process [TAS]
- innate immune response [TAS]
- intracellular signal transduction [TAS]
- mitotic cell cycle [TAS]
- neurotrophin TRK receptor signaling pathway [TAS]
- peptidyl-serine phosphorylation [IDA]
- positive regulation of cell cycle arrest [ISS]
- protein phosphorylation [NAS]
- regulation of cardiac muscle contraction [TAS]
- regulation of cardiac muscle contraction by regulation of the release of sequestered calcium ion [TAS]
- regulation of heart rate [TAS]
- regulation of insulin secretion [TAS]
- regulation of osteoblast differentiation [IDA]
- regulation of proteasomal protein catabolic process [IDA]
- regulation of protein binding [TAS]
- regulation of ryanodine-sensitive calcium-release channel activity [TAS]
- regulation of tight junction assembly [IDA]
- signal transduction [TAS]
- small molecule metabolic process [TAS]
- sperm capacitation [ISS]
- transmembrane transport [TAS]
- triglyceride catabolic process [TAS]
- water transport [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
CDKN1A
Gene Ontology Biological Process
- DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest [IDA, TAS]
- Fc-epsilon receptor signaling pathway [TAS]
- G1/S transition of mitotic cell cycle [IDA, TAS]
- G2/M transition of mitotic cell cycle [IMP]
- Ras protein signal transduction [IEP]
- cell cycle arrest [IDA, IMP]
- cellular response to DNA damage stimulus [IMP]
- cellular response to extracellular stimulus [IMP]
- cellular response to ionizing radiation [IMP]
- cellular senescence [IMP]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- innate immune response [TAS]
- intrinsic apoptotic signaling pathway [TAS]
- mitotic cell cycle [TAS]
- negative regulation of G1/S transition of mitotic cell cycle [IGI]
- negative regulation of cell growth [IDA]
- negative regulation of cell proliferation [IDA, IMP]
- negative regulation of phosphorylation [IDA]
- neurotrophin TRK receptor signaling pathway [TAS]
- phosphatidylinositol-mediated signaling [TAS]
- positive regulation of fibroblast proliferation [IMP]
- positive regulation of protein kinase activity [IDA]
- positive regulation of reactive oxygen species metabolic process [IMP]
- protein phosphorylation [IDA]
- regulation of cyclin-dependent protein serine/threonine kinase activity [TAS]
- stress-induced premature senescence [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
Akt-dependent phosphorylation of p21(Cip1) regulates PCNA binding and proliferation of endothelial cells.
The protein kinase Akt is activated by growth factors and promotes cell survival and cell cycle progression. Here, we demonstrate that Akt phosphorylates the cell cycle inhibitory protein p21(Cip1) at Thr 145 in vitro and in intact cells as shown by in vitro kinase assays, site-directed mutagenesis, and phospho-peptide analysis. Akt-dependent phosphorylation of p21(Cip1) at Thr 145 prevents the complex ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID