Aliases for CDKN1A Gene
External Ids for CDKN1A Gene
Previous Symbols for CDKN1A Gene
This gene encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, and thus functions as a regulator of cell cycle progression at G1. The expression of this gene is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. This protein can interact with proliferating cell nuclear antigen (PCNA), a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation. Multiple alternatively spliced variants have been found for this gene. [provided by RefSeq, Nov 2010]
GeneCards Summary for CDKN1A Gene
CDKN1A (Cyclin-Dependent Kinase Inhibitor 1A (P21, Cip1)) is a Protein Coding gene. Diseases associated with CDKN1A include thoracic cancer and bladder transitional cell carcinoma. Among its related pathways are PI3K-Akt signaling pathway and PI-3K cascade. GO annotations related to this gene include protein complex binding and cyclin-dependent protein serine/threonine kinase inhibitor activity. An important paralog of this gene is CDKN1B.
UniProtKB/Swiss-Prot for CDKN1A Gene
May be the important intermediate by which p53/TP53 mediates its role as an inhibitor of cellular proliferation in response to DNA damage. Binds to and inhibits cyclin-dependent kinase activity, preventing phosphorylation of critical cyclin-dependent kinase substrates and blocking cell cycle progression. Functions in the nuclear localization and assembly of cyclin D-CDK4 complex and promotes its kinase activity towards RB1. At higher stoichiometric ratios, inhibits the kinase activity of the cyclin D-CDK4 complex.