p16INK4A protein family specifically inhibit cyclin-dependent kinase 4-mediated phosphorylation of the retinoblastoma (Rb) susceptibility gene product. p16INK4A, has been identified as a tumor suppressor in many human cancers and inactivation of p16INK4A in tumors is thought to be required in order for many malignant cell types to enter S-phase (1). p16INK4A expression is required for the reduction in cdk4- and cdk6-mediated Rb kinase activity observed in response to DNA damage. p16INK4A gene is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene (2).
CDKN2A, ARF, MLM, p14, p16, p19, CMM2, INK4, MTS1, TP16, CDK4I, CDKN2, INK4a, p14ARF, p16INK4
1. Smith-Sørensen, B. et al: CDKN2A (p16INK4A) somatic and germline mutations. Hum. Mutat. 1996; 7 (4): 294-303.
2. Kusy, S. et al: p14ARF, p15INK4b and p16INK4a methylation status in chronic myelogenous leukemia. Leuk, Lymphoma, 2005; 45 (10): 1989-94.
Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability, and Shipping:
Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Cancer, Cell Cycle