CDKN2A (p16-INK4a)

Cyclins and cyclin-dependent kinases (cdks) form active complexes that regulate key events during the progression of the cell cycle and are evolutionarily highly conserved. The p16 protein has been identified as a specific inhibitor of cdk4 because it blocks cdk4 substrate phosphorylation. p16 inhibits cdk4 dependent phosphorylation of the tumor suppressor retinoblastoma protein (Rb) and Rb related proteins, p107 and p130. The biochemical properties of p16 suggest that it may be a tumor suppressor gene product. Recently a gene cloned from the short arm of human chromosome 9, Multiple Tumor Suppressor 1 (MTS1) has been identified as the gene for p16. The gene, now also known as the CDKN2 gene, has been found to be mutated in a very high percentage of tumors, including 75% of melanoma cell lines.

Cyclins and cyclin-dependent kinases (cdks) form active complexes that regulate key events during the progression of the cell cycle and are evolutionarily highly conserved. The p16 protein has been identified as a specific inhibitor of cdk4 because it blocks cdk4 substrate phosphorylation. p16 inhibits cdk4 dependent phosphorylation of the tumor suppressor retinoblastoma protein (Rb) and Rb related proteins, p107 and p130. The biochemical properties of p16 suggest that it may be a tumor suppressor gene product. Recently a gene cloned from the short arm of human chromosome 9, Multiple Tumor Suppressor 1 (MTS1) has been identified as the gene for p16. The gene, now also known as the CDKN2 gene, has been found to be mutated in a very high percentage of tumors, including 75% of melanoma cell lines.

G175-405

Western blot (Routinely Tested) Immunohistochemistry-frozen, Immunohistochemistry-paraffin, Immunoprecipitation (Tested During Development)

Human (QC Testing)

p16-INK4, p16-INK4a, ARF, MTS1, CDKN2, CDK4l

研发参考(7) 1. Kamb A, Gruis NA, Weaver-Feldhaus J, et al. A cell cycle regulator potentially involved in genesis of many tumor types. Science. 1994; 264(5157):436-440. (Biology). 2. Li Y, Nichols MA, Shay JW, Xiong Y. Transcriptional repression of the D-type cyclin-dependent kinase inhibitor p16 by the retinoblastoma susceptibility gene product pRb. Cancer Res. 1994; 54(23):6078-6082. (Biology). 3. Marx J. Link to hereditary melanoma brightens mood for p16 gene. Science. 1994; 265(5177):1364-1365. (Biology). 4. Serrano M, Hannon GJ, Beach . A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4. Nature. 1993; 366(6456):704-707. (Immunogen). 5. Shapiro GI, Edwards CD, Kobzik L, et al. Reciprocal Rb inactivation and p16INK4 expression in primary lung cancers and cell lines. Cancer Res. 1995; 55(3):505-509. (Biology). 6. Tam SW, Shay JW, Pagano M. Differential expression and cell cycle regulation of the cyclin-dependent kinase 4 inhibitor p16Ink4. Cancer Res. 1994; 54(22):5816-5820. (Clone-specific: Immunohistochemistry). 7. Yeager T, Stadler W, Belair C, Puthenveettil J, Olopade O, Reznikoff C. Increased p16 levels correlate with pRb alterations in human urothelial cells. Cancer Res. 1995; 55(3):493-497. (Clone-specific).