|Other Names||Cyclin-dependent kinase inhibitor 2A, isoforms 1/2/3, Cyclin-dependent kinase 4 inhibitor A, CDK4I, Multiple tumor suppressor 1, MTS-1, p16-INK4a, p16-INK4, p16INK4A, CDKN2A, CDKN2, MTS1|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP3183a was selected from the region of human Phospho-p16-INK4A-S140. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.|
|Cellular Location||Cytoplasm. Nucleus|
|Tissue Location||Widely expressed but not detected in brain or skeletal muscle. Isoform 3 is pancreas-specific|
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Provided below are standard protocols that you may find useful for product applications.
p16-INK4A functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, MDM1, a protein responsible for the degradation of p53. This protein acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein. The gene for this protein is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene.
Ausserlechner, M.J., et al., Leukemia 19(6):1051-1057 (2005).Kawamata, N., et al., Eur. J. Haematol. 74(5):424-429 (2005).Wang, J.L., et al., Mod. Pathol. 18(5):629-637 (2005).Kuroda, H., et al., Cancer Genet. Cytogenet. 158(2):172-179 (2005).Fu, G.H., et al., FEBS Lett. 579(10):2105-2110 (2005).
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