|Application ||WB, IF|
|Calculated MW||16533 Da|
|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||A full length p16/INK4A protein with GST tag was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||p16/INK4a Antibody is for research use only and 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.
The division cycle of eukaryotic cells is regulated by a family of protein kinases known as the cyclin-dependent kinases (CDKs). The sequential activation of individual members of this family and their consequent phosphorylation of critical substrates promotes orderly progression through the cell cycle. It has been reported that p16 binds to CDK4 and inhibits the catalytic activity of the CDK4/cyclin D enzymes. p16 seems to act in a regulatory feedback circuit with CDK4, D-type cyclins and retinoblastoma protein (1). The INK4 (inhibitor of cyclin-dependent kinase 4) family consists of four tumor-suppressor proteins: p15(INK4B), p16(INK4A), p18(INK4C), and p19(INK4D). While their sequences and structures are highly homologous, they show appreciable differences in conformational flexibility, stability, and aggregation tendency (2). Cell cycle arrest at the G1 checkpoint allows completion of critical macromolecular events prior to S phase. Regulators of the G1 checkpoint include an inhibitor of cyclin-dependent kinase, p16INK4; two tumor-suppressor proteins, p53 and RB and cyclin D1. p16INK4 is a tumor-suppressor protein and that genetic and epigenetic abnormalities in genes controlling the G1 checkpoint can lead to both escape from senescence and cancer formation (3).
1. Serrano M et al. Nature 366(6456):704-7, 1993
2. Yuan C et al. J Mol Biol 294(1):201-11, 1999
3. Okamoto A et al. Proc Natl Acad Sci 91(23):11045-9, 1994
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