Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
p16 INK4A Antibody detects endogenous levels of p16 INK4A protein.
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues within the carboxy-terminal region of human p16 INK4A. Antibodies are purified by protein A and peptide affinity chromatography.
Cyclin-dependent kinases (CDKs) are activated in part by forming complexes with cyclins. For example, CDK4 and CDK6 associate with the D-type cyclins and phosphorylate the retinoblastoma protein. This phosphorylation is a necessary event for cells to enter S-phase (1). The inhibitors of CDK4 (INK4) family include p15 INK4B, p16 INK4A, p18 INK4C and p19 INK4D. p18 has been shown to function as a haploinsufficient tumor suppressor in vivo (2). All INK4 proteins are composed of 32 amino acid ankyrin motifs and selectively inhibit CDK4/6 activity. Mutational analyses of p18 implicate the third and the amino-terminal portion of the fourth ankyrin repeat in mediating binding to CDK4/6 (3). The interaction of INK4 family members can be a binary complex with CDK4/6 or ternary complex with cyclin D-bound CDK4/6 and ultimately results in the inhibition of cell cycle progression (4,5).
p16 INK4A directly inhibits the activity of cyclin D, thereby inhibiting S-phase entry (6,7). As such, expression of p16 INK4A is commonly associated with cellular senescence, and disruption of the p16 INK4A gene is frequently observed in human cancers.
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