Product Pathways - Cell Cycle / Checkpoint
p16 INK4A Antibody #4824
| Applications | Reactivity | MW (kDa) | Source |
|---|---|---|---|
| W | H | 16 | Rabbit |
Applications Key:
W=Western Blotting
Reactivity Key:
H=Human
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.
Specificity / Sensitivity
p16 INK4A Antibody detects endogenous levels of p16 INK4A protein.
Source / Purification
Polyclonal antibodies are produced by immunizing rabbits with a synthetic peptide (KLH-coupled) corresponding to residues within the carboxy-terminal region of human p16 INK4A. Antibodies are purified by protein A and peptide affinity chromatography.
Western Blotting
Western blot analysis of extracts from HeLa and SK-N-MC cells, using p16 INK4A Antibody.
Background
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.
- Lukas, J. et al. (1996) Mol. Cell. Biol. 16, 6917-6925.
- Bai, F. et al. (2003) Mol. Cell. Biol. 23, 1269-1277.
- Noh, S.J. et al. (1999) Cancer Res. 59, 558-564.
- Guan, K.L. et al. (1994) Genes Dev. 8, 2939-2952.
- Hirai, H. et al. (1995) Mol. Cell. Biol. 15, 2672-2681.
- Sherr, C.J. (2001) Nat. Rev. Mol. Cell Biol. 2, 731-737.
- Lowe, S.W. and Sherr, C.J. (2003) Curr. Opin. Genet. Dev. 13, 77-83.
Application References
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