Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

p15 INK4B Antibody #4822

Applications Reactivity Sensitivity MW (kDa) Source
W F H M R Endogenous 15 Rabbit

Applications Key:  W=Western Blotting  F=Flow Cytometry
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

p15 INK4B Antibody detects endogenous levels of p15 INK4B.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the amino terminus of human p15 INK4B. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of whole cell extracts from 293, HeLa, HT29, C6, and NIH/3T3 cells, using p15 INK4B Antibody.

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of untreated C6 cells, using p15 INK4B Antibody versus propidium iodide (DNA content). Boxed population indicates p15 INK4B-positive cells.

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).

The gene encoding p15 INK4B is often silenced by hypermethylation in acute myeloid leukemia and deleted in acute lymphocytic leukemia (6).

  1. Lukas, J. et al. (1996) Mol. Cell. Biol. 16, 6917-6925.
  2. Bai, F. et al. (2003) Mol. Cell. Biol. 23, 1269-1277.
  3. Noh, S.J. et al. (1999) Cancer Res. 59, 558-564.
  4. Guan, K.L. et al. (1994) Genes Dev. 8, 2939-2952.
  5. Hirai, H. et al. (1995) Mol. Cell. Biol. 15, 2672-2681.
  6. Drexler, H.G. (1998) Leukemia 12, 845-859.

Application References

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Companion Products

This product is intended for research purposes only. The product is not intended to be used for therapeutic or diagnostic purposes in humans or animals.

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