Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

p21 Waf1/Cip1 (DCS60) Mouse mAb #2946

Applications Reactivity MW (kDa) Source Isotype
W IP IHC-P H Mk 21 Mouse IgG2a

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IHC-P=Immunohistochemistry (Paraffin)
Reactivity Key:  H=Human  Mk=Monkey
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.

Specificity / Sensitivity

p21 Waf1/Cip1 (DCS60) Mouse mAb detects endogenous levels of total p21 protein. The antibody does not cross-react with other cdk inhibitors.

Source / Purification

Monoclonal antibody is produced by immunizing mice with recombinant human p21 corresponding to the amino-terminal portion of p21.

Western Blotting

Western Blotting

Western blot analysis of extracts from 293, MCF-7 and COS cells, using p21 Waf1/Cip1 (DCS60) Mouse mAb.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast carcinoma, showing nuclear and cytoplasmic localization, using p21 Waf1/Cip1 (DCS60) Mouse mAb.

Background

The tumor suppressor protein p21 Waf1/Cip1 acts as an inhibitor of cell cycle progression. It functions in stoichiometric relationships forming heterotrimeric complexes with cyclins and cyclin-dependent kinases. In association with CDK2 complexes, it serves to inhibit kinase activity and block progression through G1/S (1). However, p21 may also enhance assembly and activity in complexes of CDK4 or CDK6 and cyclin D (2). The carboxy-terminal region of p21 is sufficient to bind and inhibit PCNA, a subunit of DNA polymerase, and may coordinate DNA replication with cell cycle progression (3). Upon UV damage or during cell cycle stages when cdc2/cyclin B or CDK2/cyclin A are active, p53 is phosphorylated and upregulates p21 transcription via a p53 responsive element (4). Protein levels of p21 are downregulated through ubiquitination and proteasomal degradation (5).

  1. Pestell, R.G. et al. (1999) Endocrine Rev. 20, 501-534.
  2. Cheng, J. et al. (1999) EMBO J. 18, 1571-1583.
  3. Flores-Rozas, H. et al. (1994) Proc. Natl. Acad. Sci. USA 91, 8655-8659.
  4. Wang, Y. and Prives, C. (1995) Nature 376, 88-91.
  5. Sheaff, R.J. et al. (2000) Cell 5, 403-410.

Application References

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