Cell-cycle arrest and inhibition of Cdk4 activity by small peptides based on the carboxy-terminal domain of p21WAF1

K L Ball, S Lain, R Fâhraeus, C Smythe, D P Lane

Research output: Contribution to journalArticlepeer-review

Abstract

A common event in the development of human neoplasia is the inactivation of a damage-inducible cell-cycle checkpoint pathway regulated by p53. One approach to the restoration of this pathway is to mimic the activity of key downstream effectors. The cyclin-dependent kinase (Cdk) inhibitor p21(WAF1) is one such molecule, as it is a major mediator of the p53-dependent growth-arrest pathway, and can, by itself, mediate growth suppression. The primary function of the p21(WAF1) protein appears to be the inhibition of G1 cyclin-Cdk complexes. Thus, if we can identify the region(s) of p21(WAF1) that contain its inhibitor activity they may provide a template from which to develop novel anti-proliferative drugs for use in tumours with a defective p53 pathway.
Original languageEnglish
Pages (from-to)71-80
Number of pages10
JournalCurrent biology : CB
Volume7
Issue number1
DOIs
Publication statusPublished - 1 Jan 1997

Keywords

  • Amino Acid Sequence
  • Cell Cycle
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclin-Dependent Kinases
  • Cyclins
  • Humans
  • Molecular Sequence Data

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