[Cyclin-dependent kinase inhibitors in mammal cells]

Sheng Li Ke Xue Jin Zhan. 1996 Apr;27(2):107-12.
[Article in Chinese]

Abstract

In recent two years, a group of protein factors have been found to combine with the cyclin-dependent kinases (CDKs) and block the activation of cyclin/CDK complexes. They are named CDK inhibitors (CKIs) as p21, p16, p15, p27 and CDI1. The p21 and p27 have certain homology and can inhibit the activity of multiple CDKs; p16 and p15 have higher homology and can specifically combine with CDK4 and CDK6; and the combination specificity of CDI1 needs further research. The expression of p21 is regulated positively by p53. TGF-beta can upregulate the expression of p15 and the inhibitory activity of p27. The above findings demonstrate that CKIs are not only the regulators of CDKs' activity but also the direct linkers between cancer inhibitors and cell-cycle regulation.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Animals
  • Carrier Proteins / physiology
  • Cell Cycle / physiology
  • Cell Cycle Proteins*
  • Cyclin-Dependent Kinase Inhibitor p15
  • Cyclin-Dependent Kinase Inhibitor p16 / physiology
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclin-Dependent Kinases / antagonists & inhibitors*
  • Cyclin-Dependent Kinases / physiology*
  • Cyclins / physiology
  • Enzyme Inhibitors*
  • Humans
  • Tumor Suppressor Proteins*

Substances

  • CDKN1A protein, human
  • CDKN2B protein, human
  • Carrier Proteins
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p15
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Enzyme Inhibitors
  • Tumor Suppressor Proteins
  • Cyclin-Dependent Kinases