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p15INK4B is a potential effector of TGF-beta-induced cell cycle arrest

G J Hannon1, D Beach

  • 1Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, New York 11724.

Nature
|September 15, 1994
PubMed

Insights

Transforming growth factor-beta (TGF-beta) induces cell cycle arrest by upregulating p15INK4B, a new protein in the p16INK4 family. This suggests p15INK4B is a key mediator of TGF-beta

Area of Science:

  • Molecular Biology
  • Cell Cycle Regulation
  • Cancer Genetics

Background:

  • Transforming growth factor-beta (TGF-beta) is a key regulator of cell proliferation, inducing G1-phase cell cycle arrest.
  • Progression through the G1 phase is controlled by cyclin-dependent protein kinases CDK4 and CDK6, which are inhibited by the p16INK4 protein family.

Purpose of the Study:

  • To identify and characterize novel members of the p16INK4 family.
  • To investigate the role of new p16INK4 family members in TGF-beta-mediated cell cycle arrest.

Main Methods:

  • Isolation and characterization of a new p16INK4 family member, p15INK4B.
  • Quantification of p15INK4B gene expression in human keratinocytes treated with TGF-beta.

Main Results:

  • A novel p16INK4 family member, designated p15INK4B, was isolated.
  • p15INK4B expression was induced approximately 30-fold in human keratinocytes upon TGF-beta treatment.
  • The gene encoding p15INK4B is located on chromosome 9p21, a region frequently altered in human tumors, adjacent to the p16 gene.

Conclusions:

  • p15INK4B is a novel inhibitor of CDK4/CDK6 and a likely mediator of TGF-beta-induced G1 cell cycle arrest.
  • The chromosomal location of p15INK4B (9p21) suggests its potential involvement in tumorigenesis.

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