Functions of Wild-Type and Mutant Forms of p53 in Breast Cancer.

Abstract

Cells induced to accumulate the p53 tumor suppressor protein have been shown to arrest in G1. This arrest is characterized by accumulation of the cyclin dependent kinase (CDK) inhibitor p2l (WAF1/CIP1) and of underphosphorylated forms of retinoblastoma protein (pRB). We show here that accumulation of the wild-type pS3 protein in either human or murine cells markedly increases expression of cyclin Dl. The induction of cyclin Dl can also be mediated by a target of p53, the p21 (WAF1/CIP1) inhibitor of cyclin-dependent kinases. The relationship between the induction of cyclin Dl and G1 arrest defines a new cellular response to p53.

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Document Details

Document Type
Technical Report
Publication Date
Aug 17, 1995
Accession Number
ADA300399

Entities

People

  • Xinbin Chen

Organizations

  • Columbia University

Tags

DTIC Thesaurus Topics

  • Biomedical Research
  • Breast Cancer
  • Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Eukaryotes
  • Fungi
  • Growth Factors
  • Inhibitors
  • Materials
  • Neoplasms
  • New York
  • Programmed Cell Death
  • Proteins
  • Tissue Extracts

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics