Stimulation of p53-Dependent Transcription by the Growth Suppressor, c-Abl

Abstract

Although it is known that c-Abl stimulates p53-dependent transcription, a function required for c-Abl growth suppressor activity, the molecular mechanism by which this occurs remain elusive. The results obtained with this grant award show that c-Abl interacts with the C-terminal regulatory domain of tetrameric form of p53 and functions to activate the p53 DNA-binding. In an effort to assess the mechanism of c-Abl activation, we also show that c-Abl activates p53 DNA-binding by stabilizing the p33-DNA complex. Collectively, these results suggest a model for c-Abl activation. In this model c-Abl activates latent p53 by relieving the C-terminal inhibitory domain of p53 and enhances p53 DNA-binding by forming a stable p53-DNA complex (see text).

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2001
Accession Number
ADA398668

Entities

People

  • John Cogan
  • Xuan Liu

Organizations

  • University of California, Riverside

Tags

DTIC Thesaurus Topics

  • Biomedical Research
  • Breast Cancer
  • Cancer
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Genetics
  • Laboratory Animals
  • Materials
  • Molecular Biology
  • Neoplasms
  • New York
  • Proteins
  • Recombinant Dna
  • Suppressors
  • Terminals
  • Transcription Factors

Fields of Study

  • Computer science

Readers

  • Breast cancer cell signaling and growth regulation.
  • Molecular and Cellular Biochemistry
  • Molecular and Cellular Biology