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ATM is a target for positive regulation by E2F-1

Eli Berkovich1, Doron Ginsberg

  • 1Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.

Oncogene
|January 16, 2003
PubMed

Insights

The transcription factor E2F-1 increases ATM levels and p53 phosphorylation. This reveals a new link between the RB/E2F pathway and p53, impacting cell growth and viability.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Cancer Research

Background:

  • The RB/E2F pathway regulates cell proliferation, with E2F-1 activation promoting growth.
  • Deregulation of E2F-1 can lead to oncogenic stress and apoptosis.
  • ATM kinase is crucial for responding to genotoxic stress and activating p53.

Purpose of the Study:

  • To investigate the regulatory relationship between E2F-1 and ATM.
  • To explore the functional link between the RB/E2F pathway and p53.

Main Methods:

  • Analysis of ATM promoter activity.
  • Measurement of ATM mRNA and protein levels.
  • Assessment of p53 phosphorylation.
  • Expression of HPV16 E7 protein to disrupt RB/E2F complexes.

Main Results:

  • E2F-1 was found to increase ATM promoter activity, leading to higher ATM mRNA and protein levels.
  • E2F-1 also induced increased phosphorylation of p53.
  • HPV16 E7 expression mimicked these effects, implicating endogenous E2F.

Conclusions:

  • ATM is transcriptionally regulated by E2F-1.
  • ATM acts as a novel, ARF-independent link connecting the RB/E2F pathway to p53.
  • This interaction influences cell growth control and viability pathways.

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