Cdc25 cell-cycle phosphatase as a target of c-myc

Nature. 1996 Aug 8;382(6591):511-7. doi: 10.1038/382511a0.

Abstract

The product of the proto-oncogene c-myc, in partnership with Max, forms a transcription factor that can promote either oncogenic transformation or apoptosis. The Myc/Max heterodimer binds to elements in the cdc25A gene and activates transcription. Like myc, cdc25A, itself a proto-oncogene, can induce apoptosis in cells depleted of growth factor, and Myc-induced apoptosis also requires cdc25A. These findings indicate that cdc25A is a physiologically relevant transcriptional target of c-myc.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3T3 Cells
  • Animals
  • Apoptosis / genetics
  • Binding Sites
  • Cell Cycle Proteins / genetics*
  • Cell Cycle Proteins / metabolism
  • Cell Line
  • Cell Transformation, Neoplastic / genetics
  • Cloning, Molecular
  • DNA
  • Gene Expression Regulation
  • Humans
  • Mice
  • Molecular Sequence Data
  • Phosphoprotein Phosphatases / genetics*
  • Phosphoprotein Phosphatases / metabolism
  • Protein Binding
  • Proto-Oncogene Proteins c-myc / metabolism*
  • RNA, Messenger / metabolism
  • Transcription, Genetic
  • cdc25 Phosphatases

Substances

  • Cell Cycle Proteins
  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • DNA
  • Phosphoprotein Phosphatases
  • cdc25 Phosphatases