Myc-Max-Mad: a transcription factor network controlling cell cycle progression, differentiation and death

Curr Opin Genet Dev. 1994 Feb;4(1):102-8. doi: 10.1016/0959-437x(94)90098-1.

Abstract

The Myc oncoprotein dimerizes with its partner, Max, to bind DNA, activate transcription, and promote cell proliferation, as well as programmed cell death. Max also forms homodimers or heterodimers with its alternative partners, Mad and Mxi-1. These complexes behave as antagonists of Myc/Max through competition for common DNA targets, and perhaps permit cellular differentiation.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Base Sequence
  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
  • Basic-Leucine Zipper Transcription Factors
  • Binding Sites
  • Cell Cycle / physiology
  • Cell Differentiation / physiology
  • DNA / genetics
  • DNA / metabolism
  • DNA-Binding Proteins / physiology
  • Helix-Loop-Helix Motifs / physiology
  • Humans
  • Leucine Zippers / physiology
  • Proto-Oncogene Proteins c-myc / physiology
  • Repressor Proteins*
  • Transcription Factors / physiology*

Substances

  • Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
  • Basic-Leucine Zipper Transcription Factors
  • DNA-Binding Proteins
  • MAX protein, human
  • MXD1 protein, human
  • Myc associated factor X
  • Proto-Oncogene Proteins c-myc
  • Repressor Proteins
  • Transcription Factors
  • DNA