The c-Myc protein induces cell cycle progression and apoptosis through dimerization with Max

B. Amati, T. D. Littlewood, G. I. Evan, H. Land

Research output: Contribution to journalArticle

Abstract

The c-Myc protein (Myc) is involved in cellular transformation and mitogenesis, but is also a potent inducer of programmed cell death, or apoptosis. Whether these apparently opposite functions are mediated through common or distinct molecular mechanisms remains unclear. Myc and its partner protein, Max, dimerize and bind DNA in vitro and in vivo through basic/helix-loop-helix/leucine zipper motifs (bHLH-LZ). By using complementary leucine zipper mutants (termed MycEG and MaxEG), which dimerize efficiently with each other but not with their wild-type partners, we demonstrate that both cell cycle progression and apoptosis in non-transformed rodent fibroblasts are induced by Myc-Max dimers. MycEG or MaxEG alone are inactive, but co-expression restores ability to prevent withdrawal from the cell cycle and to induce cell death upon removal of growth factors. Thus, Myc can control two alternative cell fates through dimerization with a single partner, Max.

Original languageEnglish
Pages (from-to)5083-5087
Number of pages5
JournalEMBO Journal
Volume12
Issue number13
Publication statusPublished - 1993

Keywords

  • Apoptosis
  • Cell cycle
  • Max
  • Myc
  • Oncogenes

ASJC Scopus subject areas

  • Cell Biology
  • Genetics

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    Amati, B., Littlewood, T. D., Evan, G. I., & Land, H. (1993). The c-Myc protein induces cell cycle progression and apoptosis through dimerization with Max. EMBO Journal, 12(13), 5083-5087.