JunD protects cells from p53-dependent senescence and apoptosis

Jonathan B. Weitzman, Laurence Fiette, Koichi Matsuo, Moshe Yaniv

Research output: Contribution to journalArticlepeer-review

211 Citations (Scopus)


JunD is the most broadly expressed member of the Jun family and the AP-1 transcription factor complex. Primary fibroblasts lacking JunD displayed p53-dependent growth arrest, upregulated p19(Arf) expression, and premature senescence. In contrast, immortalized cell lines lacking JunD showed increased proliferation and higher cyclinD1 levels. These properties are reminiscent of the effects of oncogenic Ras expression on primary and established cell cultures. Furthermore, JunD(-/-) fibroblasts exhibited increased p53-dependent apoptosis upon ultraviolet irradiation and were sensitive to the cytotoxic effects of TNF-α. The anti-apoptotic role of JunD was confirmed using an in vivo model of TNF-mediated hepatitis. We propose that JunD protects cells from senescence, or apoptotic responses to stress stimuli, by acting as a modulator of the signaling pathways that link Ras to p53.

Original languageEnglish
Pages (from-to)1109-1119
Number of pages11
JournalMolecular Cell
Issue number5
Publication statusPublished - 2000
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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