JunD protects cells from p53-dependent senescence and apoptosis

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

研究成果: Article査読

202 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)1109-1119
ページ数11
ジャーナルMolecular Cell
6
5
DOI
出版ステータスPublished - 2000
外部発表はい

ASJC Scopus subject areas

  • 分子生物学
  • 細胞生物学

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