The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs

Yuko Atsumi, Aki Inase, Tomoyuki Osawa, Eiji Sugihara, Ryo Sakasai, Hiroaki Fujimori, Hirobumi Teraoka, Hideyuki Saya, Masamoto Kanno, Fumio Tashiro, Hitoshi Nakagama, Mitsuko Masutani, Ken Ichi Yoshioka

研究成果: Article査読

23 被引用数 (Scopus)

抄録

Background: It is unclear how DNA-damaging agents target cancer cells over normal somatic cells. Results: Arf/p53-dependent down-regulation of H2AX enables normal cells to survive after DNA damage. Conclusion: Transformed cells, which harbor mutations in either Arf or p53, are more sensitive to DNA-damaging agents. Significance: Cellular transformation renders cells more susceptible to some DNA-damaging agents.

本文言語English
ページ(範囲)13269-13277
ページ数9
ジャーナルJournal of Biological Chemistry
288
19
DOI
出版ステータスPublished - 2013 5月 10

ASJC Scopus subject areas

  • 生化学
  • 分子生物学
  • 細胞生物学

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