Molecular mechanisms of DNA damage response and repair

Japanese

Laboratory of Anti-tumor Research

(Leader: Toshinori Ozaki, PhD)

Summary of research:

Upon DNA damage, p53 family members become activated and exert their pro-apoptotic function. Unfortunately, almost half of human tumor carry loss of function mutations and sometimes exhibits the drug-resistant phenotype. In contrast to p53, p73 is rarely mutated in human tumors and has a pro-apoptotic function. Thus, it seems to be important to clarify the precise molecular mechanisms by which p73 is activated in response to anti-tumor agents. Our studies provide a novel strategy to treat human tumors which show drug-resistant phenotype.

Keywords:

p53 family、DNA damage, Anti-cancer drug, Apoptosis

Recent main publications:

• Koida et al., J.Biol.Chem., 2008, 283: 8555-8563.
• Okoshi R et al., J.Biol.Chem., 2008, 283:3979-3987.
• Furuya K, et al., J.Biol.Chem., 2007, 282: 18365-18378.