A paradigm shift by two Ku80: New model of the radiation-induced DNA damage response mechanism in human cells

Research Project

Project/Area Number	24510077
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Risk sciences of radiation/Chemicals
Research Institution	National Institute of Radiological Sciences
Principal Investigator	KOIKE MANABU 独立行政法人放射線医学総合研究所, 放射線防護研究センター, 主任研究員 (70280740)
Co-Investigator(Renkei-kenkyūsha)	KOIKE Aki 独立行政法人放射線医学総合研究所, 放射線防護研究センター, 技術員 (50415410)
Project Period (FY)	2012-04-01 – 2015-03-31
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000) Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000) Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000) Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Keywords	Ku80
Outline of Final Research Achievements	Ku (the heterodimer of Ku70 and Ku80) plays a pivotal role in the DNA double-strand break (DSB) repair pathway (non-homologous end-joining (NHEJ). It has reported that two isoforms of Ku80 encoded by the same genes are expressed and function in primate cells, but not in rodent cells. In this study, our data suggested the possibility that nuclear localization signal of one isoform is localized not only in the C-terminal region, but also in the N-terminal region. In addition, we generated a transgenic mouse that were introduced GFP-KARP-1(1-88). These information and the mouse generated might be useful for study of KARP-1(1-88) functions and the DSB repair pathway.