| Project/Area Number |
15390323
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | TOKYO MEDICAL AND DENTAL UNIVERSITY |
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Principal Investigator |
MIZUTANI Shuki TOKYO MEDICAL AND DENTAL UNIVERSITY, DEPARTEMNT OF PEDIATRICS., PROFESSOR, 大学院・医歯学総合研究科, 教授 (60126175)
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| Co-Investigator(Kenkyū-buntansha) |
NAGASAWA Masayuki TOKYO MEDICAL AND DENTAL UNIVERSITY, DEPARTEMNT OF GENERAL MEDICINE., ASSOCIATE PROFESSOR, 大学院・医歯学総合研究科, 講師 (90262196)
峯岸 克行 東京医科歯科大学, 大学院・医歯学総合研究科, 助教授 (10343154)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥14,800,000 (Direct Cost: ¥14,800,000)
Fiscal Year 2004: ¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 2003: ¥7,700,000 (Direct Cost: ¥7,700,000)
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| Keywords | DNA STRAND BREAKS / ATM / MLL / G2 / M / ARTEMIS / DNA-PK / MRN complex / 乳児白血病 / TopoIIインヒビター |
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| Research Abstract |
ATM is a gene involved in the pathogenesis of Ataxia Telangiectasia and plays an important role in genome surveillance system. We found ATM mutation allow cells to override G2/M checkpoint in response to topoisomerase II (Topo II) inhibitor. Topo II inhibitor also cleaves MLL gene. These finding led us to investigate possible MLL translocation by Topo II inhibitor in ATM deficient cells. As the result we demonstrated frequent MLL translocation in these conditions by FISH analyses.
Artemis is a molecule involved in the development of primary immune deficiency and phosphorylated by DNA-PKcs. We found ATM is phosphorylated at S645 in ATM dependent manner in response to XIR. These findings placed Artemtis at the crossing road between ATM and DNA-Pkcs.
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