DNA double-strand break repair proteins in mitochondria of mammalian cells
| Project/Area Number |
17510057
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | National Institute of Radiological Sciences |
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Principal Investigator |
KOIKE MANABU National Institute of Radiological Sciences, Research Center for Radiation Protection, Senior Researcher, 放射線防護研究センター, 主任研究員 (70280740)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2005: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | Radiation / Gene / Protein / Cell tissue / Mitochondria / DNA repair / DSB / 放射線 / 遺伝子 / 蛋白質 / 細胞組織 / 酵素 / 非相同末端結合 / Ku / DNA損傷 / ミトコンドリア / 可視化 |
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| Research Abstract |
DNA double-strand break (DSB) is the most dangerous DNA damage. One DNA DSB can be sufficient to kill a cell, if it is not repaired. DNA DSB can be induced both exogenously, e.g., by ionizing radiation (IR), chemicals, and chemotherapeutics, and endogenously, e.g., in the process of recombination and replication or due to oxidative stresses. Two major pathways exist in mammalian cells for the repair of DNA DSB : nonhomologous DNA-end-joining (NHEJ) repair and homologous recombination (HR). The NHEJ repair process requires Ku70, Ku80, XRCC4, DNA Ligase IV, and DNA-PKcs. The HR repair process requires Rad51 and Rad52. The NHEJ repair process, which is responsible for repairing a major fraction of DNA DSB in somatic cells of all multicellular eukaryotes, is thought to begin with the binding of Ku. The mechanism of Ku-end recognition has been suggested by the recent resolution of the crystal structure of Ku: ring-like structure with high affinity DNA binding site around the central pore. Evidence for the importance of Ku in the NHEJ repair process has been reported. Cells genetically deficient in Ku are sensitive to ionizing radiation and other agents (e.g. etoposide) that generate DNA DSB. Mammals possess two cellular genomes, one in the nucleus and the other in the mitochondria. It is not well known whether in contrast to the nucleus, mammalian mitochondria are able to repair DSB, although it was reported that Ku80 is localized in mammalian mitochondria and functions in a DNA-end binding activity. In this study, I could not detect DSB-repair proteins, i.e., Ku70, Ku80, XRCC4 and Rad52 in mammal' s mitochondria examined.
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Report
(3 results)
Research Products
(4 results)
