involvement of INO80 chromatin remodeling factor in 11q23 chromosome translocations
| Project/Area Number |
26430114
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Tumor biology
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| Research Institution | Hiroshima University |
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Principal Investigator |
Sun Jiying 広島大学, 原爆放射線医科学研究所, 講師 (80397926)
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| Co-Investigator(Kenkyū-buntansha) |
田代 聡 広島大学, 原爆放射線医科学研究所, 教授 (20243610)
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| Co-Investigator(Renkei-kenkyūsha) |
HARATA MASAHIKO 東北大学, 農学研究科, 准教授 (70218642)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 染色体転座形成 / DNA repair / クロマチン変換複合体 / 染色体転座 / INO80 / RAD51 |
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| Outline of Final Research Achievements |
Chromosome translocations induced by ionizing radiation and chemotherapeutic agents, has been shown to lead to malignant transformation. However, the mechanism of chromosome translocations is still unclear. Chromosome translocations involving the MLL gene on 11q23 are the most frequent chromosome abnormalities in secondary leukemias associated with chemotherapy employing etoposide. Dysfunction of ATM, a DNA damage signaling regulator, increases the incidence of 11q23 chromosome translocations. We showed that ATM deficiency results in the excessive binding of the DNA recombinase RAD51 at the translocation breakpoint cluster region (BCR) of MLL gene after etoposide exposure. In this study, we showed that a phosphorylated subunit of INO80 complex by ATM, plays an important role in the appropriate regulation of INO80 and RAD51 binding to the BCR of MLL gene and prevention of 11q23 chromosome translocations after etoposide treatment.
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Report
(4 results)
Research Products
(21 results)
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[Journal Article] hCAS/CSE1L regulates RAD51 distribution and focus formation for homologous recombinational repair2015
Author(s)
1.Okimoto S, Sun J, Fukuto A, Horikoshi Y, Matsuda S, Matsuda T, Ikura M, Ikura T, Machida S, Kurumizaka H, Miyamoto Y, Oka M, Yoneda Y, Kiuchi Y, Tashiro S.
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Journal Title
Genes Cells.
Volume: 20
Issue: 9
Pages: 681-94
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] The transcription repressors Bach2 and Bach1 promote B cell development by repressing myeloid program.2014
Author(s)
Itoh-Nakadai A, Hikota R, Muto A, Kometani K, Matsui-Watanabe M, Sato Y, Kobayashi M, Nakamura A, Miura Y, Yano Y, Tashiro S, Sun J, Ikawa T, Ochiai K, Kurosaki T, and Igarashi K.
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Journal Title
Nature Immunol.
Volume: 15
Issue: 12
Pages: 1171-1180
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Reorganization of Damaged Chromatin by the Exchange of Histone Variant H2A.Z-22014
Author(s)
Nishibuchi I, Suzuki H, Kinomura A, Sun J, Liu NA, Horikoshi Y, Shima H, Kusakabe M, Harata M, Fukagawa T, Ikura T, Ishida T, Nagata Y, Tashiro
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Journal Title
Int J Radiat Oncol Biol Phys.
Volume: 89
Pages: 736-44
Related Report
Peer Reviewed / Open Access
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[Journal Article] Nap1 stimulates homologous recombination by RAD51 and RAD54 in higher-ordered chromatin containing histone H1.2014
Author(s)
Machida, S., Takaku, M., Ikura, M., Sun, J., Suzuki, H., Kobayashi, W., Kinomura, A., Osakabe, A., Tachiwana, H., Horikoshi, Y., Fukuto, A., Matsuda, R., Ura, K., Tashiro, S., Ikura, T., and Kurumizaka, H.
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Journal Title
Scientific Rep.
Volume: 4
Issue: 1
Pages: 4863-4863
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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