2011 Fiscal Year Final Research Report
DNA-protein cross-links : Repair and chromosome damage induction
| Project/Area Number |
21310037
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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 |
Risk sciences of radiation/Chemicals
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| Research Institution | Hiroshima University |
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Principal Investigator |
IDE Hiroshi 広島大学, 大学院・理学研究科, 教授 (30223126)
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| Co-Investigator(Kenkyū-buntansha) |
NAKANO Toshiaki 広島大学, 大学院・理学研究科, 助教 (10526122)
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| Project Period (FY) |
2009 – 2011
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| Keywords | ゲノム / 損傷 / 修復 |
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| Research Abstract |
Proteins are often covalently trapped on DNA, generating DNA-protein cross-links(DPCs), when cells are exposed to DNA-damaging agents. However, not much is known about how cells mitigate the adverse effects of DPCs. In the present study, we have developed novel methods for the detection of DPCs. Genomic DPCs were primarily eliminated by spontaneous hydrolysis, and excision repair played no significant role in the removal of DPCs. It was suggested that DPCs initially activated the ATR DNA-damage response pathway, followed by the ATM pathway.
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Research Products
(13 results)
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[Journal Article] Homolo go usre combination but not nucleotideexcision repair plays a pivotal role intolerance to DNA-protein crosslinks inmammalian cells2009
Author(s)
Nakano T., Katafuchi A., Matsubara M., Terato H., Tsuboi T., Masuda T., Tatsumoto T., Pack S. P., Makino K., Croteau D. L., Van Houten B., Iijima K., Tauchi H., and Ide H.
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Journal Title
J. Biol., Chem.
Volume: 284
Pages: 27065-27076
DOI
Peer Reviewed
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