2011 Fiscal Year Final Research Report
Activation mechanism and physiological role of the ATM checkpoint kinase in response to oxidative stress
Project/Area Number |
22710052
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Risk sciences of radiation/Chemicals
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Research Institution | Kanazawa University |
Principal Investigator |
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Project Period (FY) |
2010 – 2011
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Keywords | 応答 / ATM |
Research Abstract |
The sulfhydryl-reactive oxidative stress agents 15d-PGJ_2, ONE and 8-nitro-cGMP induce phosphorylation and accumulation of p53 and apoptosis but DNA damage response. The ATM activation by 15d-PGJ_2 does not require a disulfide-cross-linked dimer formation of ATM, unlike the case by hydrogen peroxide. 15d-PGJ_2 affects the ATM-dependent metabolic regulation. These results obtained in this study characterize the mechanism of the ATM-dependent oxidative stress response that is different from DNA damage response and indicate involvement of the oxidative stress response in regulation of the metabolic system.
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