2012 Fiscal Year Final Research Report
Regulation of MUTYH expression by p53 plays a critical role in cell death
| Project/Area Number |
22501014
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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 |
Tumor biology
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| Research Institution | Kyushu University |
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Principal Investigator |
OKA Sugako 九州大学, 生体防御医学研究所, 特任助教 (80467894)
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| Co-Investigator(Kenkyū-buntansha) |
NAKABEPPU Yusaku 九州大学, 生体防御医学研究所, 教授 (30180350)
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| Project Period (FY) |
2010 – 2012
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| Keywords | シグナル伝達と遺伝子発現 |
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| Research Abstract |
MUTYH, adenine DNA glycosylase excises adenine inserted opposite 8-oxoguanine (8-oxoG), a major form of spontaneous oxidative DNA damage, and whose deficiency is known to cause MUTYH-associated familial adenomatous polyposis. We have shown that accumulation of 8-oxoG in nuclear and mitochondrial DNA independently triggers two distinct MUTYH-dependent cell death programs. In the present study, we found that expression of MUTYH is regulated by p53 and identified functional p53-binding site in MUTYH gene. These results suggest that MUTYH is a potential mediator of p53 tumor suppression.
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[Journal Article] MutT Homolog-1 Attenuates Oxidative DNA Damage and Delays Photoreceptor Cell Death in Inherited Retinal Degeneration2012
Author(s)
Murakami Y, Ikeda Y, Yoshida N, Notomi S, Hisatomi T, Oka S, De Luca G, Yonemitsu Y, Bignami M, Nakabeppu Y, Ishibashi T
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Journal Title
Am J Pathol
Volume: 181(4)
Pages: 1378-86
Peer Reviewed
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