2013 Fiscal Year Final Research Report
Roles of 53BP1 in elimination of an apoptotic cell
Project/Area Number |
24651056
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Single-year Grants |
Research Field |
Risk sciences of radiation/Chemicals
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Research Institution | Kanazawa Medical University |
Principal Investigator |
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Co-Investigator(Renkei-kenkyūsha) |
NAKAMURA Akira 金沢医科大学, 医学部, 教授 (20344723)
SUNATANI Yumi 金沢医科大学, 医学部, 助教 (70581057)
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Project Period (FY) |
2012-04-01 – 2014-03-31
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Keywords | アポトーシス |
Research Abstract |
p53 binding protein-1(53BP1) accumulates at sites of DNA double-strand breaks, where it suppresses DNA end resection, and facilitates repair of DNA double-strand breaks by non-homologous end joining. In this study, we found that in apoptotic cells 53BP1 is cleaved to generate a fragment of 53BP1 in a caspase-dependent manner. This 53BP1 fragment is localized on the surface of apoptotic cells. Our data suggest that 53BP1 regulates clearance of apoptotic cells by a macrophage.
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[Journal Article] DHX36 enhances RIG-I signaling by facilitating PKR-mediated antiviral stress granule formation2014
Author(s)
Yoo JS, Takahasi K, Ng CS, Ouda R, Onomoto K, Yoneyama M, Lai JC, Lattmann S, Nagamine Y, Matsui T, Iwabuchi K, Kato H, Fujita T
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Journal Title
PLoS Pathog
Volume: 10(3)
Pages: e1004012
Peer Reviewed
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