2013 Fiscal Year Final Research Report
Roles of 53BP1 in progression of apoptosis
| Project/Area Number |
23310041
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Risk sciences of radiation/Chemicals
|
|---|
| Research Institution | Kanazawa Medical University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Mitsumasa 金沢医科大学, 一般教育機構, 准教授 (70293975)
ISHIGAKI Yasuhito 金沢医科大学, 総合医学研究所, 准教授 (20232275)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
SUNATANI Yumi 金沢医科大学, 医学部, 助教 (70581057)
|
|---|
| Project Period (FY) |
2011-04-01 – 2014-03-31
|
| Keywords | アポトーシス |
|---|
| Research Abstract |
p53 binding protein-1 (53BP1) facilitates non-homologous end joining repair of DNA double-strand breaks. In this study, we examined functional interaction between 53BP1 and p53 in apoptotic cells. We found that 53BP1 is cleaved into a fragment of 53BP1 in a caspase-dependent manner. 53BP1 cleavage is observed in both cells with wild-type and mutant p53. Some of the 53BP1 fragments are localized on the surface of apoptotic cells, suggesting a role of 53BP1 in elimination of apoptotic cells by a macrophage. Downregulation of 53BP1 reduces transcription of several p53 target genes. However, binding of p53 on the promoter in these genes is not affected by 53BP1 downregulation, suggesting that 53BP1 regulates transcriptional activity of p53 by regulating modification of p53 on the promoter in the target genes.
|
-
[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
-
Journal Title
PLoS P athog
Volume: 10(3)
Pages: e1004012
Peer Reviewed
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
