Transcriptional repressor RP58 as neuronal maturation and maintenance
Project/Area Number |
26290016
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Nerve anatomy/Neuropathology
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Research Institution | Tokyo Metropolitan Institute of Medical Science |
Principal Investigator |
OKADO Haruo 公益財団法人東京都医学総合研究所, 脳発達・神経再生研究分野, プロジェクトリーダー (60221842)
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Co-Investigator(Kenkyū-buntansha) |
平井 志伸 公益財団法人東京都医学総合研究所, その他部局等, 研究員 (00625189)
平井 清華 公益財団法人東京都医学総合研究所, その他部局等, 研究員 (80606434)
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Co-Investigator(Renkei-kenkyūsha) |
TANAKA Kenji 慶応義塾大学, 医学部, 准教授 (30329700)
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Research Collaborator |
KANZAKI Seiji
TAKASAWA Katsuko
SHIMBO Hiroko
TANAKA Tomoko
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥14,950,000 (Direct Cost: ¥11,500,000、Indirect Cost: ¥3,450,000)
Fiscal Year 2016: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2015: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2014: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
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Keywords | RP58 / 転写抑制因子 / 脳形成 / 行動異常 / 知的障害 / 加齢性脳障害 / 脳発達 / 加齢 / 変異マウス / RP58 / 老化 / FASTシステム / 大脳皮質 |
Outline of Final Research Achievements |
It has been reported that nonsense mutation of transcriptional repressor RP58 is found in the patients of intellectual disability, and the expression of RP58 is reduced in aged prefrontal cortex. Therefore, we raise the hypothesis that the quantity of RP58 is important for brain function. To examine the hypothesis, we generated the mice, in which RP58 expression is reduced. The RP58 hetero mice (RP58+/-) show the abnormal behaviors with little abnormality of brain formation. The mice, in which the expression of RP58 is reduced to one-third, shows more sever abnormal behavior and abnormal brain formation. These results indicate that quantitative expression of RP58 is involved in behavior and brain formation.
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Report
(4 results)
Research Products
(14 results)
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[Journal Article] Altered tau isoform ratio caused by loss of Fus and Sfpq function leads to FTLD-like phenotypes2017
Author(s)
Ishigaki S, Fujioka Y, Okada Y, Riku Y, Udagawa T, Honda D, Yokoi S, Endo K, Ikenaka K, Takagi S, Iguchi Y, Sahara N, Takashima A, Okano H, Yoshida M, Warita H, Aoki M, Watanabe H, Okado H, Katsuno H, Sobue G.
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Journal Title
Cell Reports
Volume: 18
Issue: 5
Pages: 1118-1131
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Phosphorylation of TAR DNA-binding Protein of 43 kDa (TDP-43) by Truncated Casein Kinase 1δ Triggers Mislocalization and Accumulation of TDP-43.2016
Author(s)
Nonaka T, Suzuki G, Tanaka Y, Kametani F, Hirai S, Okado H, Miyashita T, Saitoe M, Akiyama H, Masai H, Hasegawa M.
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Journal Title
The journal of Biological Chemistry
Volume: 291
Issue: 11
Pages: 5473-83
DOI
Related Report
Peer Reviewed / Open Access
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