| Project/Area Number |
25293073
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Saitama Medical University |
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Principal Investigator |
KUROKAWA RIKI 埼玉医科大学, 医学部, 教授 (70170107)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIMOTO KENTA 埼玉医科大学, 医学部, 助教 (50403580)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUSITA AKIO 埼玉医科大学, 医学部, 客員講師 (50402269)
OGAWA SUMITO 東京大学, 医学部附属病院, 准教授 (20323579)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2015: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥8,710,000 (Direct Cost: ¥6,700,000、Indirect Cost: ¥2,010,000)
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| Keywords | 酵素 / 遺伝子 / 核酸 / 生体分子 / 発現制御 / メチル化 / 長鎖非コードRNA |
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| Outline of Final Research Achievements |
We have demonstrated that the promoter-associated noncoding RNA-D (pncRNA-D) transcribed from a promoter region of the cyclin D1 gene represses its expression through binding of pncRNA-D to RNA-binding protein TLS (Nature 454: 126-130, 2008). TLS is found to target the 5’ end (32-62) of pncRNA-D. At the 3’ end (44-62) of pncRNA-D forms a stem-loop structure, while TLS firmly binds to the straight chain of the 5’ end (32-44) of pncRNA. Moreover, high-osmotic treatment of HeLa cells reduced methylation of the N6-adenosine (m6A) at pncRNA-D, but induced its binding to TLS. Recently, we have been analyzing effect of methylation of TLS on its binding to pncRNA-D. Methylation of long ncRNAs (lncRNAs) might regulate their physiological function presenting another exciting issue of the lncRNA biology.
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