| Project/Area Number |
25650063
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cell biology
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| Research Institution | Nagoya University |
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Principal Investigator |
SENGA Takeshi 名古屋大学, 医学(系)研究科(研究院), 准教授 (80419431)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Akio 名古屋大学, 大学院医学系研究科, 准教授 (10343203)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | RNA / スプライシング / 細胞周期 / 細胞分裂 / アポトーシス / ＢＣＡＳ２ / ＣＤＣ５Ｌ / ＳＮＷ１ / ＲＮＡ |
|---|
| Outline of Final Research Achievements |
SNW1 is associated with RNA splicing or transcription of specific genes. We found that SNW1 depletion inhibited cell cycle progression and induced apoptosis. We identified EFTUD2 and SNRNP200 are direct binding partner of SNW1. Similar to SNW1 knockdown, suppression of either EFTUD2 or SNRNP200 inhibited cell cycle progression and induced apoptosis. Expression of mutant SNW1 or EFTUD2 that could disrupt binding of interaction between endogenous SNW1 and EFTUD2 promoted apoptosis by arresting cells in mitosis. These results indicate that inhibition of SNW1 function may inhibit cell cycle progression and promote apoptosis.
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