| Project/Area Number |
16K20910
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cell biology
Functional biochemistry
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| Research Institution | Tohoku University |
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Principal Investigator |
Nagai Tomoaki 東北大学, 生命科学研究科, 助教 (10723059)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 一次繊毛 / 中心体 / TTBK2 / Cep164 / 母中心小体 / 脊髄小脳変性症 / TTBK2キナーゼ / 細胞周期 / 細胞情報伝達機構 / 一次繊毛形成 |
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| Outline of Final Research Achievements |
Primary cilia are formed from the mother centriole in cellular quiescence. TTBK2 is a serine-threonine kinase that is essential for growth arrest-induced ciliogenesis, but its regulatory mechanism is largely unknown. In this study, I investigated the role of Cep164, a mother centriole protein known to recruit TTBK2 to the mother centriole, and ATR, a DNA damage response-related kinase, for TTBK2 activation. This study showed that an auto-interaction of TTBK2 between C-terminus and N-terminal kinase domain inhibits its kinase activity and that Cep164 interacts with the C-terminal region of TTBK2 and activate it through suppressing its autoinhibitory interaction. These results suggest that Cep164 plays an important role for not only the localization but also the activation of TTBK2.
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