| Project/Area Number |
25650024
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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 |
Structural biochemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
MAITA Ayako 徳島大学, 大学院医歯薬学研究部(医学系), 特別研究員(RPD) (60415106)
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| Research Collaborator |
TSUGITA Saki 徳島大学, 大学院医歯薬学研究部
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | カルシウム恒常性 / NMR / サルコペニア / In-cell NMR / リアノジン受容体 |
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| Outline of Final Research Achievements |
Ryanodine receptor is the sarcoplasmic reticulum calcium release channel. We tried to investigate the interaction between ryanodine receptor and its stabilizing factor, FKBP12, by in-cell NMR. However, we did not succeed to deliver the protein of interest to myogenic cells. Thus, I changed the originally planned research project for the study focused on the interaction the protein complex (uncoupling protein 3 (UCP3) and HAX-1) that was involved in the control of the calcium influx into the mitochondria. The NMR and CD experiments showed that calcium-induced folding and stabilization of the C-terminal region of HAX-1 enable it to interact with UCP3. Moreover, the NMR experiment using two different detergents suggested that the C-terminal region could bind to biological membrane.
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