2017 Fiscal Year Final Research Report
Elucidation of mechanism for coupling factor 6-induced accelerated aging and identification of its inhibitory protein
| Project/Area Number |
15K09151
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Hirosaki University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
奥村 謙 弘前大学, 医学研究科, 客員研究員 (20185549)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | coupling factor 6 / aging / autophagy / telomere / epigenetics / genomic instability / inhibitory protein 1 |
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| Outline of Final Research Achievements |
Coupling factor 6 (CF6) converts the rotation of ecto-F1Fo complex from a clockwise mode of proton export to a counter-clockwise mode of proton import. Inhibitory peptide 1 (IF1) is a unidirectional inhibitor of ATP hydrolysis. TG cells displayed the decrease in lamin and emerin and the increase in H3K4me3 and H4K20me3. LC3 II and lysosome were stained weakly in the peripheral cytoplasm in TG cells. LC3 II and P62 were increased and Atg7 was decreased in TG cells. Telomere length was shorter in TG cells. Overexpression of IF1 rescued TG cells from all aging hallmarks. IF1 suppressed CF6-induced expression of aging hallmarks, and may function as an anti-aging molecule.
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| Free Research Field |
医歯薬学
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