2017 Fiscal Year Final Research Report
Study on selective autophagy on cellular functions
| Project Area | Multidisciplinary research on autophagy: from molecular mechanisms to disease states |
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| Project/Area Number |
25111006
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| Research Category |
Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Niigata University (2014-2017)
Tokyo Metropolitan Institute of Medical Science (2013) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
和栗 聡 福島県立医科大学, 医学部, 教授 (30244908)
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| Project Period (FY) |
2013-06-28 – 2018-03-31
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| Keywords | オートファジー / タンパク質分解 / p62 / Nrf2 / 肝細胞がん |
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| Outline of Final Research Achievements |
Autophagy has long been thought of as a bulk degradation system in which cytoplasmic components are sequestered by double-membrane structures called autophagosomes, and the contents are then degraded after autophagosomes fuse with lysosomes. Genetic experiments in yeast identified a set of Autophagy-related (ATG) genes that are essential for autophagy. We have since elucidated many of the molecular underpinnings of autophagy and the physiologic roles of these processes in various systems. Moreover, growing lines of evidence have shed light on indispensable role for autophagy in cellular homeostasis, which is mediated by selective degradation of a specific substrate(s). Such selectivity allows diverse cellular regulation, similar to the ubiquitin proteasome pathway. In this research program, we have addressed the pathophysiological roles of selective autophagy.
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| Free Research Field |
病態医化学
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