2017 Fiscal Year Final Research Report
Revealing the physiological function of de-N-glycosylating enzymes in mice
| Project/Area Number |
16K18520
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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 |
Functional biochemistry
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Keywords | Ngly1 / ENGase / ubiquitin-proteasome / autophagy |
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| Outline of Final Research Achievements |
In this study, I aimed to reveal an unknown physiological function of de-N-glycosylating enzymes, peptide:N-glycanase (Ngly1) and endo-beta-N-acetylglucosaminidase (ENGase), in mammals. To this end, I performed phenotypic analyses of mice that lack Ngly1/Engase gene (Ngly1-KO, Engase-KO, Ngly1;Engase-KO mice). I found that the deletion of Ngly1 causes many defects (heart, muscle, nervous systems, body weight etc), while Engase deletion does not cause any defects. Interestingly, the defects caused by the loss of Ngly1 are partially rescued by the additional deletion of Engase gene. Therefore, there are two types of pathways that cause the defects by Ngly1-deletion, ENGase-dependent pathway and ENGase-independent pathway. Based on recent reports and my additional experiments suggested that a transcriptional factor Nrf1, which regulates the expression levels of proteasome subunits under low proteasome activity, seems to be involved in the ENGase-independent pathway.
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| Free Research Field |
糖鎖生物学
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