| Project/Area Number |
15K15062
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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 |
General medical chemistry
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| Research Institution | University of Fukui |
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Principal Investigator |
NAKAYA MAKO 福井大学, 学術研究院医学系部門, 助教 (60538552)
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| Co-Investigator(Kenkyū-buntansha) |
青木 耕史 福井大学, 学術研究院医学系部門, 教授 (40402862)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | オートファジー / ATG7 |
|---|
| Outline of Final Research Achievements |
In recent years, abnormality of genes involved in autophagy has been reported as a cause of cancer, Crohn's disease, ulcerative colitis and neurodegenerative diseases from genome-wide association analysis. We found that the homeobox protein CDX2 specifically expressed in the intestinal epithelial cells we are interested in binds to ATG7, an essential enzyme of autophagy. Furthermore, three genes that bind to ATG7 were identified among 30 screening candidates for ATG7. We also clarified that CDX2 suppresses bacterial growth in the intestine in Citrobacter rodentium infection using Cdx2 gene mutant mice.
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