| Project/Area Number |
15K10235
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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 surgery
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
白石 修一 新潟大学, 医歯学総合病院, その他 (00422600)
佐藤 征二郎 新潟大学, 医歯学系, 助教 (40646931)
小池 輝元 新潟大学, 医歯学系, 講師 (90635723)
|
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | オートファジー / 肺癌 / 大動脈疾患 / 血管内皮 / 肺扁平上皮癌 / 血管内皮障害 / ｐ62 |
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| Outline of Final Research Achievements |
1. Analysis in lung cancer cells: Changes after glutaminolysis suppression regarding glutamine-dependent proliferation, mTORC1 activity, autophagy induction ability were analyzed using a lung cancer cell line. LC3 - II level was measured as an index of autophagy induction ability. It was found that cell proliferation was suppressed via mTORC1 signal suppression and autophage induction by suppressing glutaminolysis.
2. Vascular endothelial damage model: In the mouse model, expression of p53 was found to be enhanced when the vascular endothelium was exposed to stress such as ischemia and aging. It is thought that p62 is involved in autophagy, but the direct association between P53 and P62 is unknown, and further study is required.
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