2017 Fiscal Year Final Research Report
Does nonreceptor type tyrosine kinase Fyn participate in autophagy mechanism in diabetic nephropathy ?
Project/Area Number |
15K09242
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Kidney internal medicine
|
Research Institution | Gunma University |
Principal Investigator |
Yamada Eijiro 群馬大学, 医学部附属病院, 助教 (60645563)
|
Co-Investigator(Kenkyū-buntansha) |
前嶋 明人 群馬大学, 大学院医学系研究科, 准教授 (70431707)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Keywords | Fyn / Tgm2 / オートファジー |
Outline of Final Research Achievements |
It was found that Fyn can directly phosphorylate Tgm2 in vitro. Wild type Tgm2 and phosphorylation site mutation Tgm2 were expressed in HK-2 cells, and the crosslinking of Beclin 1 was examined. It turned out that there was no change. When autophagy flux was examined in HK2 cells, autophagic activity was decreased in cells overexpressing Tgm2. This result seems to contribute to the elucidation of the mechanism of diabetic nephropathy.
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Free Research Field |
糖尿病性腎症
|