2017 Fiscal Year Final Research Report
Systems biology analysis of the pathogenesis of kidney injury caused by deficiency of a water channel protein localized in the endoplasmic reticulum
| Project/Area Number |
15H04594
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Veterinary medical science
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| Research Institution | University of Miyazaki |
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Principal Investigator |
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| Research Collaborator |
ISHIBASHI Kenichi
MATSUZAKI Toshiyuki
SONODA Hiroko
YOKOTA-IKEDA Naoko
NAGANOBU Kiyokazu
TORISU Shidow
KANEKO Yasuyuki
TAKAHASHI Saki
OSHIKAWA Sayaka
MIKODA Nobuyuki
ASVAPROMTADA Siree
HOSHINO Yuya
SINLAPADEELERDKUL Thitaporn
KATO Ayaka
KINOUCHI Minami
KOGA Moeko
KISHABA Ai
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | アクアポリン-11 / systems biology / 小胞体 / NOX2 / 酸化ストレス / アポトーシス |
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| Outline of Final Research Achievements |
Aquaporin-11 (AQP11), a member of a family of transmembrane channel proteins, is known to be localized in the endoplasmic reticulum. So far, studies with AQP11-deficient mice have suggested that loss of function of AQP11 caused kidney injury, characterized by formation of cysts. However, the mechanism underlying the kidney injury remains unclear. In this study, in order to clarify the mechanism, we examined the kidneys from AQP11-deficient mice using systems biology. Finally, we found that the pathway of NADPH oxidase 2 (NOX2) - reactive oxygen species - apoptosis might be involved in the AQP11-deficient-induced kidney injury.
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| Free Research Field |
獣医薬理学
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