| Project/Area Number |
26461240
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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 |
Kidney internal medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
富野 康日己 順天堂大学, 医学部, 名誉教授 (60130077)
鈴木 祐介 順天堂大学, 医学(系)研究科(研究院), 教授 (70372935)
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| Research Collaborator |
MAIGUMA Masayuki
TAKAHATA Akiko
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | IgA腎症 / gddYマウス / HIGAマウス / 糖鎖修飾 / 次世代シーケンス |
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| Outline of Final Research Achievements |
Pathogenesis of IgA nephrology is still unknown. There are some reports which suggest that genetic factors are related to the mutation in genetic region for IgA glucosylation. In this study, we assessed the genetic regions of IgA glucose deficiency by comparing the two mice strains originated from ddY mouse, grouped ddY (gddY) mouse and HIGA mouse. While gddY mouse has early onset of IgAN within a 100% incidence, HIGA
mouse has high serum level of IgA but does not always develop IgAN. By studying the genes using the micro-satellite markers, we found out that genetic area around D12Mit20 may be the responsible gene of glucose deficiency in IgAN. Since we need to consider other methods to compare the other genetic regions as also in full detail, we will introduce the next-genetic sequence method and continue the study.
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