A novel mouse model of diabetic nephropathy : MafA-deficient and beta cell-specific MafK-overexpressing hybrid transgenic
Project/Area Number |
19590933
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Kidney internal medicine
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Research Institution | University of Tsukuba |
Principal Investigator |
YOH Keigyou University of Tsukuba, 大学院・人間総合科学研究科, 准教授 (90323302)
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Project Period (FY) |
2007 – 2009
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Project Status |
Completed (Fiscal Year 2009)
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Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | 糖尿病 / 糖尿病性腎症 / Maf群タンパク質 / 転写因子 / Maf |
Research Abstract |
We generated hybrid transgenic mice that were MafA-deficient and also overexpressed MafK specifically in beta cells (MafA-/-MafK+). MafA-/-MafK+ mice developed severe overt diabetes mellitus within 5 weeks old. Furthermore, after uninephrectomy, these mice demonstrated three characteristics of human diabetic nephropathy : diffuse, nodular, and exudative lesions. MafA-/-MafK+ mice might be a useful model for the analysis of human diabetic nephropathy.
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Report
(4 results)
Research Products
(6 results)
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[Journal Article] MafA-deficient and beta cell-specific MafK-overexpressing hybrid transgenic mice develop human-like severe diabetic nephropathy2009
Author(s)
Shimohata H, Yoh K, Fujita A, Morito N, Ojima M, Tanaka H, Hirayama K, Kobayashi M, Kudo T, Yamagata K, Takahashi, S.
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Journal Title
Biochem Biophys Res Commun. 389(2)
Pages: 235-40
Related Report
Peer Reviewed
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