2009 Fiscal Year Final Research Report
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 |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | University of Tsukuba |
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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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| Keywords | 糖尿病 / 糖尿病性腎症 / Maf群タンパク質 / 転写因子 |
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| 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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[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
Peer Reviewed
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