The progressive nephropathy in Skp2-p27 double knockout mice.
Project/Area Number |
22790310
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Pathological medical chemistry
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Research Institution | Hamamatsu University School of Medicine |
Principal Investigator |
SUZUKI Sayuri 浜松医科大学, 医学部, 特任研究員 (80568949)
|
Project Period (FY) |
2010 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 細胞増殖 / タンパク分解 / 腎障害 / p27 / Skp2 / Cks1 |
Research Abstract |
p27, is known a Skp2 target, most increased in the UUO kidney in Skp2^<-/-> mice. The ameliorated UUO renal injure by Skp2-deficiency was canceled by the additional p27-deficiency in Skp2^<-/-> p27^<-/-> mice. These findings suggest a pathogenic role of the reduction in p27 targeted by Skp2 in the progression of nephropathy in UUO mice.
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Report
(3 results)
Research Products
(12 results)
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[Journal Article] Up-regulation of Cks1 and Skp2 with TNFα/NF-κB Signaling in Chronic Progressive Nephropathy2011
Author(s)
Suzuki S., Fukasawa H., Misaki T., Togawa A., Ohashi N., Kitagawa K., Kotake Y., Niida H., Hishida A., Yamamoto T., and Kitagawa M.
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Journal Title
Genes Cells
Volume: 16
Pages: 1110-1120
Related Report
Peer Reviewed
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[Journal Article] Reduction of transforming growth factor-b type II receptor is caused by the enhanced ubiquitin-dependent degradation in human renal cell carcinoma2010
Author(s)
Fukasawa H, Yamamoto T, Fujigaki Y, Misaki T, Ohashi N, Takayama T, Suzuki S, Mugiya S, Oda T, Uchida C, Kitagawa K, Hattori T, Hayashi H, Ozono S, Kitagawa M and Hishida A
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Journal Title
Int. J. Cancer
Volume: 127
Pages: 1517-1525
Related Report
Peer Reviewed
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