Study on the new cyst formation mechanism through the cell proliferation with the abnormal modification of RXR and examination of its mechanism-mediated suppressed effect on polycystic kidney disease
Project/Area Number |
24790393
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Experimental pathology
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Research Institution | Fujita Health University |
Principal Investigator |
KUGITA Masanori 藤田保健衛生大学, 疾患モデル教育研究センター, 助教 (50440681)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Project Status |
Completed (Fiscal Year 2014)
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Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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Keywords | 多発性嚢胞腎症 / RXR |
Outline of Final Research Achievements |
It is indicate that the expression level of retinoid X receptor (RXR) that is a ligand dependent nuclear receptor is increased by progression of polycystic kidney disease (PKD), RXR localize in nuclei of cystic epithelial cells, and there are a few kind of phosphorylated RXR in nucleus. RXR ligand and phosphatase inhibitor of RXR suppressed progression of PKD. Combination use of its reagents efficiently ameliorates pathological condition of PKD. These results suggest that RXR might be a new target molecule to create therapeutic agent for PKD.
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Report
(4 results)
Research Products
(36 results)
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[Journal Article] Global Gene ExpressionProfiling in PPAR-γ Agonist-TreatedKidneys in an Orthologous Rat Model of Human Autosomal Recessive Polycystic Kidney Disease.2012
Author(s)
Yoshihara D, Kugita M, Yamaguchi T, Aukema HM, Kurahashi H, Morita M, Hiki Y, Calvet JP, Wallace DP, Toyohara T, Abe T, Nagao S.
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Journal Title
PPAR Res
Volume: 2012
Pages: 695898-695898
DOI
Related Report
Peer Reviewed
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