Identification and characterization of a membrane protein TRAP involved in Fanconi syndrome like symptoms.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390217
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: Osaka University
• Principal Investigator: Kanai Yoshikatsu 大阪大学, 医学(系)研究科(研究院), 教授 (60204533)
• Co-Investigator(Kenkyū-buntansha): 大垣 隆一 大阪大学, 医学(系)研究科(研究院), 助教 (20467525) ; 永森 收志 大阪大学, 医学(系)研究科(研究院), 准教授 (90467572) ; 奥田 傑 大阪大学, 医学(系)研究科(研究院), 助教 (50511846)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 腎臓学 / 腎生理学

Outline of Final Research Achievements

We identified a novel membrane protein TRAP, which was specifically localized at luminal membrane of renal proximal tubules. It's KO mice showed Fanconi syndrome-like symptoms such as glucosuria, aminoaciduria and uricosuria. TRAP was co-expressed with various renal transporters. Proteomics analysis showed that TRAP interacts directly with those transporters to regulate their localization at luminal membrane of renal proximal tubules. TRAP KO mice did not maintaine normal distribution of transporters at luminal membrane. These data suggest that TRAP can regulate multiple transporters of renal proximal tubules by affecting their localization at luminal membrane.
Our results indicate that TRAP can be a new candidate gene responsible for Fanconi syndrome. They, furthermore, suggest a novel mechanism to integrate multiple transporters in solute transport.

Free Research Field

医歯薬学