A targeting mechanism of membrane protein to proteasome

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08183
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: Kyoto Gakuen University
• Principal Investigator: Niisato Naomi 京都学園大学, 健康医療学部, 教授 (00237645)
• Co-Investigator(Kenkyū-buntansha): 丸中 良典 京都府立医科大学, 医学(系)研究科(研究院), 教授 (00127036) ; 宮崎 裕明 京都府立医科大学, 医学(系)研究科(研究院), 助教 (30360027)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: proteasome / ENaC / p97 / MG132 / Ubiquitin

Outline of Final Research Achievements

In this study, we hypothesized that membrane proteins containing ENaC might be degraded in proteasome through a similar mechanism to “retrotranslocation” in ERAD (endoplasmic reticulum associated degradation. As results, we indicate that 1) a p97 (a AAA+ ATPase) inhibitor accumulated ENaC in the plasma membrane when ENaC degradation was induced by a p38 inhibitor, 2) p97 colocalized with ENaC by inducing ENaC degradation with a p38 inhibitor, 3) a composition of proteasome also colocalized with ENaC by a p38 inhibitor. Based on these results, ENaC might be degrated in proteasome through a p97-dependent mechanism.

Free Research Field

細胞生理学