analyses of molecules which are related to an ATP releasing anion channel, Maxi-Cl.

2019 Fiscal Year Final Research Report

• Project/Area Number: 16K08510
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: National Institute for Physiological Sciences
• Principal Investigator: Okada Toshiaki 生理学研究所, 生体機能調節研究領域, 研究員 (00373283)
• Project Period (FY): 2016-04-01 – 2020-03-31
• Keywords: アニオンチャネル / Maxi-Cl / ATP放出

Outline of Final Research Achievements

The molecular entity of Maxi-Cl which is an ATP-release anion channel had long been elusive. We recently identified SLCO2A1 as a core factor of Maxi-Cl in murine C127 cell line. This study aimed to clarify whether SLCO2A1 is a channel pore-forming component or other important subcomponent and whether endogenous expression of SLCO2A1 is generally contributes to Maxi-Cl functions, current generation and ATP release, not only in C127 cells but also in the variety of cells. During a survey period, these purposes were partially, at least, validated and I published one thesis in and one another thesis has been accepted by a peer-reviewed journal. I had two times of conference presentation. I also published coauthored two review articles which are related to this project.

Free Research Field

分子細胞生理学

Academic Significance and Societal Importance of the Research Achievements

細胞外に放出されたATPは恒常性を維持するという生体にとって有益な反応を誘起する一方で、生体に不利益な反応をもたらすこともあるため、生理学的・医学的観点から広く注目されている。ATP放出性チャネルとして知られるMaxi-Clの分子機構を解明することにより、チャネルを介したATP放出による様々な生理学的・病理学的現象について分子論的な理解が深まることが期待される。医療分野においても、例えば心臓や脳における虚血－再灌流時に発生するATP放出が関与する組織のダメージ（心筋梗塞、脳梗塞）を軽減するような治療法の開発などの一助となることが期待される等、今後の研究の進展により様々な貢献が期待できる。