Study on the regulatory mechanisms of L-type Ca2+ channels

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08181
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: Kagoshima University
• Principal Investigator: KAMEYAMA Masaki 鹿児島大学, 医歯学総合研究科, 客員研究員 (60150059)
• Co-Investigator(Kenkyū-buntansha): 徐 建軍 鹿児島大学, 医歯学域医学系, 講師 (10581689)
• Co-Investigator(Renkei-kenkyūsha): MINOBE Etsuko 鹿児島大学, 医歯学域医学系, 講師 (00448581) ; GAO Qinghua 鹿児島大学, 医歯学総合研究科, 特任研究員 (60813524)
• Research Collaborator: MORI Tomoyuki 京都大学, 工学研究科, 准教授 ; HAO Liying 中国医科大学, 薬学院薬理毒理学, 教授 ; ZHU Tong 東北大学, 機械工程及自動化学院, 教授 ; LYU Liting 東北大学, 機械工程及自動化学院, 大学院生 ; LEI Ming 中国医科大学, 薬学院薬理毒理学, 大学院生
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: Caチャネル / Aキナーゼ / カルモジュリン / 心筋

Outline of Final Research Achievements

We have investigated mechanisms underlying Cav1.2 Ca2+ channel regulation. We have found that: 1) the Ca2+ channels bind with protein kinase A (PKA) and protein phosphatases even in the inside-out mode; 2) there is a new interaction between CaM-binding region in the proximal C-terminal (CT1) and a region in the distal C-terminal (CT3) of alpha1C subunit; 3) PKA phosphorylation of CT1 affects the binding not only between CaM and CT1 but also the new proximal-distal (CT1-CT3) interaction. These results suggest that PKA phosphorylation regulate the Cav1.2 channel activity, at least partially, via affecting the CaM-CT1 interaction.

Free Research Field

生理学