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2021 Fiscal Year Final Research Report

Inactivation of Cav1.2 channel by 2 molecules of calmodulin

Research Project

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Project/Area Number 19K07303
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 48020:Physiology-related
Research InstitutionKagoshima University

Principal Investigator

Minobe Etsuko  鹿児島大学, 医歯学域医学系, 講師 (00448581)

Project Period (FY) 2019-04-01 – 2022-03-31
KeywordsCav1.2チャネル / 電気生理学実験 / パッチクランプ / カルモジュリン / カルシウム
Outline of Final Research Achievements

almodulin (CaM) is essential for the regulation of Cav1.2 channel activity. We reported that the Ca2+ dependent inactivation of the channel included the CaM-concentration-dependent manner but the molecular mechanism is still unclear. In this study, amino-terminal domain deletion channel maintained the CaM dependent inactivation measured by patch-clamp current recording. The carboxyl-terminal domain peptide linked with a CaM by Glycine linker bound with additional CaM. These results suggest that CaM-concentration-dependent inactivation induced without amino-terminal domain of the channel and with two CaM binding to carboxyl-terminal site.

Free Research Field

イオンチャネル

Academic Significance and Societal Importance of the Research Achievements

Cav1.2チャネルを含むL型Caチャネルは、心筋、骨格筋、神経系や分泌細胞に分布し、筋収縮、遺伝子発現、シナプス伝達、ホルモン分泌などにおいて重要な役割を持つため、本研究により得られた知見を広く応用できる。また、カルモジュリンにより制御されるチャネルはCaチャネルの他に多数あり、それらの作用機序の解明に貢献できる。カルモジュリンの遺伝子異常から病態につながる例も報告されており、カルモジュリンによるチャネルの活性調節は重要な位置づけにある。

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Published: 2023-01-30  

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