Affiliation:
1. Department of Physiology, Graduate School of Medical & Dental Sciences, Kagoshima University, Sakura-ga-oka, Kagoshima 890-8544, Japan
2. Department of Pharmaceutical Toxicology, School of Pharmacy, China Medical University, Shenyang 110012, China
Abstract
Cav1.2 Ca2+ channels, a type of voltage-gated L-type Ca2+ channel, are ubiquitously expressed, and the predominant Ca2+ channel type, in working cardiac myocytes. Cav1.2 channels are regulated by the direct interactions with calmodulin (CaM), a Ca2+-binding protein that causes Ca2+-dependent facilitation (CDF) and inactivation (CDI). Ca2+-free CaM (apoCaM) also contributes to the regulation of Cav1.2 channels. Furthermore, CaM indirectly affects channel activity by activating CaM-dependent enzymes, such as CaM-dependent protein kinase II and calcineurin (a CaM-dependent protein phosphatase). In this article, we review the recent progress in identifying the role of apoCaM in the channel ‘rundown’ phenomena and related repriming of channels, and CDF, as well as the role of Ca2+/CaM in CDI. In addition, the role of CaM in channel clustering is reviewed.
Funder
JSPS KAKENHI Grants of Japan
National Natural Science Foundation of China
Subject
Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis
Cited by
1 articles.
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1. Calcium Channels and Calcium-Binding Proteins;International Journal of Molecular Sciences;2023-09-19