ATP-sensitive voltage- and calcium-dependent chloride channels in sarcoplasmic reticulum vesicles from rabbit skeletal muscle

1997 ◽  
Vol 157 (1) ◽  
pp. 39-51 ◽  
Author(s):  
J. I. Kourie
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Chloride Channels ◽  
Rabbit Skeletal Muscle ◽  
Calcium Dependent

scholarly journals Calsequestrin: a well-known but curious protein in skeletal muscle

2020 ◽  
Vol 52 (12) ◽  
pp. 1908-1925
Author(s):  
Jin Seok Woo ◽  
Seung Yeon Jeong ◽  
Ji Hee Park ◽  
Jun Hee Choi ◽  
Eun Hui Lee
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Human Skeletal Muscle ◽  
Rabbit Skeletal Muscle ◽  
Muscle Type ◽  
Muscle Diseases ◽  
The Past ◽  
Muscle Tissues ◽  
Suitable Amount ◽  
Terminal Cisternae

AbstractCalsequestrin (CASQ) was discovered in rabbit skeletal muscle tissues in 1971 and has been considered simply a passive Ca2+-buffering protein in the sarcoplasmic reticulum (SR) that provides Ca2+ ions for various Ca2+ signals. For the past three decades, physiologists, biochemists, and structural biologists have examined the roles of the skeletal muscle type of CASQ (CASQ1) in skeletal muscle and revealed that CASQ1 has various important functions as (1) a major Ca2+-buffering protein to maintain the SR with a suitable amount of Ca2+ at each moment, (2) a dynamic Ca2+ sensor in the SR that regulates Ca2+ release from the SR to the cytosol, (3) a structural regulator for the proper formation of terminal cisternae, (4) a reverse-directional regulator of extracellular Ca2+ entries, and (5) a cause of human skeletal muscle diseases. This review is focused on understanding these functions of CASQ1 in the physiological or pathophysiological status of skeletal muscle.

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