Voltage-gated calcium channels represent the sole mechanism converting electrical signals of excitable cells into cellular functions such as contraction, secretion, and gene regulation. Specific voltage-sensing domains detect changes in membrane potentials and control channel gating. Calcium ions entering through the channel function as second messengers regulating cell functions; with the exception of skeletal muscle, where CaV1.1 is essentially not functioning as channel but activates calcium release from intracellular stores. It has long been known that calcium currents are dispensable for skeletal muscle contraction. However, the questions as to how and why the channel function of CaV1.1 is curtailed remained obscure until the recent discovery of a developmental CaV1.1 splice variant with normal channel functions. This discovery enabled new means to study the molecular mechanisms regulating the channel gating and led to the understanding that in skeletal muscle calcium currents need to be restricted to allow proper regulation of fibre type specification and to prevent mitochondrial damage.
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