When observed under a microscope, skeletal muscle exhibits striations due to the highly organized arrangement of muscle proteins that interact with one another to induce muscle contraction. Muscle contraction requires transient increases in intracellular 'Ca(2+)' concentration. In this review, Ca(2+) channels contributing to the functional integrity of intracellular Ca(2+)-release and extracellular Ca(2+)-entry during skeletal muscle contraction are reviewed in terms of their properties, newly emerging ancillary proteins to them, and their abnormalities related to human skeletal muscle diseases. Finally, the aim of this review is to show the big picture of the correlation among Ca(2+) channels that participate in the Ca(2+) homeostasis in skeletal muscle.
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