Contributes to the regulation of lumenal Ca2+ release via the sarcoplasmic reticulum calcium release channels RYR1 and RYR2, a key step in triggering skeletal and heart muscle contraction. Required for normal organization of the triad junction, where T-tubules and the sarcoplasmic reticulum terminal cisternae are in close contact. Required for normal skeletal muscle strength (PubMed:19843516). Plays a role in excitation-contraction coupling in the heart and in regulating the rate of heart beats. Homooligomer of variable subunit number; disulfide-linked. Interacts with CASQ1 and RYR1 in skeletal muscle. Interacts with CASQ2. Detected in heart (at protein level). Detected in heart. Phosphorylated by CaMK2. N-glycosylated. Mice appear normal; they are viable and fertile but have reduced muscular strength, due to defects in the structure of the triad junction, where T-tubules and the sarcoplasmic reticulum terminal cisternae are in close contact. In mutant mice, about 25% of the triads are in oblique or longitudinal orientation, instead of the normal transversal orientation (PubMed:19843516). Similar structural defects are seen in the heart, leading to impaired excitation-contraction coupling. Mutant mice are subject to stress-induced ventricular tachycardia (PubMed:19383796).