Ca(2+) signaling in striated muscle: the elusive roles of triadin, junctin, and calsequestrin.
This review focuses on molecular interactions between calsequestrin, triadin, junctin and the ryanodine receptor in the lumen of the sarcoplasmic reticulum. These interactions modulate changes in Ca(2+) release in response to changes in the Ca(2+) load within the sarcoplasmic reticulum store in striated muscle and are of fundamental importance to Ca(2+) homeostasis, since massive adaptive changes occur when expression of the proteins is manipulated, while mutations in calsequestrin lead to functional changes which can be fatal. We find that calsequestrin plays a different role in the heart and skeletal muscle, enhancing Ca(2+) release in the heart, but depressing Ca(2+) release in skeletal muscle. We also find that triadin and junctin exert independent influences on the ryanodine receptor in skeletal muscle where triadin alone modifies excitation-contraction coupling, while junctin alone supports functional interactions between calsequestrin and the ryanodine receptor.
Muscle Research Group, John Curtin School of Medical Research, Australian National University, PO Box 334, Canberra, ACT, 2601, Australia.
Nicole A
NA
Beard
Lan
L
Wei
Angela Fay
AF
Dulhunty
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology*; D002155:Calsequestrin / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism*; D006801:Humans; D009124:Muscle Proteins / Q000378:metabolism*; D054792:Muscle, Striated / Q000166:cytology* / Q000378:metabolism*; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism
D002155:Calsequestrin; D002352:Carrier Proteins; D009124:Muscle Proteins; D019837:Ryanodine Receptor Calcium Release Channel; C070048:triadin; D002118:Calcium