Alternative processing of the sarco/endoplasmic reticulum Ca(2+)-ATPase transcripts during muscle differentiation is a specifically regulated process.

Sarco / endoplasmic Reticulum Calcium ATPase - 2 ( SERCA 2 ) Expression is Regulated by ATF 6 During the Endoplasmic Reticulum Stress Response : Intracellular Signaling of Calcium Stress in a Cardiac Myocyte Model System

Modulation of SERCA2 activity: regulated splicing and interaction with phospholamban.

Ca(2+)-uptake into intracellular stores is mediated by the sarco/endoplasmic reticulum Ca(2+)ATPases (SERCAs). This review deals first with the gene structural and the characterization of the tissue-specific SERCA2 transcript processing. Secondly, the two different protein isoforms and their regulation are described. Finally, this review ends with a discussion on the possible physiological role...

Reduced sarco/endoplasmic reticulum Ca(2+) uptake activity can account for the reduced response to NO, but not sodium nitroprusside, in hypercholesterolemic rabbit aorta.

BACKGROUND Hypercholesterolemia (HC) impairs acetylcholine-induced relaxation but has little effect on that caused by the NO donor sodium nitroprusside (SNP), suggesting that acetylcholine releases less NO from the endothelium in HC. The relaxation to authentic NO gas, however, is also impaired in HC aortic smooth muscle, indicating an abnormal smooth muscle response. NO relaxes arteries by bot...

Cellular trafficking of phospholamban and formation of functional sarcoplasmic reticulum during myocyte differentiation.

Phospholamban (PLB) associates with the Ca(2+)-ATPase in sarcoplasmic reticulum (SR) membranes to permit the modulation of contraction in response to beta-adrenergic signaling. To understand how coordinated changes in the abundance and intracellular trafficking of PLB and the Ca(2+)-ATPase contribute to the maturation of functional muscle, we measured changes in abundance, location, and turnove...

Reduced Sarco/Endoplasmic Reticulum Ca Uptake Activity Can Account for the Reduced Response to NO, but Not Sodium Nitroprusside, in Hypercholesterolemic Rabbit Aorta

Background—Hypercholesterolemia (HC) impairs acetylcholine-induced relaxation but has little effect on that caused by the NO donor sodium nitroprusside (SNP), suggesting that acetylcholine releases less NO from the endothelium in HC. The relaxation to authentic NO gas, however, is also impaired in HC aortic smooth muscle, indicating an abnormal smooth muscle response. NO relaxes arteries by bot...