The protein encoded by this gene specifies the cardiac muscle family member of the calsequestrin family. Calsequestrin is localized to the sarcoplasmic reticulum in cardiac and slow skeletal muscle cells. The protein is a calcium binding protein that stores calcium for muscle function. Mutations in ...
Acute aerobic exercise regulation of myocardial calcium homeostasis involves CASQ1, CASQ2, and TRDNdoi:10.1152/japplphysiol.00299.2023bioinformaticscalcium overloadLangendorffmyocardiumRNA-seqExercise maintains cardiac calcium homeostasis and promotes cardiovascular health. This study explored temporal changes of ...
Gene SummaryThe protein encoded by this gene specifies the cardiac muscle family member of the calsequestrin family. Calsequestrin is localized to the sarcoplasmic reticulum in cardiac and slow skeletal muscle cells. The protein is a calcium binding protein that stores calcium for muscle function. Muta...
Timothy syndrome is a multisystem disorder associated with QT interval prolongation and ventricular cardiac arrhythmias. The syndrome has been linked to mutations in Ca(V)1.2 resulting in gain of function of the L-type calcium current (I... S Sicouri,L Zhang,KW Timothy,... - 《Heart Rhythm...
Calcium homeostasis, the basis of cardiac function, relies on the release (RyR2 and FKBP12.6), uptake (SERCA2a and phospholamban, PLB), and storage (calsequestin 2, CASQ2) of Ca2+ in the SR. RyR2, FKBP12.6, SERCA2a, and PLB were found to be downregulated in failing hearts and ...
Deletion of either CASQ2 or HRC results in relatively mild phenotypes characterized by preserved cardiac structure and function, although CASQ2 knockout (KO), or Cnull, shows increased arrhythmia burden under conditions of catecholaminergic stress. We hypothesized that given the apparent overlap of ...
Deletion of either CASQ2 or HRC results in relatively mild phenotypes characterized by preserved cardiac structure and function, although CASQ2 knockout (KO), or Cnull, shows increased arrhythmia burden under conditions of catecholaminergic stress. We hypothesized that given the apparent overlap of ...
Young mutant mice had structurally normal hearts but stress-induced ventricular arrhythmias; aging produced cardiac hypertrophy and reduced contractile function. Mutant myocytes had reduced CASQ2 and increased calreticulin and RyR2 (with normal phosphorylated proportions) but unchanged calstabin levels, as ...