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Calsequestrin 2

CASQ2, calsequestrin 2
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 this gene cause stress-induced polymorphic ventricular tachycardia, also referred to as catecholaminergic polymorphic ventricular tachycardia 2 (CPVT2), a disease characterized by bidirectional ventricular tachycardia that may lead to cardiac arrest. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Calsequestrin, RyR2, CAN, HAD, Triadin
Papers on CASQ2
Sudden death during struggle in the setting of heterozygosity for a mutation in calsequesterin 2.
Pollanen et al., Toronto, Canada. In Forensic Sci Med Pathol, Jan 2016
Post-mortem molecular testing demonstrated this man to be heterozygous for a catecholaminergic polymorphic ventricular tachycardia (CPVT) associated mutation (Phe189Leu) in the calsequestrin 2 (CASQ2) gene.
David Triggle: Research collaborations and scientific exchanges with the China Pharmaceutical University, Nanjing, China.
Dai, Nanjing, China. In Biochem Pharmacol, Dec 2015
sarco/endoplasmic reticulum Ca(2+)ATPse (SERCA2A) and calsequens 2 (CASQ2), calcium leak at the diastole and endoplasmic reticulum stress, were evaluated and are discussed.
Ablation of HRC alleviates cardiac arrhythmia and improves abnormal Ca handling in CASQ2 knockout mice prone to CPVT.
Györke et al., Columbus, United States. In Cardiovasc Res, Dec 2015
AIMS: Cardiac calsequestrin (CASQ2) and histidine-rich Ca-binding protein (HRC) are sarcoplasmic reticulum (SR) Ca-binding proteins that regulate SR Ca release in mammalian heart.
Left Cardiac Sympathetic Denervation in Patients with CASQ2-Associated Catecholaminergic Polymorphic Ventricular Tachycardia.
Khoury et al., In Isr Med Assoc J, Sep 2015
OBJECTIVES: To report our experience with LCSD in calsequestrin (CASQ2) mutation-associated CPVT.
CPUY11018, an azimilide derivative, ameliorates isoproterenol-induced cardiac insufficiency through relieving dysfunctional mitochondria and endoplasmic reticulum.
Dai et al., Nanjing, China. In J Pharm Pharmacol, Aug 2015
CASQ2 and SERCA2a was also remarkable in vivo and in vitro implying an abnormal ER.
Functional abnormalities in iPSC-derived cardiomyocytes generated from CPVT1 and CPVT2 patients carrying ryanodine or calsequestrin mutations.
Binah et al., Haifa, Israel. In J Cell Mol Med, Aug 2015
CPVT is caused by abnormal intracellular Ca(2+) handling resulting from mutations in the RyR2 or CASQ2 genes.
Targeted next-generation sequencing (NGS) of nine candidate genes with custom AmpliSeq in patients and a cardiomyopathy risk group.
Baranov et al., Saint Petersburg, Russia. In Clin Chim Acta, Jul 2015
METHODS: We developed a custom AmpliSeq panel for NGS sequencing of the coding sequences of ACTC1, MYBPC3, MYH7, MYL2, MYL3, TNNI3, TNNT2, TPM1, and CASQ2.
Impaired calcium-calmodulin-dependent inactivation of Cav1.2 contributes to loss of sarcoplasmic reticulum calcium release refractoriness in mice lacking calsequestrin 2.
Knollmann et al., Nashville, United States. In J Mol Cell Cardiol, May 2015
We recently reported that the SR luminal Ca(2+) binding protein calsequestrin 2 (Casq2) contributes to release refractoriness in intact mouse hearts, but the underlying mechanisms remain unclear.
Comprehensive Identification of Sexual Dimorphism-Associated Differentially Expressed Genes in Two-Way Factorial Designed RNA-Seq Data on Japanese Quail (Coturnix coturnix japonica).
Lee et al., Seoul, South Korea. In Plos One, 2014
Several of the genes identified in the present study as significant sex-related genes have been previously found in avian gene expression analyses (NIPBL, UBAP2), and other genes found differentially expressed in this study and not previously associated with sex-related differences may be considered potential candidates for molecular sexing (TERA, MYP0, PPR17, CASQ2).
Genetic Analysis of Arrhythmogenic Diseases in the Era of NGS: The Complexity of Clinical Decision-Making in Brugada Syndrome.
Brugada et al., Girona, Spain. In Plos One, 2014
Twenty-eight genes were resequenced: AKAP9, ANK2, CACNA1C, CACNB2, CASQ2, CAV3, DSC2, DSG2, DSP, GPD1L, HCN4, JUP, KCNE1, KCNE2, KCNE3, KCNH2, KCNJ2, KCNJ5, KCNQ1, NOS1AP, PKP2, RYR2, SCN1B, SCN3B, SCN4B, SCN5A, SNTA1, and TMEM43.
Common Variants in TRDN and CALM1 Are Associated with Risk of Sudden Cardiac Death in Chronic Heart Failure Patients in Chinese Han Population.
Pu et al., Beijing, China. In Plos One, 2014
BACKGROUND: Recent studies suggest that variants in two calcium handling genes (RyR2 and CASQ2) associated with sudden cardiac death (SCD) and non-sudden cardiac death (NSCD) in subjects with heart failure and coronary artery disease, respectively.
Inherited calcium channelopathies in the pathophysiology of arrhythmias.
Priori et al., Pavia, Italy. In Nat Rev Cardiol, 2012
Firstly, we discuss mutations in the genes encoding the ryanodine receptor 2 (RYR2) and calsequestrin 2 (CASQ2).
Regulation of sarco(endo)plasmic reticulum Ca2+-ATPase and calsequestrin gene expression in the heart.
Fragoso-Medina et al., Mexico. In Can J Physiol Pharmacol, 2012
Calsequestrin (Casq2) is the main protein in the SR lumen, functioning as a Ca(2+) buffer and participating in Ca(2+) release by interacting with the ryanodine receptor 2 (RyR2) Ca(2+)-release channel.
Calsequestrin mutations and catecholaminergic polymorphic ventricular tachycardia.
Knollmann et al., Nashville, United States. In Pediatr Cardiol, 2012
Cardiac calsequestrin (Casq2) is the major Ca2+ binding protein in the sarcoplasmic reticulum, which is the principle Ca2+ storage organelle of cardiac muscle.
Importance of ventricular tachycardia storms not terminated by implantable cardioverter defibrillators shocks in patients with CASQ2 associated catecholaminergic polymorphic ventricular tachycardia.
Boulos et al., Haifa, Israel. In Am J Cardiol, 2012
patients with CASQ2-associated CPVT should be recommended to receive ICDs to prevent sudden death when medical therapy is not effective.
Modulation of SR Ca2+ release by the triadin-to-calsequestrin ratio in ventricular myocytes.
Kirchhefer et al., Münster, Germany. In Am J Physiol Heart Circ Physiol, 2012
The triadin-to-calsequestrin ratio is a critical modulator of the sarcoplasmic reticulum Ca(2+) signaling in ventricular myocytes.
Cardiomyocytes generated from CPVTD307H patients are arrhythmogenic in response to β-adrenergic stimulation.
Binah et al., Haifa, Israel. In J Cell Mol Med, 2012
Aspartate to histidine casq2 mutation causes arrhythmia in cardiomyocytes generated from catecholaminergic polymorphic ventricular tachycardia patients.
Guidelines for the diagnosis and management of Catecholaminergic Polymorphic Ventricular Tachycardia.
Davis et al., Melbourne, Australia. In Heart Lung Circ, 2012
CPVT can be caused by mutations the cardiac ryanodine receptor gene (RYR2) or mutations in the cardiac calsequestrin gene CASQ2.
Role of Junctin protein interactions in cellular dynamics of calsequestrin polymer upon calcium perturbation.
Kwon et al., Taejŏn, South Korea. In J Biol Chem, 2012
Ca(2+) and JNT-dependent disassembly of the CSQ2 polymer
Functional consequences of stably expressing a mutant calsequestrin (CASQ2D307H) in the CASQ2 null background.
Periasamy et al., Columbus, United States. In Am J Physiol Heart Circ Physiol, 2012
Suggest that CASQ2(D307H) point mutation may affect Ca(2+) buffering capacity and Ca(2+) release in cardiac myocytes.
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