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anti-Mouse (Murine) CASQ2 Antibodies:
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Human Polyclonal CASQ2 Primary Antibody for WB - ABIN1881138
Kirchhefer, Wehrmeister, Postma, Pohlentz, Mormann, Kucerova, Müller, Schmitz, Schulze-Bahr, Wilde, Neumann: The human CASQ2 mutation K206N is associated with hyperglycosylation and altered cellular calcium handling. in Journal of molecular and cellular cardiology 2010
Show all 2 Pubmed References
Human Monoclonal CASQ2 Primary Antibody for ELISA, WB - ABIN560181
Leatherbury, Yu, Chatterjee, Walker, Yu, Tian, Lo: A novel mouse model of X-linked cardiac hypertrophy. in American journal of physiology. Heart and circulatory physiology 2008
we show that Fam20C phosphorylates several SR proteins involved in Ca(2+) signaling, including calsequestrin2 and Stim1, whose biochemical activities are dramatically regulated by Fam20C mediated phosphorylation
CASQ2-/- causes increase in calsequestrin 1 (CASQ1) expression.
These data suggest a functional role of CSQ2 not only in the ventricle but also in the atrium of mammalian hearts
Calcium entry activated by ablation of both JP45-CASQ1 and JP45-CASQ2 complexes supports tetanic force development in slow twitch soleus muscles.
The minimal KEKE motif of TRN involved in the interactions with CSQ2, HRC and RyR2 within the Ca2+ release units of cardiac sarcoplasmic reticulum has been defined.
While CASQ2 stabilizes RyR2 rendering it refractory in the diastolic phase, HRC enhances RyR2 activity facilitating RyR2 recovery from refractoriness.
Results show that CASQ2 deletion causes abnormal sarcoplasmic reticulum Ca(2+) release and selective interstitial fibrosis in the atrial pacemaker complex, which disrupt SAN pacemaking and increase susceptibility to atrial fibrillation
Viral gene transfer of wild-type CASQ2 into the heart of R33Q mice prevents and reverts severe manifestations of catecholaminergic polymorphic ventricular tachycardia.
Cardiac hypertrophy and calcium waves in CASQ2-null cardiac muscle are governed by the ryanodine receptor (Ryr)2 Ca2+ sensor.
Expression of CASQ2-R33Q influences molecular and ultra-structural heart development; post-natal, adaptive changes appear capable of ensuring until adulthood a new pathophysiological equilibrium.
Mutant CASQ2(D307H) protein retains some of its physiological function. Its expression decreases with age and is inversely related to arrhythmia severity.
Qualitatively similar results were obtained in a hybrid strain created by crossing CASQ2 knockout mice with mice deficient in phospholamban.
Aberrant disordered calcium release events can become synchronized in the intact myocardium, leading to triggered activity and the resultant diastolic contractions in the settings of a cardiac rhythm disorder.
The triadin-to-calsequestrin ratio is a critical modulator of the sarcoplasmic reticulum Ca(2+) signaling in ventricular myocytes.
The results presented in this paper support the idea of Casq2 acting both as a buffer and a direct regulator of the Ca(2+) release process.
Ca(2+) and JNT-dependent disassembly of the CSQ2 polymer
Suggest that CASQ2(D307H) point mutation may affect Ca(2+) buffering capacity and Ca(2+) release in cardiac myocytes.
The results presented in this paper unmask a differential effect of CASQ1&2 ablation in fast versus slow fibers
Report prevention of ventricular arrhythmia and calcium dysregulation in a catecholaminergic polymorphic ventricular tachycardia mouse model carrying calsequestrin-2 mutation.
Calsequestrin not only stores Ca(2+), but also varies its affinity in ways that progressively increase the ability of the store to deliver Ca(2+) as it becomes depleted, a novel feedback mechanism of potentially valuable functional implications.
We show for the first time a heterozygous CASQ2 variant causing autosomal dominant CPVT in a large family with a severe phenotype.
a direct interaction exists between RyR2 and CSQ2, is reported.
induced Pluripotent Stem Cell-derived cardiomyocytes are useful for investigating the similarities/differences in the pathophysiological consequences of RyR2 versus CASQ2 mutations underlying Catecholaminergic polymorphic ventricular tachycardia.
Mutations in the MYBPC3 and CASQ2 genes and six combinations between loci in the MYBPC3, MYH7 and CASQ2 genes were responsible for cardiomyopathy risk in a studied cohort.
We observed association between a CASQ2 polymorphism and SCA due to VA in patients with CAD adjusting for CHF and independent associations between CASQ2 SNPs and CHF adjusting for SCA.
The sarcoplasmic reticulum calcium content in human type II fibres is primarily determined by the CSQ1 abundance, and in type I fibres, by the combined amounts of both CSQ1 and CSQ2.
Molecular analysis of the CASQ2 gene in 43 probands with Catecholaminergic polymorphic ventricular tachycardia were performed and eight mutations in five patients, were identified.
Genetic background of catecholaminergic polymorphic ventricular tachycardia in Japan.
In a consanguineous family, a novel homozygous CASQ2 mutation (p.L77P) was identified in a child with CPVT who required implantation of a cardioverter defibrillator due to episodes of syncope while on medical therapy
A review of the physiology of Casq2 in cardiac Ca2+ handling and discuss pathophysiological mechanisms that lead to catecholaminergic polymorphic ventricular tachycardia caused by CASQ2 mutations.
patients with CASQ2-associated CPVT should be recommended to receive ICDs to prevent sudden death when medical therapy is not effective.
Aspartate to histidine casq2 mutation causes arrhythmia in cardiomyocytes generated from catecholaminergic polymorphic ventricular tachycardia patients.
Two causative genes of CPVT have been identified: RYR2, encoding the cardiac ryanodine receptor (RyR2) Ca(2+) release channel, and CASQ2, encoding cardiac calsequestrin. Their mutation have been found in 60% of patients with CPVT.
Common variations in or near CASQ2, GPD1L, and NOS1AP are associated with increased risk of sudden cardiac death in patients with coronary artery disease
Studies identified two phosphorylation sites, Ser(385) and Ser(393 in hCASQ2 by mass-spectroscopy.
Catecholaminergic polymorphic ventricular tachycardia (CPTV) mutations modify CASQ2 behaviour, including folding, aggregation/polymerization and selectivity towards Ca2+.
up-regulation of casq2 gene in the thyroid of patients with Graves' Hyperthyroidism may lead to the production of autoantibodies and sensitized T-lymphocytes, which cross-react with calsequestrin of patients who develop ophthalmopathy.
A regulatory role of CASQ2 on cytosolic Ca(2+) and hERG channels which may contribute to the etiology of CPVT.
The human CASQ2 mutation K206N is associated with hyperglycosylation and altered cellular calcium handling.
endogenous ankyrin repeat domain 1 protein and CASQ2 are co-enriched in piglet cardiac Purkinje cells
data shows that phosphorylated calsequestrin is required for high capacity calcium buffering and suggest that ryanodine receptor inhibition by calsequestrin is mediated by junctin
chief role of calsequestrin in skeletal muscle
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.
calsequestrin 2 (cardiac muscle)
, calsequestrin, cardiac muscle isoform
, cardiac calsequestrin
, calsequestrin 2, fast-twitch, cardiac muscle
, SR calcium binding protein
, calsequestrin homologue
, calsequestrin, skeletal muscle isoform
, laminin-binding protein