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Calmodulin (CaM) has three separate nonallelic genes that encode for three identical proteins.
We discovered a novel CPVT mutation in the CALM3 gene that shares functional characteristics with established CPVT-associated mutations in CALM1. A small proportion of A103V-CaM is sufficient to evoke arrhythmogenic Ca disturbances via ryanodine receptor 2 dysregulation, which explains the autosomal dominant inheritance.
the spectrum and prevalence of pathogenic CaM variants in a cohort of genetically elusive long QT syndrome, were determined.
CALM3 had the highest ranking in the 1629-gene LQTS nodal network of the 7 genes identified through our filtering process.
the association of EGFR (显示 EGFR 蛋白), CALM3 and SMARCD1 (显示 SMARCD1 蛋白) gene polymorphisms with bone mineral density in white women, as conducted.
Differentiation paralleled the activation of Wnt5 (显示 WNT5A 蛋白)/Calmodulin signalling by autocrine/paracrine intense secretion of Wnt5a (显示 WNT5A 蛋白) and Wnt5b (显示 WNT5B 蛋白)
The rat and mouse 3'-UTR region had an identity of approximately 80% with the human. Three common polyadenylation signals in the 3'-UTR may account for the multiple CaM III transcripts.
These findings demonstrate that physical interaction of CaM with recombinant and native 5-HT(2C) receptors is critical for G protein-independent, arrestin (显示 SAG 蛋白)-dependent receptor signaling.
data suggest that the -34T>A CALM3 polymorphism is a modifier gene for Familial Hypertrophy Cardiomyopathy, potentially by affecting expression level of CALM3 and therefore Ca(2 (显示 CA2 蛋白)+)-handling and development of hypertrophy.
Calmodulin mediates the control of a large number of enzymes, ion channels and other proteins by Ca(2+). Among the enzymes to be stimulated by the calmodulin-Ca(2+) complex are a number of protein kinases and phosphatases. Together with CEP110 and centrin, is involved in a genetic pathway that regulates the centrosome cycle and progression through cytokinesis.
, Calmodulin III
, prepro-calmodulin 3