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Calmodulin (CaM) has three separate nonallelic genes that encode for three identical proteins.
the spectrum and prevalence of pathogenic CaM (show CALM1 Proteins) variants in a cohort of genetically elusive long QT syndrome, were determined.
CALM3 (show CALM1 Proteins) had the highest ranking in the 1629-gene LQTS nodal network of the 7 genes identified through our filtering process.
the association of EGFR (show EGFR Proteins), CALM3 (show CALM1 Proteins) and SMARCD1 (show SMARCD1 Proteins) gene polymorphisms with bone mineral density in white women, as conducted.
Differentiation paralleled the activation of Wnt5 (show WNT5A Proteins)/Calmodulin (show CALM1 Proteins) signalling by autocrine/paracrine intense secretion of Wnt5a (show WNT5A Proteins) and Wnt5b (show WNT5B Proteins)
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 (show CALM1 Proteins) III transcripts.
These findings demonstrate that physical interaction of CaM (show CALM1 Proteins) with recombinant and native 5-HT(2C (show HTR2C Proteins)) receptors is critical for G protein-independent, arrestin (show SAG Proteins)-dependent receptor signaling.
data suggest that the -34T>A CALM3 (show CALM1 Proteins) polymorphism is a modifier gene for Familial Hypertrophy Cardiomyopathy, potentially by affecting expression level of CALM3 (show CALM1 Proteins) and therefore Ca(2 (show CA2 Proteins)+)-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