| http://purl.uniprot.org/citations/30167506 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/30167506 | http://www.w3.org/2000/01/rdf-schema#comment | "Heterozygous mice (αMHC403/+ ) expressing the human disease-causing mutation Arg403Gln exhibit cardinal features of hypertrophic cardiomyopathy (HCM) including hypertrophy, myocyte disarray, and increased myocardial fibrosis. Treatment of αMHC403/+ mice with the L-type calcium channel (ICa-L) antagonist diltiazem has been shown to decrease left ventricular anterior wall thickness, cardiac myocyte hypertrophy, disarray, and fibrosis. However, the role of the ICa-L in the development of HCM is not known. In addition to maintaining cardiac excitation and contraction in myocytes, the ICa-L also regulates mitochondrial function through transmission of movement of ICa-L via cytoskeletal proteins to mitochondrial voltage-dependent anion channel. Here, the authors investigated the role of ICa-L in regulating mitochondrial function in αMHC403/+ mice. Whole-cell patch clamp studies showed that ICa-L current inactivation kinetics were significantly increased in αMHC403/+ cardiac myocytes, but that current density and channel expression were similar to wild-type cardiac myocytes. Activation of ICa-L caused a significantly greater increase in mitochondrial membrane potential and metabolic activity in αMHC403/+ . These increases were attenuated with ICa-L antagonists and following F-actin or β-tubulin depolymerization. The authors observed increased levels of fibroblast growth factor-21 in αMHC403/+ mice, and altered mitochondrial DNA copy number consistent with altered mitochondrial activity and the development of cardiomyopathy. These studies suggest that the Arg403Gln mutation leads to altered functional communication between ICa-L and mitochondria that is associated with increased metabolic activity, which may contribute to the development of cardiomyopathy. ICa-L antagonists may be effective in reducing the cardiomyopathy in HCM by altering metabolic activity."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.jacbts.2015.12.001"xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Seidman C.E."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Seidman J.G."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Semsarian C."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Filipovska A."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Hool L.C."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Viola H.M."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Richman T.R."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Tsoutsman T."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Johnstone V.P.A."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/author | "Cserne Szappanos H."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/name | "JACC Basic Transl Sci"xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/pages | "61-72"xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/title | "The Role of the L-Type Ca2+ Channel in Altered Metabolic Activity in a Murine Model of Hypertrophic Cardiomyopathy."xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://purl.uniprot.org/core/volume | "1"xsd:string |
| http://purl.uniprot.org/citations/30167506 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/30167506 |
| http://purl.uniprot.org/citations/30167506 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/30167506 |
| http://purl.uniprot.org/uniprot/#_A0A2I3BPY4-mappedCitation-30167506 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30167506 |
| http://purl.uniprot.org/uniprot/#_B2RQQ1-mappedCitation-30167506 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30167506 |
| http://purl.uniprot.org/uniprot/#_B8JJH3-mappedCitation-30167506 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30167506 |
| http://purl.uniprot.org/uniprot/#_Q2TAW4-mappedCitation-30167506 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30167506 |
| http://purl.uniprot.org/uniprot/#_Q3UQQ3-mappedCitation-30167506 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30167506 |