| http://purl.uniprot.org/citations/24747296 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24747296 | http://www.w3.org/2000/01/rdf-schema#comment | "In cardiomyocytes, Ca2+ entry through voltage-dependent Ca2+ channels (VDCCs) binds to and activates RyR2 channels, resulting in subsequent Ca2+ release from the sarcoplasmic reticulum (SR) and cardiac contraction. Previous research has documented the molecular coupling of small-conductance Ca2+-activated K+ channels (SK channels) to VDCCs in mouse cardiac muscle. Little is known regarding the role of RyRs-sensitive Ca2+ release in the SK channels in cardiac muscle. In this study, using whole-cell patch clamp techniques, we observed that a Ca2+-activated K+ current (IK,Ca) recorded from isolated adult C57B/L mouse atrial myocytes was significantly decreased by ryanodine, an inhibitor of ryanodine receptor type 2 (RyR2), or by the co-application of ryanodine and thapsigargin, an inhibitor of the sarcoplasmic reticulum calcium ATPase (SERCA) (p<0.05, p<0.01, respectively). The activation of RyR2 by caffeine increased the IK,Ca in the cardiac cells (p<0.05, p<0.01, respectively). We further analyzed the effect of RyR2 knockdown on IK,Ca and Ca2+ in isolated adult mouse cardiomyocytes using a whole-cell patch clamp technique and confocal imaging. RyR2 knockdown in mouse atrial cells transduced with lentivirus-mediated small hairpin interference RNA (shRNA) exhibited a significant decrease in IK,Ca (p<0.05) and [Ca2+]i fluorescence intensity (p<0.01). An immunoprecipitated complex of SK2 and RyR2 was identified in native cardiac tissue by co-immunoprecipitation assays. Our findings indicate that RyR2-mediated Ca2+ release is responsible for the activation and modulation of SK channels in cardiac myocytes."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0094905"xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/author | "Chen Y."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/author | "Zhang Q."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/author | "Wang Q."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/author | "Duan P."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/author | "Zhao W.C."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/author | "Tu H.Y."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/author | "Zhao W.D."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/author | "Mu Y.H."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/pages | "e94905"xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/title | "RyR2 modulates a Ca2+-activated K+ current in mouse cardiac myocytes."xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://purl.uniprot.org/core/volume | "9"xsd:string |
| http://purl.uniprot.org/citations/24747296 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24747296 |
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