http://purl.uniprot.org/citations/16289269 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/16289269 | http://www.w3.org/2000/01/rdf-schema#comment | "In cardiac muscle, junctin forms a quaternary protein complex with the ryanodine receptor (RyR), calsequestrin, and triadin 1 at the luminal face of the junctional sarcoplasmic reticulum (jSR). By binding directly the RyR and calsequestrin, junctin may mediate the Ca(2+)-dependent regulatory interactions between both proteins. To gain more insight into the underlying mechanisms of impaired contractile relaxation in transgenic mice with cardiac-specific overexpression of junctin (TG), we studied cellular Ca(2+) handling in these mice. We found that the SR Ca(2+) load was reduced by 22% in cardiomyocytes from TG mice. Consistent with this, the frequency of Ca(2+) sparks was diminished by 32%. The decay of spontaneous Ca(2+) sparks was prolonged by 117% in TG. This finding was associated with a lower Na(+)-Ca(2+) exchanger (NCX) protein expression (by 67%) and a higher basal RyR phosphorylation at Ser(2809) (by 64%) in TG. The shortening- and Delta[Ca](i)-frequency relationships (0.5-4 Hz) were flat in TG compared to wild-type (WT) which exhibited a positive staircase for both parameters. Furthermore, increasing stimulation frequencies hastened the time of relaxation and the decay of [Ca](i) by a higher percentage in TG. We conclude that the impaired relaxation in TG may result from a reduced NCX expression and/or a higher SR Ca(2+) leak. The altered shortening-frequency relationship in TG seems to be a consequence of an impaired excitation-contraction coupling with depressed SR Ca(2+) release at higher rates of stimulation. Our data suggest that the more prominent frequency-dependent hastening of relaxation in TG results from a stimulation of SR Ca(2+) transport reflected by corresponding changes of [Ca](i)."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ceca.2005.10.004"xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/author | "Schmitz W."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/author | "Lipp P."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/author | "Jones L.R."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/author | "Kirchhefer U."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/author | "Neumann J."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/author | "Kaestner L."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/author | "Hanske G."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/author | "Justus I."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/name | "Cell Calcium"xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/pages | "131-142"xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/title | "Overexpression of junctin causes adaptive changes in cardiac myocyte Ca(2+) signaling."xsd:string |
http://purl.uniprot.org/citations/16289269 | http://purl.uniprot.org/core/volume | "39"xsd:string |
http://purl.uniprot.org/citations/16289269 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16289269 |
http://purl.uniprot.org/citations/16289269 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16289269 |
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