http://purl.uniprot.org/citations/16129693 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/16129693 | http://www.w3.org/2000/01/rdf-schema#comment | "S100A1 is an EF-hand type Ca2+-binding protein with a muscle-specific expression pattern. The highest S100A1 protein levels are found in cardiomyocytes, and it is expressed already at day 8 in the heart during embryonic development. Since S100A1 is known to be involved in the regulation of Ca2+ homeostasis, we tested whether extracellular S100A1 plays a role in regulating the L-type Ca2+ current (I(Ca)) in ventricular cardiomyocytes. Murine embryonic (day 16.5 postcoitum) ventricular cardiomyocytes were incubated with S100A1 (0.001-10 microM) for different time periods (20 min to 48 h). I(Ca) density was found to be significantly increased as early as 20 min (from -10.8 +/-1 pA/pF, n = 18, to -22.9 +/- 1.4 pA/pF; +112.5 +/-13%, n = 9, p < 0.001) after the addition of S100A1 (1 microM). S100A1 also enhanced I(Ca) current density in neonatal rat cardiomyocytes. Fluorescence and capacitance measurements evidenced a fast translocation of rhodamine-coupled S100A1 from the extracellular space into cardiomyocytes. S100A1 treatment did not affect cAMP levels. However, protein kinase inhibitor, a blocker of cAMP-dependent protein kinase A (PKA), abolished the S100A1-induced enhancement of I(Ca). Accordingly, measurements of PKA activity yielded a significant increase in S100A1-treated cardiomyocytes. In vitro reconstitution assays further demonstrated that S100A1 enhanced PKA activity. We conclude that the Ca2+-binding protein S100A1 augments transsarcolemmal Ca2+ influx via an increase of PKA activity in ventricular cardiomyocytes and hence represents an important regulator of cardiac function."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m504750200"xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Tang M."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Duan Y."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Hescheler J."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Nurnberg B."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Fleischmann B.K."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Roell W."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Sasse P."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Reppel M."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Piekorz R."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/author | "Kletke A."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/pages | "36019-36028"xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/title | "S100A1 enhances the L-type Ca2+ current in embryonic mouse and neonatal rat ventricular cardiomyocytes."xsd:string |
http://purl.uniprot.org/citations/16129693 | http://purl.uniprot.org/core/volume | "280"xsd:string |
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