http://purl.uniprot.org/citations/23035250 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/23035250 | http://www.w3.org/2000/01/rdf-schema#comment | "Protein kinase A (PKA) is activated during sympathetic stimulation of the heart and phosphorylates key proteins involved in cardiac Ca(2+) handling, including the L-type Ca(2+) channel (Ca(V)1.2) and phospholamban (PLN). This results in acceleration and amplification of the beat-to-beat changes in cytosolic Ca(2+) in cardiomyocytes and, in turn, an increased rate and force of contraction. PKA is held in proximity to its substrates by protein scaffolds called A kinase anchoring proteins (AKAPs). It has been suggested that the short and long isoforms of AKAP7 (also called AKAP15/18) localize PKA in complexes with Ca(V)1.2 and PLN, respectively. We generated an AKAP7 KO mouse in which all isoforms were deleted and tested whether Ca(2+) current, intracellular Ca(2+) concentration, or Ca(2+) reuptake were impaired in isolated adult ventricular cardiomyocytes following stimulation with the β-adrenergic agonist isoproterenol. KO cardiomyocytes responded normally to adrenergic stimulation, as measured by whole-cell patch clamp or a fluorescent intracellular Ca(2+) indicator. Phosphorylation of Ca(V)1.2 and PLN were also unaffected by genetic deletion of AKAP7. Immunoblot and RT-PCR revealed that only the long isoforms of AKAP7 were detectable in ventricular cardiomyocytes. The results indicate that AKAP7 is not required for regulation of Ca(2+) handling in mouse cardiomyocytes."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.1215219109"xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/author | "Scott J.D."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/author | "Su T."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/author | "Catterall W.A."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/author | "Westenbroek R.E."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/author | "Nichols C.B."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/author | "McKnight G.S."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/author | "Brunet S."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/author | "Jones B.W."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/author | "Gilbert M.L."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/pages | "17099-17104"xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/title | "Cardiomyocytes from AKAP7 knockout mice respond normally to adrenergic stimulation."xsd:string |
http://purl.uniprot.org/citations/23035250 | http://purl.uniprot.org/core/volume | "109"xsd:string |
http://purl.uniprot.org/citations/23035250 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23035250 |
http://purl.uniprot.org/citations/23035250 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/23035250 |
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