| http://purl.uniprot.org/citations/16415078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16415078 | http://www.w3.org/2000/01/rdf-schema#comment | "The deficiency of dystrophin, a critical membrane stabilizing protein, in the mdx mouse causes an elevation in intracellular calcium in myocytes. One mechanism that could elicit increases in intracellular calcium is enhanced influx via the L-type calcium channels. This study investigated the effects of the dihydropyridines BAY K 8644 and nifedipine and alterations in dihydropyridine receptors in dystrophin-deficient mdx hearts. A lower force of contraction and a reduced potency of extracellular calcium (P < 0.05) were evident in mdx left atria. The dihydropyridine agonist BAY K 8644 and antagonist nifedipine had 2.7- and 1.9-fold lower potencies in contracting left atria (P < 0.05). This corresponded with a 2.0-fold reduction in dihydropyridine receptor affinity evident from radioligand binding studies of mdx ventricular homogenates (P < 0.05). Increased ventricular dihydropyridine receptor protein was evident from both radioligand binding studies and Western blot analysis and was accompanied by increased mRNA levels (P < 0.05). Patch-clamp studies in isolated ventricular myocytes showed no change in L-type calcium current density but revealed delayed channel inactivation (P < 0.05). This study indicates that a deficiency of dystrophin leads to changes in dihydropyridine receptors and L-type calcium channel properties that may contribute to enhanced calcium influx. Increased influx is a potential mechanism for the calcium overload observed in dystrophin-deficient cardiac muscle."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpheart.00844.2005"xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/author | "Lu S."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/author | "Watson M."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/author | "Brown L."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/author | "Xiao X.H."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/author | "Woolf P.J."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/author | "Cornford-Nairn R."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/author | "Hoey A.J."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/author | "Holroyd S.M."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/name | "Am J Physiol Heart Circ Physiol"xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/pages | "H2439-45"xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/title | "Alterations in dihydropyridine receptors in dystrophin-deficient cardiac muscle."xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://purl.uniprot.org/core/volume | "290"xsd:string |
| http://purl.uniprot.org/citations/16415078 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16415078 |
| http://purl.uniprot.org/citations/16415078 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16415078 |
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