| http://purl.uniprot.org/citations/17363698 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17363698 | http://www.w3.org/2000/01/rdf-schema#comment | "Increased relative expression of the slow molecular motor of the heart (beta-myosin heavy chain [MyHC]) is well known to occur in many rodent models of cardiovascular disease and in human heart failure. The direct effect of increased relative beta-MyHC expression on intact cardiac myocyte contractility, however, is unclear. To determine the direct effects of increased relative beta-MyHC expression on cardiac contractility, we used acute genetic engineering with a recombinant adenoviral vector (AdMYH7) to genetically titrate beta-MyHC protein expression in isolated rodent ventricular cardiac myocytes that predominantly expressed alpha-MyHC (fast molecular motor). AdMYH7-directed beta-MyHC protein expression and sarcomeric incorporation was observed as soon as 1 day after gene transfer. Effects of beta-MyHC expression on myocyte contractility were determined in electrically paced single myocytes (0.2 Hz, 37 degrees C) by measuring sarcomere shortening and intracellular calcium cycling. Gene transfer-based replacement of alpha-MyHC with beta-MyHC attenuated contractility in a dose-dependent manner, whereas calcium transients were unaffected. For example, when beta-MyHC expression accounted for approximately 18% of the total sarcomeric myosin, the amplitude of sarcomere-length shortening (nanometers, nm) was depressed by 42% (151.0+/-10.7 [control] versus 87.0+/-5.4 nm [AdMYH7 transduced]); and genetic titration of beta-MyHC, leading to 38% beta-MyHC content, attenuated shortening by 57% (138.9+/-13.0 versus 59.7+/-7.1 nm). Maximal isometric cross-bridge cycling rate was also slower in AdMYH7-transduced myocytes. Results indicate that small increases of beta-MyHC expression (18%) have Ca2+ transient-independent physiologically relevant effects to decrease intact cardiac myocyte function. We conclude that beta-MyHC is a negative inotrope among the cardiac myofilament proteins."xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.org/dc/terms/identifier | "doi:10.1161/01.res.0000264102.00706.4e"xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/author | "Vandenboom R."xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/author | "Edwards T."xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/author | "Herron T.J."xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/author | "Metzger J.M."xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/author | "Fomicheva E."xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/author | "Mundada L."xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/name | "Circ Res"xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/pages | "1182-1190"xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/title | "Calcium-independent negative inotropy by beta-myosin heavy chain gene transfer in cardiac myocytes."xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://purl.uniprot.org/core/volume | "100"xsd:string |
| http://purl.uniprot.org/citations/17363698 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17363698 |
| http://purl.uniprot.org/citations/17363698 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17363698 |
| http://purl.uniprot.org/uniprot/#_P02564-mappedCitation-17363698 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17363698 |
| http://purl.uniprot.org/uniprot/P02564 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/17363698 |