| http://purl.uniprot.org/citations/19233194 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19233194 | http://www.w3.org/2000/01/rdf-schema#comment | "Mutations in cardiac troponin T (TnT) are a cause of familial hypertrophic cardiomyopathy (FHC). Transgenic mice expressing a missense mutation (R92Q) or a splice site donor mutation (Trunc) in the cardiac TnT gene have mutation-specific phenotypes but mice of both models have smaller hearts compared to wild type and exhibit hemodynamic dysfunction. Because growth-related signaling pathways in the hearts of mice expressing TnT mutations are not known, we evaluated the impact of increased Akt or glycogen synthase kinase-3beta (GSK-3beta) activity in both mutant TnT mice; molecules that increase heart size via physiologic pathways and block pathologic growth, respectively. Expression of activated Akt dramatically augments heart size in both R92Q and Trunc mice; however, this increase in heart size is not beneficial, since Akt also increases fibrosis in both TnT mutants and causes some pathologic gene expression shifts in the R92Q mice. Activated GSK-3beta results in further decreases in left ventricular size in both R92Q and Trunc hearts, but this decrease is associated with significant mutation-specific phenotypes. Among many pathologic consequences, activating GSK-3beta in R92Q hearts decreases phosphorylation of troponin I and results in early mortality. In contrast, increased GSK-3beta activity in Trunc hearts does not significantly impact cardiac phenotypes. These findings demonstrate that increased Akt and its downstream target, GSK-3beta can impact both cardiac size and phenotype in a mutation-specific manner. Moreover, increased activity of these molecules implicated in beneficial cardiac phenotypes exacerbates the progression of disease in the R92Q TnT mutant."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.yjmcc.2009.02.010"xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/author | "Leinwand L.A."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/author | "Olson E.N."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/author | "Walker L.A."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/author | "Rosenzweig A."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/author | "Luckey S.W."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/author | "Smyth T."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/author | "Mansoori J."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/author | "Messmer-Kratzsch A."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/name | "J Mol Cell Cardiol"xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/pages | "739-747"xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/title | "The role of Akt/GSK-3beta signaling in familial hypertrophic cardiomyopathy."xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://purl.uniprot.org/core/volume | "46"xsd:string |
| http://purl.uniprot.org/citations/19233194 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19233194 |
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