http://purl.uniprot.org/citations/12847114 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/12847114 | http://www.w3.org/2000/01/rdf-schema#comment | "Caveolae are omega-shaped organelles of the cell surface. The protein caveolin-3, a structural component of cardiac caveolae, is associated with cellular signaling. To investigate the effect of adenovirus-mediated overexpression of caveolin-3 on hypertrophic responses in cardiomyocytes, we constructed an adenovirus that encoded human wild-type caveolin-3 (Ad.Cav-3), mutant caveolin-3 (Ad.Cav-3Delta), or bacterial beta-galactosidase (Ad.LacZ). This mutant has been reported to cause human limb-girdle muscular dystrophy. It lacks 9 nucleotides in the caveolin scaffolding domain and behaves in a dominant-negative fashion. Rat neonatal cardiomyocytes were infected with the virus and then harvested 36 hours after infection. In noninfected cells, phenylephrine (PE) and endothelin-1 (ET) increased cell size and [3H]leucine incorporation, along with the induction of sarcomeric reorganization and the reexpression of beta-myosin heavy chain, indicating myocyte hypertrophy. Infection with Ad.LacZ had no effect on those parameters. Ad.Cav-3 prevented the PE- and ET-induced increases in cell size, leucine incorporation, sarcomeric reorganization, and reexpression of beta-myosin heavy chain. Ad.Cav-3 also blocked the PE- and ET-induced phosphorylations of extracellular signal-regulated kinases (ERKs) but did not affect c-Jun amino-terminal kinase and p38 mitogen-activated protein kinase activities. In contrast, Ad.Cav-3Delta significantly augmented hypertrophic responses to ET, which were associated with increased ET-induced phosphorylation of ERK1/2. These results suggest that caveolin-3 behaves as a negative regulator of hypertrophic responses, probably through suppression of ERK1/2 activity."xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.org/dc/terms/identifier | "doi:10.1161/01.hyp.0000082926.08268.5d"xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/author | "Kato S."xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/author | "Kikuchi T."xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/author | "Oka N."xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/author | "Imaizumi T."xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/author | "Miyazaki H."xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/author | "Koga A."xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/name | "Hypertension"xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/pages | "213-219"xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/title | "Adenovirus-mediated overexpression of caveolin-3 inhibits rat cardiomyocyte hypertrophy."xsd:string |
http://purl.uniprot.org/citations/12847114 | http://purl.uniprot.org/core/volume | "42"xsd:string |
http://purl.uniprot.org/citations/12847114 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/12847114 |
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