| http://purl.uniprot.org/citations/15367668 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15367668 | http://www.w3.org/2000/01/rdf-schema#comment | "The adult heart responds to stress signals by hypertrophic growth, which is often accompanied by activation of a fetal cardiac gene program and eventual cardiac demise. We showed previously that histone deacetylase 9 (HDAC9) acts as a suppressor of cardiac hypertrophy and that mice lacking HDAC9 are sensitized to cardiac stress signals. Here we report that mice lacking HDAC5 display a similar cardiac phenotype and develop profoundly enlarged hearts in response to pressure overload resulting from aortic constriction or constitutive cardiac activation of calcineurin, a transducer of cardiac stress signals. In contrast, mice lacking either HDAC5 or HDAC9 show a hypertrophic response to chronic beta-adrenergic stimulation identical to that of wild-type littermates, suggesting that these HDACs modulate a specific subset of cardiac stress response pathways. We also show that compound mutant mice lacking both HDAC5 and HDAC9 show a propensity for lethal ventricular septal defects and thin-walled myocardium. These findings reveal central roles for HDACs 5 and 9 in the suppression of a subset of cardiac stress signals as well as redundant functions in the control of cardiac development."xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.24.19.8467-8476.2004"xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/author | "Chang S."xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/author | "Zhang C.L."xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/author | "Hill J.A."xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/author | "Olson E.N."xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/author | "Richardson J.A."xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/author | "McKinsey T.A."xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/name | "Mol Cell Biol"xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/pages | "8467-8476"xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/title | "Histone deacetylases 5 and 9 govern responsiveness of the heart to a subset of stress signals and play redundant roles in heart development."xsd:string |
| http://purl.uniprot.org/citations/15367668 | http://purl.uniprot.org/core/volume | "24"xsd:string |
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