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http://purl.uniprot.org/citations/17336904http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17336904http://www.w3.org/2000/01/rdf-schema#comment"Chondrocyte hypertrophy is essential for endochondral bone development. Unexpectedly, we discovered that MEF2C, a transcription factor that regulates muscle and cardiovascular development, controls bone development by activating the gene program for chondrocyte hypertrophy. Genetic deletion of Mef2c or expression of a dominant-negative MEF2C mutant in endochondral cartilage impairs hypertrophy, cartilage angiogenesis, ossification, and longitudinal bone growth in mice. Conversely, a superactivating form of MEF2C causes precocious chondrocyte hypertrophy, ossification of growth plates, and dwarfism. Endochondral bone formation is exquisitely sensitive to the balance between MEF2C and the corepressor histone deacetylase 4 (HDAC4), such that bone deficiency of Mef2c mutant mice can be rescued by an Hdac4 mutation, and ectopic ossification in Hdac4 null mice can be diminished by a heterozygous Mef2c mutation. These findings reveal unexpected commonalities in the mechanisms governing muscle, cardiovascular, and bone development with respect to their regulation by MEF2 and class II HDACs."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.org/dc/terms/identifier"doi:10.1016/j.devcel.2007.02.004"xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"Kim Y."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"Qi X."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"Bassel-Duby R."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"Olson E.N."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"Richardson J.A."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"Shelton J.M."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"Arnold M.A."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"Phan D."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"McAnally J."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/author"Czubryt M.P."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/name"Dev Cell"xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/pages"377-389"xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/title"MEF2C transcription factor controls chondrocyte hypertrophy and bone development."xsd:string
http://purl.uniprot.org/citations/17336904http://purl.uniprot.org/core/volume"12"xsd:string
http://purl.uniprot.org/citations/17336904http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17336904
http://purl.uniprot.org/citations/17336904http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17336904
http://purl.uniprot.org/uniprot/Q8CFN5#attribution-0BEE99874F2F283CA8F37C3CDD6087C2http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17336904
http://purl.uniprot.org/uniprot/Q8CFN5#attribution-6E327A63425DE4607E595C8DA64A27ADhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17336904
http://purl.uniprot.org/uniprot/Q63943#attribution-6E327A63425DE4607E595C8DA64A27ADhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17336904
http://purl.uniprot.org/uniprot/#_A0A0G2JDK0-mappedCitation-17336904http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17336904
http://purl.uniprot.org/uniprot/#_A0A0G2JDQ1-mappedCitation-17336904http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17336904