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http://purl.uniprot.org/SHA-384/648F767AAAE98A3657D28F975E8541B1EAF6149BFFC0EB9166D8FFEA3CF75538A7BE5A20804F10F7ED4B06D3F8668159http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/648F767AAAE98A3657D28F975E8541B1EAF6149BFFC0EB9166D8FFEA3CF75538A7BE5A20804F10F7ED4B06D3F8668159http://www.w3.org/2000/01/rdf-schema#comment"Myofibrogenesis in cultured Npr2(+/)(-) fibroblasts was insensitive to CNP treatment. Aged Npr2(+/)(-) and Npr2(+/)(-);Ldlr-/- mice developed cardiac dysfunction and ventricular fibrosis. Aortic valve function was impaired in Npr2(+/)(-) and Npr2(+/)(-);Ldlr(-/)(-) mice with increased valve thickening myofibrogenesis osteogenesis proteoglycan synthesis collagen accumulation and calcification."xsd:string
http://purl.uniprot.org/uniprot/#_70017F1869C9FC6584AAA93E71FE90B019041093E6FA59A7EB8CCCF7246807016AB09CDD26C68939F05E8B2217C83E1Bhttp://www.w3.org/1999/02/22-rdf-syntax-ns#subjecthttp://purl.uniprot.org/SHA-384/648F767AAAE98A3657D28F975E8541B1EAF6149BFFC0EB9166D8FFEA3CF75538A7BE5A20804F10F7ED4B06D3F8668159
http://purl.uniprot.org/uniprot/O55009http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/648F767AAAE98A3657D28F975E8541B1EAF6149BFFC0EB9166D8FFEA3CF75538A7BE5A20804F10F7ED4B06D3F8668159
http://purl.uniprot.org/uniprot/#_O55009-mappedCitation-29273600http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/648F767AAAE98A3657D28F975E8541B1EAF6149BFFC0EB9166D8FFEA3CF75538A7BE5A20804F10F7ED4B06D3F8668159