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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RAYSTFaowkRoWaAdE7Erd7bvBNVZVSUz1UkHd3SHNms0g#_1
http://purl.obolibrary.org/obo/RO_0002204
http://rgd.mcw.edu/rgdweb/report/gene/main.html?id=69051
http://www.tkuhn.ch/bel2nanopub/RAYSTFaowkRoWaAdE7Erd7bvBNVZVSUz1UkHd3SHNms0g#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_33697
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http://purl.obolibrary.org/obo/BFO_0000066
http://purl.bioontology.org/ontology/MSH/D006321
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http://www.w3.org/2000/01/rdf-schema#label
a(CHEBI:aldosterone) -> r(RGD:Tgfb1)
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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1.4
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http://www.w3.org/ns/prov#value
Aldosterone provoked expression of hypertrophic markers (NPPA, NPPB, and ACTA1) in rat cardiac myocytes by phosphorylation of protein kinase D (PKD) and expression of collagens (COL1A1, COL1A2, and COL3A1) and transforming growth factor-beta1 in rat cardiac fibroblasts by upregulation of phosphoinositide 3-kinase (PI3K)-p100delta. Inhibition of PKD and PI3K-p110delta abrogated the hypertrophic and profibrotic effects, respectively, as did the mineralocorticoid receptor (MR) antagonist spironolactone
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http://www.w3.org/ns/prov#wasQuotedFrom
http://www.ncbi.nlm.nih.gov/pubmed/14993121
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http://www.w3.org/2000/01/rdf-schema#label
Selventa
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http://www.w3.org/ns/prov#hadPrimarySource
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http://purl.org/dc/terms/created
2014-07-03T14:30:21.202+02:00
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