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http://www.tkuhn.ch/bel2nanopub/RAimSp6n87-dmLI1Kvi33nq3AFoUBnzNsM1G_WboOhjFY#_1
http://purl.obolibrary.org/obo/RO_0002204
http://rgd.mcw.edu/rgdweb/report/gene/main.html?id=1562954
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a(CHEBI:glucocorticoid) -> r(RGD:Akr1c19)
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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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Upstream from the NRE are three distal imperfect glucocorticoid response elements (GRE1, GRE2, and GRE3); in addition, a proximal imperfect GRE (GRE4) is adjacent to an Oct binding site in the NRE. When rat hepatocytes were cultured on Matrigel and exposed to dexamethasone (Dex), steady state levels of 3alpha-HSD/DD mRNA were increased 4-fold in a dose-dependent manner, yielding an EC50 value of 10 nM. Time to maximal response was 24 hr, and the effect was blocked with the anti-glucocorticoid RU486. Measurement of the half-life of 3alpha-HSD/DD mRNA, with and without Dex treatment, indicated that the increase in steady state mRNA levels was not due to increased mRNA stability. By contrast, nuclear run-off experiments using nuclei obtained from Dex-stimulated hepatocytes indicated that Dex increased transcription of the rat 3alpha-HSD/DD gene.
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Selventa
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2014-07-03T14:34:05.001+02:00
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