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http://www.tkuhn.ch/bel2nanopub/RACYLM34Rj69xQoy6wGf6ubX_CneAOzc2ETe_uPVoAXcM#_1
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http://www.ebi.ac.uk/chebi/searchId.do?chebiId=4461
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a(CHEBI:dexamethasone) -| (kin(p(SFAM:"AKT Family")) =| kin(p(HGNC:GSK3B)))
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http://www.w3.org/2000/01/rdf-schema#label
kin(p(SFAM:"AKT Family")) =| kin(p(HGNC:GSK3B))
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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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Dexamethasone treatment decreased the ability of insulin to stimulate glucose uptake, glycogen synthesis and glycogen synthase fractional activity. In addition, the dephosphorylation of glycogen synthase by insulin was blocked. These defects were paralleled by reduced insulin-stimulated protein kinase B (PKB) and GSK-3 phosphorylation. We demonstrated that chronic dexamethasone treatment impairs insulin-stimulated PKB and GSK-3 phosphorylation, which may contribute to insulin resistance in skeletal muscles.
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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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2014-07-03T14:32:48.291+02:00
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