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http://www.nanopub.org/nschema#hasProvenance
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http://www.tkuhn.ch/bel2nanopub/RANsaMqqdmAQuHUbSMv4TwZ4ulaM_kyfqMshlj897Wlts
http://www.nanopub.org/nschema#hasPublicationInfo
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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RANsaMqqdmAQuHUbSMv4TwZ4ulaM_kyfqMshlj897Wlts#_1
http://www.selventa.com/vocabulary/variantOf
http://www.ncbi.nlm.nih.gov/gene/56718
http://www.tkuhn.ch/bel2nanopub/RANsaMqqdmAQuHUbSMv4TwZ4ulaM_kyfqMshlj897Wlts#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.ebi.ac.uk/ontology-lookup/?termId=MOD:00000
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http://www.w3.org/2000/01/rdf-schema#label
a(CHEBI:"insulin (human)") -> p(EGID:56718,pmod(P,S,2448))
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http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel
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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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http://www.w3.org/ns/prov#value
We show that in freshly isolated rat adipocytes, insulin stimulates the phosphorylation of mTOR on serine 2448, a protein kinase B (PKB) consensus phosphorylation site. This site is also phosphorylated by amino acids, which in contrast to insulin do not activate PKB. Moreover, insulin and amino acids have an additive effect on mTOR phosphorylation, indicating that they act via two independent pathways. Importantly, amino acids, notably leucine, permit insulin to stimulate PKB when PI 3-kinase is inhibited
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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://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel
http://www.tkuhn.ch/bel2nanopub/RANsaMqqdmAQuHUbSMv4TwZ4ulaM_kyfqMshlj897Wlts#assertion
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2014-07-03T14:32:33.307+02:00
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