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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAZxs4dp2B2Zylp7CEY4jjXpBCzCMybA30O9ckUkmL9Hc#_7 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAZxs4dp2B2Zylp7CEY4jjXpBCzCMybA30O9ckUkmL9Hc#_6 http://www.w3.org/ns/prov#value Tyrosine phosphorylation of IRS-1, as well as its association with p85{alpha} and activation of IRS-1-associated PI 3-kinase activity, decreased after 15-30 min of insulin stimulation in PTP1B+/+ neonatal hepatocytes (Fig. 4, upper panel). In sharp contrast, the effect of insulin on IRS-1 tyrosine phosphorylation in PTP1B-/- neonatal hepatocytes was prolonged; tyrosine phosphorylation of IRS-1, IRS-1/p85{alpha} association, and IRS-1-associated PI 3-kinase activity was sustained for 4 h in PTP1B-/- neonatal hepatocytes (Fig. 4, lower panel). Similar to findings for IRS-1, IRS-2 tyrosine phosphorylation, its binding to p85{alpha}, and activation of IRS-2-associated PI 3-kinase activity decreased between 15 and 60 min in insulin-stimulated PTP1B+/+ neonatal hepatocytes (Fig. 5, upper panel). 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