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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/RAUnatTAx72bZIAiovFmF7SSrKuiJ9NThgm9Hb9Udz2ik#_5 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAUnatTAx72bZIAiovFmF7SSrKuiJ9NThgm9Hb9Udz2ik#_4 http://www.w3.org/ns/prov#value IL-6 treatment led to activation of the mitogen-activated protein kinase (MAPK) and the phosphatidylinositol 3'-kinase (PI3K) pathways. Inhibition of MAPK or PI3K activity reversed IL-6- and oncostatin M-stimulated migration. For transient transfections, plasmids were introduced into the cells using Superfect transfection reagent (Qiagen). A HA-tagged MAPK (Erk2) construct (kindly provided by M. El-Shemerly and Y. Nagamine; Friedrich Miescher Institute, Basel, Switzerland) was cotransfected with a DN EGF receptor construct lacking 533 COOH-terminal amino acids MAPK kinase inhibitors PD98059 (20 uM; New England Biolabs) or UO126 (50 uM; Promega, Madison, WI PD98059, which is known to specifically inhibit the ERK-activating kinase MEK1, has been widely used to assess the effects of dampening ERK activation. 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