sub:provenance {
beldoc: dce:description "Approximately 61,000 statements." ;
dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved." ;
dce:title "BEL Framework Large Corpus Document" ;
pav:authoredBy sub:_5 ;
pav:version "20131211" .
sub:_4 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. MEK inhibitor UO126 (Promega, MEK Inhibitor U0126 is a chemically synthesized organic compound that inhibits activation of MAPK (ERK 1/2) by inhibiting the kinase activity of MAP Kinase Kinase (MAPKK or MEK 1/2)." ;
prov:wasQuotedFrom pubmed:11196191 .
sub:_5 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:11196191 ;
prov:wasDerivedFrom beldoc: ,
sub:_4 .
}