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 "1.4" .
  sub:_4 prov:value "2 potential AP-1 binding sites located at positions -1000 to -994 and -943 to -937 was identified in the 248-bp fragment of the gonadotropin releasing hormone receptor (Gnrhr). A decrease in human GnRHR promoter activity was observed after GnRHa (GnRH agonists) treatment. GnRHa- and TPA-mediated decrease in the human GnRHR promoter activity was reversed by a specific protein kinase C inhibitor. These findings indicate that the activation of the PKC pathway is important in regulating the human GnRHR gene expression. EMSA studies with alphaT3-1 cells transfected with the Gnrhr reporter construct using anti-c-jun antibody demonstrated the binding of c-jun to the AP-1 binding site of the Gnrhr promoter. It was also demonstrated that mutation of the AP-1 binding site at -1000 to -994 abolished the GnRHa (GnRH agonists) induced inhibition. Thus, AP-1-binding site located at -1000 to -994 of the human GnRHR5'-flanking region has been identified to be involved in mediating the down-regulatory effect." ;
    prov:wasQuotedFrom pubmed:11014215 .
  sub:_5 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:11014215 ;
    prov:wasDerivedFrom beldoc: , sub:_4 .
}