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:_6 ;
    pav:version "20131211" .
  sub:_5 prov:value "As shown in Fig. 3A, activins AB and B augmented (SBE)4-lux reporter activity in MIN6 cells. To verify that activin isoforms signal is mediated via ALK7 in MIN6 cells, we measured the activity of the dominant negative ALK7 construct (D/N ALK7 cDNA). D/N ALK7 cDNA lacks the intracellular kinase domain but retains the extracellular and transmembrane domains. The specificity of D/N ALK7 was confirmed in HEK293 cells (Fig. 3B). The activity of ALK4-dependent activin signaling was barely affected in the D/N ALK7 construct, but the ALK7-augmented response to activins B and AB was significantly inhibited. Thus, D/N ALK7 is a dominant negative inhibitor of ALK7 signaling but not of the ALK4 pathway ( Fig. 3B). As shown in Fig. 3C, D/N ALK7 completely blocked the responses of MIN6 cells to activins AB and B, confirming that activin isoforms signal via ALK7 in MIN6 cells" ;
    prov:wasQuotedFrom pubmed:15196700 .
  sub:_6 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:15196700 ;
    prov:wasDerivedFrom beldoc: , sub:_5 .
}