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 "Repression of these SMC1{beta} promoter constructs by E2F6 was confirmed by inhibition of reporter gene expression by overexpressed E2F6 (Fig. 2C). A point mutant of E2F6 defective in DNA binding (E68) (6) had no effect on reporter gene expression, demonstrating that repression of SMC1{beta} by E2F6 depends on sequence-specific DNA-binding. The -26 promoter had equal activity in wild-type and E2f6-/- cells and was not repressed by the coexpression of E2F6. This finding suggests that an E2F6-responsive site is located between nucleotides -26 and -129 of the SMC1{beta} promoter. Examination of this part of the promoter sequence showed that it contains a potential E2F binding site (see Fig. 2D). To test whether this E2F site is required for repression of the SMC1{beta} promoter by E2F6, we mutated the E2F element and analyzed the activity of the mutated reporter construct in E2f6+/+ and E2f6-/- cells (Fig. 2E). The mutated reporter gene had equal activity in E2f6+/+ and E2f6-/- cells, demonstrating that the E2F site is required for repression by E2F6. " ;
    prov:wasQuotedFrom pubmed:16236716 .
  sub:_6 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:16236716 ;
    prov:wasDerivedFrom beldoc: , sub:_5 .
}