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 "Studies of the MCK and MLC1/3 gene enhancers have demonstrated cooperativity in MEF-2 and MyoD binding at their respective sites (22 ,46 ,54 -57 ). Whether a similar mechanism is operating within the dystrophin gene and contributes to selective utilization of adjoining E box and MEF-2 motifs remains to be determined The core enhancer region was delimited to a 195 bp Spe I- Acc I fragment and sequence analysis identified three MEF-1/E box and two MEF-2/AT-rich motifs as potential muscle-specific regulatory domains. EMSA competition and DNase footprinting indicated that sequences within a 30 bp region containing single adjoining MEF-1/E box and MEF-2/AT-rich motifs are target binding sites for trans -acting factors expressed in H9C2(2-1) myotubes but not in L6 or C2C12 myotubes. The core enhancer region was delimited to a 195 bp Spe I- Acc I fragment and sequence analysis identified three MEF-1/E box and two MEF-2/AT-rich motifs as potential muscle-specific regulatory domains. EMSA competition and DNase footprinting indicated that sequences within a 30 bp region containing single adjoining MEF-1/E box and MEF-2/AT-rich motifs are target binding sites for trans -acting factors expressed in H9C2(2-1) myotubes but not in L6 or C2C12 myotubes. Site-specific mutations within these motifs resulted in a significant reduction in enhancer activity in H9C2(2-1) myotubes." ;
    prov:wasQuotedFrom pubmed:9092671 .
  sub:_6 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:9092671 ;
    prov:wasDerivedFrom beldoc: , sub:_5 .
}