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:_7 ;
pav:version "1.4" .
sub:_6 prov:value "More recently, ERBB transactivation has been shown to involve other physiological ligands (FIG. 2). The binding of WNT to its seven-pass membrane receptor Frizzled (FZD) transactivates EGFR. The mechanism seems to be similar to that described for GPCRs, as it is rapid and blocked by metalloproteinase inhibitors; however, the target ligand has not been identified. WNT?FZD-mediated transactivation has been observed in normal mammary cells43 and in breast cancer cells (T. Schlange and N.E.H., unpublished observations). Oestradiol (E2) bindingto plasma-membrane-associated oestrogen receptor (ER) has also been shown to rapidly transactivate ERBBs. According to one report, E2-stimulated activation of MMP2 and MMP9 leads to the release of HB-EGF. Tamoxifen, a selective ER modifier (SERM) was shown to transactivate EGFR and ERBB2, and in ERBB2-overexpressing breast cancer cells this reduced the antiproliferative activity of the SERM" ;
prov:wasQuotedFrom pubmed:15864276 .
sub:_7 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:15864276 ;
prov:wasDerivedFrom beldoc: ,
sub:_6 .
}