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 "Although the growth-inhibitory effect of TGF-B is believed to be mediated by the Smad dependent TGF-B signaling pathway, there have been reports of TGF-B mediated inhibition of proliferation in Smad4 null cells.22 Proposed alternative mechanisms for resistance to TGF-B include decreased expression of TBRI,34 TBRII,35 or TBRIII36 on the cell surface; increased expression of the inhibitory Smad, Smad7; repression of TGF-B signaling by a variety of oncoproteins including p53,38 Myc,39 E1A,40 Ras,41 Ski/ SnoN,42,43 and Evi-1 44; reduced expression or inactivation of tumor suppressors that directly regulate the TGF-B signaling pathway including Menin,45 Disabled-2 ,46 and RUNX3; and activation of other signaling pathways includings protein kinase C (PKC). TGF-B is able to increase the production of mitogenic growth factors, including platelet-derived growth factor,51 fibroblast growth factor,52 TGF-B,53 and connective tissue growth factor,54 and to increase expression of the platelet derived growth factor receptor,55 and the epithelial growth factor receptor.56 In addition, TGF-B can activate Smad independent pathways, including the Ras/Raf/MAPK pathway,20-22,57,58 which often mediates the proliferative signal of growth factors. Indeed, it is in conjunction with oncogenic forms of Ras (Ha-Ras or Ki-Ras), that TGF-B drives Smad-independent proliferation of human colon and prostate cancer cells.3,49" ;
    prov:wasQuotedFrom pubmed:15774796 .
  sub:_5 rdfs:label "Selventa" .
  sub:assertion prov:hadPrimarySource pubmed:15774796 ;
    prov:wasDerivedFrom beldoc: , sub:_4 .
}