Nanopublications

Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RATfS7ugwIZ7wdVBSrywbRSQ16s2OlSEzlBP_pfulgatE#provenance>. }

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_4 label "Selventa" provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
large_corpus.bel version "20131211" provenance.
large_corpus.bel authoredBy _4 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _3 provenance.
assertion hadPrimarySource 12559172 provenance.
_3 wasQuotedFrom 12559172 provenance.
_3 value "Enforced expression of Bcl-2 protein from plasmid vectors, in contrast, abrogates sensitivity to the apoptosis promoting effects of antiestrogens in breast cancer lines, while antisense BCL-2 prevents estrogen-mediated apoptosis suppression, thus establishing a direct functional connection between ER, Bcl-2, and suppression of apoptosis (Teixeira et al., 1995). expression of Bcl-2 or Bcl-XL can be downregulated in specific types of cancer and leukemia cells by smallmolecule drugs that modulate the activity of retinoic acid receptors (RAR), retinoid X receptors (RXR), PPAR?, vitamin D receptors (VDR), and certain other members of the SRTF superfamily. RAR and RXR ligands are already approved for treatment of some types of leukemia and lymphoma, and are in advanced clinical testing for solid tumors. PPAR? modulators have demonstrated antitumor activity in xenograft models of breast and prostate cancer (Kubota et al., 1998), sometimes displaying synergy with retinoids, probably due in part to the fact that PPAR? binds DNA as a heterodimer with RXR. antiapoptotic members of the Bcl-2-family (Bcl-2, Bcl-XL, Mcl-1, Bcl-W, Bfl-1, Bcl-B)" provenance.