sub:provenance { sub:assertiondcterms:description "[Results of the present study indicate that 1) PGE(2) promotes survival of human endometriotic cells through EP2 and EP4 receptors by activating ERK1/2, AKT, nuclear factor-kappaB, and beta-catenin signaling pathways; 2) selective inhibition of EP2 and EP4 suppresses these cell survival pathways and augments interactions between proapoptotic proteins (Bax and Bad) and antiapoptotic proteins (Bcl-2/Bcl-XL), facilitates the release of cytochrome c, and thus activates caspase-3/poly (ADP-ribose) polymerase-mediated intrinsic apoptotic pathways; and 3) these PGE(2) signaling components are more abundantly expressed in ectopic endometriosis tissues compared with eutopic endometrial tissues during the menstrual cycle in women.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ; wi:evidencedgn-void:source_evidence_curated ; sio:SIO_000772miriam-pubmed:19407222 ; prov:wasDerivedFromdgn-void:CTD_human ; prov:wasGeneratedByeco:ECO_0000218 . dgn-void:CTD_humanpav:importedOn "2017-01-25"^^xsd:date . dgn-void:source_evidence_curatedaeco:ECO_0000205 ; rdfs:comment "Gene-disease associations manually curated."@en ; rdfs:label "DisGeNET evidence - CURATED"@en . }