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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAt4P7b0N_Jj74mfPomHAWyrOGsEjG49KQry1TUyynOyU#_5 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAt4P7b0N_Jj74mfPomHAWyrOGsEjG49KQry1TUyynOyU#_4 http://www.w3.org/ns/prov#value The expression of the GATA5 antisense cDNA had no effect on the morphology or proliferation of undifferentiated cells (Fig. 5D and data not shown). However, in the absence of GATA5 protein, treatment with RA did not lead to the appearance of endothelial-like morphological and biochemical changes nor to a decrease in cell proliferation as in control cells, even with increasing concentration (10–4 M) and time (5 days) of RA treatment (Fig. 5D). Furthermore, unlike control cells, endothelial markers like ET-1, Flt1, and EPAS1 were not induced in cell lines lacking GATA5 indicating that GATA5 expression is required for endocardial differentiation (Fig. 5E). In order to molecularly define the stage at which differentiation was arrested, RT-PCR analyses were carried out. 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