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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/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0#_5 http://www.w3.org/ns/prov#value The Hey basic helix-loop-helix transcription factors are downstream effectors of Notch signaling in the cardiovascular system. Mice lacking Hey2 develop cardiac hypertrophy, often associated with congenital heart defects, whereas combined Hey1/Hey2 deficiency leads to severe vascular defects and embryonic lethality around embryonic day E9.5. The molecular basis of these disorders is poorly understood, however, since target genes of Hey transcription factors in the affected tissues remain elusive. To identify genes regulated by Hey factors we have generated a conditional Hey1 knockout mouse. This strain was used to generate paired Hey2- and Hey1/2-deficient embryonic stem cell lines. Comparison of these cell lines by microarray analysis identified GATA4 and GATA6 as differentially expressed genes. Loss of Hey1/2 leads to elevated GATA4/6 and ANF mRNA levels in embryoid bodies, while forced expression of Hey factors strongly represses expression of the GATA4 and GATA6 promoter in various cell lines. In addition, the promoter activity of the GATA4/6 target gene ANF was inhibited by Hey1, Hey2, and HeyL. Protein interaction and mutation analyses suggest that repression is due to direct binding of Hey proteins to GATA4 and GATA6, blocking their transcriptional activity. In Hey2-deficient fetal hearts we observed elevated mRNA levels of ANF and CARP. Expression of ANF and Hey2 is normally restricted to the trabecular and compact myocardial layer, respectively. Intriguingly, loss of Hey2 leads to ectopic ANF expression in the compact layer, suggesting a direct role for Hey2 in limiting ANF expression in this cardiac compartment. http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0#_5 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/16199874 http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0#_6 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/16199874 http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0#_5 http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0#pubinfo http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0 http://purl.org/dc/terms/created 2014-07-03T14:30:38.411+02:00 http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0 http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RACWjcHO0IXGGjI93V274fRzEoVM9t-Y57rs04pZGSxW0 http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234