{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T03:19:31Z","timestamp":1792984771374,"version":"4.5.0"},"reference-count":41,"publisher":"National Academy of Sciences","issue":"24","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2003,11,25]]},"abstract":"<jats:p>\n                    GATA transcription factors, together with Friend of GATA (FOG) cofactors, are required for the differentiation of diverse cell types. Multiple aspects of hematopoiesis are controlled by the interaction of FOG-1 with the GATA-1\/2\/3 subfamily. Likewise, FOG-2 is coexpressed with the GATA-4\/5\/6 subfamily at other sites, including the heart and gonads. FOG-2 and GATA-4 are required for cardiac development. Through transgenic rescue of hematopoietic defects of FOG-1\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    embryos we define an unsuspected role for FOG-1 in heart development. In particular, rescued FOG-1\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    mice die at embryonic day (E) 14.5 with cardiac defects that include double outlet right ventricle and a common atrioventricular valve. Using conditional inactivation of\n                    <jats:italic>Fog<\/jats:italic>\n                    -\n                    <jats:italic>1<\/jats:italic>\n                    we assign the cell of origin in which FOG-1 function is required. Neural crest cells migrate properly into FOG-1\n                    <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    hearts and mice with FOG-1 conditionally excised from neural crest derivatives fail to develop cardiac abnormalities. In contrast, conditional inactivation of FOG-1 in endothelial-derived tissues by means of Tie-2-expressed Cre recapitulates the rescue-knockout defects. These findings establish a nonredundant requirement for FOG-1 in the outlet tract and atrioventricular valves of the heart that depend on expression in endothelial-derived tissue and presumably reflect cooperation with the GATA-4\/5\/6 subfamily.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1936250100","type":"journal-article","created":{"date-parts":[[2003,11,25]],"date-time":"2003-11-25T15:59:06Z","timestamp":1069775946000},"page":"14030-14035","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":37,"title":["Endothelial lineage-mediated loss of the GATA cofactor Friend of GATA 1 impairs cardiac development"],"prefix":"10.1073","volume":"100","author":[{"given":"Samuel G.","family":"Katz","sequence":"first","affiliation":[{"name":"Division of Hematology\/Oncology, Children's Hospital and Dana\u2013Farber Cancer Institute, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA 02115; and Department of Medicine, Cardiology Division and Department of Cell and Developmental Biology, University of Pennsylvania Health System, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aimee","family":"Williams","sequence":"additional","affiliation":[{"name":"Division of Hematology\/Oncology, Children's Hospital and Dana\u2013Farber Cancer Institute, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA 02115; and Department of Medicine, Cardiology Division and Department of Cell and Developmental Biology, University of Pennsylvania Health System, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jifu","family":"Yang","sequence":"additional","affiliation":[{"name":"Division of Hematology\/Oncology, Children's Hospital and Dana\u2013Farber Cancer Institute, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA 02115; and Department of Medicine, Cardiology Division and Department of Cell and Developmental Biology, University of Pennsylvania Health System, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuko","family":"Fujiwara","sequence":"additional","affiliation":[{"name":"Division of Hematology\/Oncology, Children's Hospital and Dana\u2013Farber Cancer Institute, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA 02115; and Department of Medicine, Cardiology Division and Department of Cell and Developmental Biology, University of Pennsylvania Health System, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alice P.","family":"Tsang","sequence":"additional","affiliation":[{"name":"Division of Hematology\/Oncology, Children's Hospital and Dana\u2013Farber Cancer Institute, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA 02115; and Department of Medicine, Cardiology Division and Department of Cell and Developmental Biology, University of Pennsylvania Health System, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan A.","family":"Epstein","sequence":"additional","affiliation":[{"name":"Division of Hematology\/Oncology, Children's Hospital and Dana\u2013Farber Cancer Institute, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA 02115; and Department of Medicine, Cardiology Division and Department of Cell and Developmental Biology, University of Pennsylvania Health System, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stuart H.","family":"Orkin","sequence":"additional","affiliation":[{"name":"Division of Hematology\/Oncology, Children's Hospital and Dana\u2013Farber Cancer Institute, Harvard Medical School, and Howard Hughes Medical Institute, Boston, MA 02115; and Department of Medicine, Cardiology Division and Department of Cell and Developmental Biology, University of Pennsylvania Health System, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2003,11,12]]},"reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V80.3.575.575"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(17)31636-8"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.16.5.2238"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.3.950"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)80318-9"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/339446a0"},{"key":"e_1_3_2_7_2","first-page":"1759","volume":"120","year":"1994","unstructured":"Yomogida, K., Ohtani, H., Harigae, H., Ito, E., Nishimune, Y., Engel, J. 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