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Cell, v.101 no.7, 2000년, pp.729 - 739
Tevosian, Sergei G (Division of Hematology-Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School and, Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA) , Deconinck, Anne E (Division of Hematology-Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School and, Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA) , Tanaka, Makoto (Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School and, Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA) , Schinke, Martina (Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School and, Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA) , Litovsky, Silvio H (Departments of Pediatrics and Pathology, Children's Hospital and Dana Farber Cancer Institute, Beth Israel Deaconess Medical Center, Harvard Medical School and, Howard Hughes Medical Institute, Boston, Massachusetts 02115, USA) , Izumo, Seigo (Division of Cardiology, Department of Medicine, Beth Israel Deaconess Med) , Fujiwara, Yuko , Orkin, Stuart H
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AbstractWe disrupted the FOG-2 gene in mice to define its requirement in vivo. FOG-2−/− embryos die at midgestation with a cardiac defect characterized by a thin ventricular myocardium, common atrioventricular canal, and the tetralogy of Fallot malformation. Remarkably, coronary vascul...
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