Journal article
E2F3 plays an essential role in cardiac development and function
Cell cycle (Georgetown, Tex.), Vol.7(23), pp.3775-3780
12/2008
DOI: 10.4161/cc.7.23.7240
PMCID: PMC2723769
PMID: 19029823
Abstract
The E2F transcription factors are key downstream targets of the retinoblastoma protein tumor suppressor. They are known to regulate the expression of genes that control fundamental biological processes including cellular proliferation, apoptosis and differentiation. However, considerable questions remain about the precise roles of the individual E2F family members. This study shows that E2F3 is essential for normal cardiac development. E2F3-loss impairs the proliferative capacity of the embryonic myocardium and most
E2f3
−/−
mice die
in utero
or perinatally with hypoplastic ventricular walls and/or severe atrial and ventricular septal defects. A small fraction of the
E2f3
−/−
neonates have hearts that appear grossly normal and they initially survive. However, these animals develop ultrastructural defects in the cardiac muscle and ultimately die as a result of congestive heart failure. These data demonstrate a clear link between E2F3’s role in the proliferative capacity of the myocardium and cardiac function during both development and adulthood.
Details
- Title: Subtitle
- E2F3 plays an essential role in cardiac development and function
- Creators
- Jennifer C King - Koch Institute for Integrative Cancer Research @ MIT, Cambridge, MA 02139Ivan P. G Moskowitz - Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115Patrick G Burgon - Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115Ferhaan Ahmad - Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115James R Stone - Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114Jonathan G Seidman - Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115Jacqueline A Lees - Koch Institute for Integrative Cancer Research @ MIT, Cambridge, MA 02139
- Resource Type
- Journal article
- Publication Details
- Cell cycle (Georgetown, Tex.), Vol.7(23), pp.3775-3780
- DOI
- 10.4161/cc.7.23.7240
- PMID
- 19029823
- PMCID
- PMC2723769
- ISSN
- 1538-4101
- eISSN
- 1551-4005
- Language
- English
- Date published
- 12/2008
- Academic Unit
- Radiology; Molecular Physiology and Biophysics; Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
- Record Identifier
- 9984025406102771
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