| http://purl.uniprot.org/citations/25196150 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25196150 | http://www.w3.org/2000/01/rdf-schema#comment | "FOG-2 is a multi-zinc finger protein that binds the transcriptional activator GATA4 and modulates GATA4-mediated regulation of target genes during heart development. Our previous work has demonstrated that the Nucleosome Remodeling and Deacetylase (NuRD) complex physically interacts with FOG-2 and is necessary for FOG-2 mediated repression of GATA4 activity in vitro. However, the relevance of this interaction for FOG-2 function in vivo has remained unclear. In this report, we demonstrate the importance of FOG-2/NuRD interaction through the generation and characterization of mice homozygous for a mutation in FOG-2 that disrupts NuRD binding (FOG-2(R3K5A)). These mice exhibit a perinatal lethality and have multiple cardiac malformations, including ventricular and atrial septal defects and a thin ventricular myocardium. To investigate the etiology of the thin myocardium, we measured the rate of cardiomyocyte proliferation in wild-type and FOG-2(R3K5A) developing hearts. We found cardiomyocyte proliferation was reduced by 31±8% in FOG-2(R3K5A) mice. Gene expression analysis indicated that the cell cycle inhibitor Cdkn1a (p21(cip1)) is up-regulated 2.0±0.2-fold in FOG-2(R3K5A) hearts. In addition, we demonstrate that FOG-2 can directly repress the activity of the Cdkn1a gene promoter, suggesting a model by which FOG-2/NuRD promotes ventricular wall thickening by repression of this cell cycle inhibitor. Consistent with this notion, the genetic ablation of Cdkn1a in FOG-2(R3K5A) mice leads to an improvement in left ventricular function and a partial rescue of left ventricular wall thickness. Taken together, our results define a novel mechanism in which FOG-2/NuRD interaction is required for cardiomyocyte proliferation by directly down-regulating the cell cycle inhibitor Cdkn1a during heart development."xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ydbio.2014.08.030"xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/author | "Gao Z."xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/author | "Martens S."xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/author | "Svensson E.C."xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/author | "Earley J.U."xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/author | "Broman M."xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/author | "Garnatz A.S."xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/name | "Dev Biol"xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/pages | "50-61"xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/title | "FOG-2 mediated recruitment of the NuRD complex regulates cardiomyocyte proliferation during heart development."xsd:string |
| http://purl.uniprot.org/citations/25196150 | http://purl.uniprot.org/core/volume | "395"xsd:string |
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