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- W3096202250 abstract "Significance Mutation of CHD7 causes multiple developmental disorders, including CHARGE syndrome, in which conotruncal anomalies are the most prevalent form of heart defects. Our study provides mouse genetic evidence demonstrating that CHD7 cell-autonomously regulates cardiac neural crest cell (cNCC) development to promote normal conotruncal morphogenesis, clarifying a long-standing controversy. Furthermore, through comprehensive in vitro and in vivo analyses, we reveal that CHD7 acts in cNCCs through both nucleosome remodeling and recruiting histone modifying enzymes to target loci. Our study provides fundamental insights regarding the etiology of CHD7-related congenital cardiovascular disorders. Importantly, our data suggest that patients carrying truncation mutations versus missense mutations will likely display different molecular alterations; these patients might therefore require personalized therapeutic interventions." @default.
- W3096202250 created "2020-11-09" @default.
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- W3096202250 date "2020-10-30" @default.
- W3096202250 modified "2023-10-09" @default.
- W3096202250 title "CHD7 regulates cardiovascular development through ATP-dependent and -independent activities" @default.
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- W3096202250 doi "https://doi.org/10.1073/pnas.2005222117" @default.
- W3096202250 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7682373" @default.
- W3096202250 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33127760" @default.
- W3096202250 hasPublicationYear "2020" @default.
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