NKX2-5 mutations causative for congenital heart disease retain functionality and are directed to hundreds of targets

NKX2-5 mutations causative for congenital heart disease retain functionality and are directed to hundreds of targets

We take a functional genomics approach to congenital heart disease mechanism. We used DamID to establish a robust set of target genes for NKX2-5 wild type and disease associated NKX2-5 mutations to model loss-of-function in gene regulatory networks. NKX2-5 mutants, including those with a crippled ho...

Täydet tiedot

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Bibliografiset tiedot
Päätekijät: Romaric Bouveret, Ashley J. Waardenberg, Nicole Schönrock, Mirana Ramialison, Tram B. Doan, Daniëlle de Jong, Antoine Bondue, Gurpreet Kaur, Stephanie Mohamed, Hananeh Fonoudi, C.M. Chen, Merridee A. Wouters, Shoumo Bhattacharya, Nicolas Plachta, Sally L. Dunwoodie, Gavin Chapman, Cédric Blanpain, Richard P. Harvey
Aineistotyyppi: Artigo
Kieli:englanti
Julkaistu: 2015
Linkit:https://doi.org/10.7554/elife.06942
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Internet

https://doi.org/10.7554/elife.06942

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