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A G542X cystic fibrosis mouse model for examining nonsense mutation directed therapies

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By Daniel McHugh, Miarasa S. Steele, Dana M. Valerio, Alexander Miron
| PLOS
Nonsense mutations are present in 10% of patients with CF, produce a premature termination codon in CFTR mRNA causing early termination of translation, and lead to lack of CFTR function. There are no currently available animal models which contain a nonsense mutation in the endogenous Cftr locus that can be utilized to test nonsense mutation therapies. In this study, we create a CF mouse model carrying the G542X nonsense mutation in Cftr using CRISPR/Cas9 gene editing.
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