Suppressing ‘nonsense’ in cystic fibrosis
Author:
Affiliation:
1. INSERM U1151 Institut Necker Enfants Malades Paris France
2. Université Paris Descartes Paris France
3. School of Physiology Pharmacology and Neuroscience University of Bristol Bristol UK
Publisher
Wiley
Subject
Physiology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1113/JP279267
Reference7 articles.
1. Alternate Translation Initiation Codons Can Create Functional Forms of Cystic Fibrosis Transmembrane Conductance Regulator
2. Correctors and Potentiators Rescue Function of the Truncated W1282X-Cystic Fibrosis Transmembrane Regulator (CFTR) Translation Product
3. Aminoglycoside antibiotics restore CFTR function by overcoming premature stop mutations
4. Functional rescue of c.3846G>A (W1282X) in patient-derived nasal cultures achieved by inhibition of nonsense mediated decay and protein modulators with complementary mechanisms of action
5. Capitalizing on the heterogeneous effects of CFTR nonsense and frameshift variants to inform therapeutic strategy for cystic fibrosis
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