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- W2767356064 endingPage "131" @default.
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- W2767356064 abstract "Premature termination codons (PTC) originate from nucleotide substitution introducing an in-frame PTC. They induce truncated, usually non-functional, proteins, degradation of the PTC containing transcripts by the nonsense-mediated decay (NMD) pathway and abnormal exon skipping. Readthrough compounds facilitate near cognate amino-acyl-tRNA incorporation, leading potentially to restoration of a functional full-length protein. Splicing mutations can lead to aberrantly spliced transcripts by creating a cryptic splice site or destroying a normal site. Most mutations result in disruption of the open reading frame and activation of NMD. Antisense oligonucleotides are single stranded short synthetic RNA-like molecules chemically modified to improve their stability and ability to recognize their target RNAs and modify the splice site. This review focuses on recent developments in therapies aiming to improve the health of CF patients carrying nonsense or splicing mutations." @default.
- W2767356064 created "2017-11-17" @default.
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- W2767356064 date "2017-06-01" @default.
- W2767356064 modified "2023-10-14" @default.
- W2767356064 title "The suppression of premature termination codons and the repair of splicing mutations in CFTR" @default.
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- W2767356064 doi "https://doi.org/10.1016/j.coph.2017.09.017" @default.
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