Drug‐induced readthrough of premature stop codons leads to the stabilization of laminin α2 chain mRNA in CMD myotubes

The most common form of congenital muscular dystrophy is caused by a deficiency in the α2 chain of laminin‐211, a protein of the extracellular matrix. A wide variety of mutations, including 20 to 30% of nonsense mutations, have been identified in the corresponding gene, LAMA2. A promising approach for the treatment of genetic disorders due to premature termination codons (PTCs) is the use of drugs to force stop codon readthrough.

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