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Suppression of premature termination codons as a therapeutic approach.
The designer aminoglycoside NB84 significantly reduces glycosaminoglycan accumulation associated with MPS I-H in the Idua-W392X mouse.
Characterization of an MPS I-H knock-in mouse that carries a nonsense mutation analogous to the human IDUA-W402X mutation.
AAV-delivered suppressor tRNA overcomes a nonsense mutation in mice.
Ataluren suppresses a premature termination codon in an MPS I-H mouse.