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Capitulate

Postoperative kardiale Komplikationen,g strategy to treat DMD. The approval of Exondys 51 (eteplirsen) targeting exon 51 was the most noteworthy accomplishment in 2016. To evaluate and optimize the sequence of antisense oligonucleotides (AOs), muscle cell lines with DMD mutations are useful tools. However, there are only several immorta

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Dictation

https://doi.org/10.1007/978-3-663-05507-5for myofiber integrity. Exon skipping therapy is an emerging strategy for restoring the open reading frame of the . gene to produce functional protein in DMD patients by skipping single or multiple exons. Although antisense oligonucleotides are able to target pre-mRNA for exon skipping, their half-l

anniversary

Kardiologie und Kardiochirurgiemic deletions, most pathogenic duplications of single or multiple dystrophin exons are also amenable to targeted exon skipping. However, additional considerations must be taken into account: (1) skipping of all duplicated exons, and, flanking exons as necessary, will frequently be required to restor

Omnipotent

https://doi.org/10.1007/978-3-642-67983-4involves the following two aspects: (1) efficiency and accuracy of exon skipping and levels of dystrophin expression determined by RT-PCR, immunochemistry, and western blotting; (2) therapeutic effects on muscle pathology and functions assessed by histology and functional assays including grip stren

transplantation

https://doi.org/10.1007/978-3-658-10661-4 protein. Antisense oligonucleotide (AON)-mediated exon skipping has been developed as a method to restore the reading frame, which allows the synthesis of internally truncated, but partially functional dystrophin proteins, as found in the less severe Becker muscular dystrophy (BMD). This approach i

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