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10.1038/mtna.2015.39 http://scihub22266oqcxt.onion/10.1038/mtna.2015.39 C5014533!5014533 !26623937     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26623937 &cmd=llinks): Failed to open stream: HTTP request failed! 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Evaluation of 2 -Deoxy-2 -fluoro Antisense Oligonucleotides for Exon Skipping in Duchenne Muscular Dystrophy |pdf=|usr=}}{{26623937 }} gab.com Text Evaluation of 2 -Deoxy-2 -fluoro Antisense Oligonucleotides for Exon Skipping in Duchenne Muscular Dystrophy JO: Mol Ther Nucleic Acids http://www.kidney.de/pget.php?&tw=1&pmid=26623937 #FOAvip Duchenne muscular dystrophy (DMD) is a severe muscle wasting disorder typically caused by frame-shifting mutations in the DMD gene. Restoration of the reading frame would allow the production of a shorter but partly functional dystrophin protein as seen in Becker muscular dystrophy patients. This can be achieved with antisense oligonucleotides (AONs) that induce skipping of specific exons during pre-mRNA splicing. Different chemical modifications have been developed to improve AON properties. The 2'-deoxy-2'-fluoro (2F) RNA modification is attractive for exon skipping due to its ability to recruit ILF2/3 proteins to the 2F/pre-mRNA duplex, which resulted in enhanced exon skipping in spinal muscular atrophy models. In this study, we examined the effect of two different 2'-substituted AONs (2'-F phosphorothioate (2FPS) and 2'-O-Me phosphorothioate (2OMePS)) on exon skipping in DMD cell and animal models. In human cell cultures, 2FPS AONs showed higher exon skipping levels than their isosequential 2OMePS counterparts. Interestingly, in the mdx mouse model, 2FPS was less efficient than 2OMePS and suggested safety issues as evidenced by increased spleen size and weight loss. Our results do not support a clinical application for 2FPS AON. Twit Text FOAVip Evaluation of 2 -Deoxy-2 -fluoro Antisense Oligonucleotides for Exon Skipping in Duchenne Muscular Dystrophy ????Mol Ther Nucleic Acids http://www.kidney.de/pget.php?&tw=1&pmid=26623937 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26623937 #FOAvip English Wikipedia <ref>{{Cite pmid|26623937 }}</ref> Evaluation of 2 -Deoxy-2 -fluoro Antisense Oligonucleotides for Exon Skipping in Duchenne Muscular Dystrophy #MMPMID26623937 Jirka SM ; Tanganyika-de Winter CL ; Boertje-van der Meulen JW ; van Putten M ; Hiller M ; Vermue R ; de Visser PC ; Aartsma-Rus A Mol Ther Nucleic Acids 2015[Dec]; 4 (12 ): e265 PMID26623937 show ga Duchenne muscular dystrophy (DMD) is a severe muscle wasting disorder typically caused by frame-shifting mutations in the DMD gene. Restoration of the reading frame would allow the production of a shorter but partly functional dystrophin protein as seen in Becker muscular dystrophy patients. This can be achieved with antisense oligonucleotides (AONs) that induce skipping of specific exons during pre-mRNA splicing. Different chemical modifications have been developed to improve AON properties. The 2'-deoxy-2'-fluoro (2F) RNA modification is attractive for exon skipping due to its ability to recruit ILF2/3 proteins to the 2F/pre-mRNA duplex, which resulted in enhanced exon skipping in spinal muscular atrophy models. In this study, we examined the effect of two different 2'-substituted AONs (2'-F phosphorothioate (2FPS) and 2'-O-Me phosphorothioate (2OMePS)) on exon skipping in DMD cell and animal models. In human cell cultures, 2FPS AONs showed higher exon skipping levels than their isosequential 2OMePS counterparts. Interestingly, in the mdx mouse model, 2FPS was less efficient than 2OMePS and suggested safety issues as evidenced by increased spleen size and weight loss. Our results do not support a clinical application for 2FPS AON. äEvaluation of 2 -Deoxy-2 -fluoro Antisense Oligonucleotides for Exon S(epmc).pdf DeepDyve Pubget Overpricing