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生成两条无基因组整合的 DMD iPSC 系,其突变影响所有肌营养不良蛋白异构体,并且可能适合外显子跳跃。

Generation of two genomic-integration-free DMD iPSC lines with mutations affecting all dystrophin isoforms and potentially amenable to exon-skipping.

机构信息

Department of Cell and Developmental Biology, University College London, WC1E 6DE London, United Kingdom.

Dubowitz Neuromuscular Centre, Great Ormond Street Institute of Child Health, University College London, London WC1N 1EH, United Kingdom; NIHR Great Ormond Street Hospital Biomedical Research Centre, London, United Kingdom.

出版信息

Stem Cell Res. 2020 Mar;43:101688. doi: 10.1016/j.scr.2019.101688. Epub 2020 Feb 1.

Abstract

Duchenne muscular dystrophy (DMD) is the most common paediatric muscular dystrophy and is caused by mutations in the DYSTROPHIN gene. We generated two induced pluripotent stem cell (iPSC) lines from DMD patients with nonsense mutations in exons 68 (UCLi011-A) or 70 (UCLi012-A) by transfecting reprogramming mRNAs. Both mutations affect expression of all dystrophin isoforms. iPSCs expressed pluripotency-associated markers, differentiated into cells of the three germ layers in vitro and had normal karyotypes. The selected mutations are potentially amenable to read-through therapies, exon-skipping and gene-editing. These new iPSCs are also relevant to study DYSTROPHIN role in tissues other than skeletal muscle.

摘要

杜氏肌营养不良症(DMD)是最常见的儿科肌肉疾病,由 DYSTROPHIN 基因突变引起。我们通过转染重编程 mRNA ,从具有外显子 68(UCLi011-A)或 70(UCLi012-A)无义突变的 DMD 患者中生成了两条诱导多能干细胞(iPSC)系。这两种突变均影响所有肌营养不良蛋白异构体的表达。iPSC 表达多能性相关标志物,在体外分化为三个胚层的细胞,且具有正常核型。所选突变可能适用于通读疗法、外显子跳跃和基因编辑。这些新的 iPSC 也与研究除骨骼肌以外的组织中 DYSTROPHIN 的作用有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1187/7057262/b321a17005ad/gr1.jpg

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