| Literature DB >> 27879217 |
Stefan Hauser1, Stefanie Schuster2, Yvonne Theurer3, Matthis Synofzik4, Ludger Schöls4.
Abstract
Human skin fibroblasts were isolated from a 48-year-old patient carrying compound heterozygous mutations (c.610+364G>A and c.1311A>G) in OPA1, responsible for early onset optic atrophy complicated by ataxia and pyramidal signs (Behr syndrome; OMIM #210000). Fibroblasts were reprogrammed using episomal plasmids carrying hOCT4, hSOX2, hKLF4, hL-MYC and hLIN28. The generated transgene-free line iPS-OPA1-BEHR showed no additional genomic aberrations, maintained the disease-relevant mutations, expressed important pluripotency markers and was capable to differentiate into cells of all three germ layers in vitro. The generated iPS-OPA1-BEHR line might be a useful platform to study the pathomechanism of early onset complicated optic atrophy syndromes.Entities:
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Year: 2016 PMID: 27879217 DOI: 10.1016/j.scr.2016.09.012
Source DB: PubMed Journal: Stem Cell Res ISSN: 1873-5061 Impact factor: 2.020