| Literature DB >> 17902024 |
Biagio Didona1, Andrea Codispoti2, Enrico Bertini3, Wiliam B Rizzo4, Gael Carney4, Giovanna Zambruno5, Carlo Dionisi-Vici3, Mauro Paradisi6, Cristina Pedicelli6, Gerry Melino7,8,9, Alessandro Terrinoni10.
Abstract
Sjögren-Larsson syndrome (SLS; MIM#270200) is an autosomal recessive neurocutaneous disease caused by mutations in the ALDH3A2 gene for fatty aldehyde dehydrogenase (FALDH), a microsomal enzyme that catalyzes the oxidation of medium- and long- chain aliphatic aldehydes fatty acids. We studied two unrelated Italian SLS patients with ichthyosis, developmental delay, spastic diplegia and brain white matter disease. One patient was homozygous for a novel ALDH3A2 insertion mutation (c.767insA) in exon 5. The other SLS patient was a compound heterozygote for two previously reported mutations: a slice site mutation (c.1094C > T; S365L) in exon 7. Analysis of fibroblast RNA by RT-PCR indicated that the spice-site mutation caused skipping of exons 2 and 3. The c.1094C > T mutation, previously associated with two ALDH3A2 haplotypes, was found on a third distinct haplotype in our patient, which indicates that arose independently in this kindred. These results add to understanding of the genetic basis of SLS and will be useful for DNA diagnosis of this disease.Entities:
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Year: 2007 PMID: 17902024 PMCID: PMC3057174 DOI: 10.1007/s10038-007-0180-z
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172