Human Mutation · 2004 · 70 citations · 7 references
Life SciencesGeneticsMolecular GeneticsGenodermatosesHuman GeneticsMedical GeneticsGenetic DisordersGenetic SyndromesGenotype-phenotype Association AnalysisGenotype-phenotype CorrelationPigmentary DisordersSyndromic GenodermatosesAdar EnzymesCongenital Pigmentary DisordersHypomelanotic MaculesMutationSkin Disease GeneticsSkin GenodermatosesSkin Pigmentation Genetics
Dyschromatosis symmetrica hereditaria (DSH) is an autosomal dominant pigmentary genodermatosis characterized by hyperpigmented and hypopigmented macules of on the extremities and caused by the mutations in the ADAR gene(also called DSRAD) encoding for RNA-specific adenosine deaminase. Here we reported clinical and molecular findings of 6 Chinese multi-generation families and 2 sporadic patients with DSH. We found that the same mutation could lead to different phenotypes even in the same family and we did not establish a clear correlation between genotypes and phenotypes. Seven novel heterozygous mutations of ADAR were identified, which were c.2433_2434delAG (p.T811fs), c.2197G>T (p.E733X), c.3286C>T (p.R1096X), c.2897G>T (p.C966F), c.2797C>T (p.Q933X), c.2375delT (p.L792fs) and c.3203-2A>G respectively. Our data add new variants to the repertoire of ADAR mutations in DSH.
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Requirement of the RNA Editing Deaminase ADAR1 Gene for Embryonic Erythropoiesis
Q. Wang, Jaspal S. Khillan, Paul Gadue et al. · Science · 2000 · 443 citations
Yi Wang, Yong Zeng, John M. Murray et al. · Journal of Molecular Biology · 1995 · 79 citations · Full text