| Literature DB >> 24509478 |
Kálmán Tory1, Dóra K Menyhárd2, Stéphanie Woerner3, Fabien Nevo3, Olivier Gribouval3, Andrea Kerti4, Pál Stráner2, Christelle Arrondel3, Evelyne Huynh Cong3, Tivadar Tulassay5, Géraldine Mollet3, András Perczel6, Corinne Antignac7.
Abstract
Monogenic disorders result from defects in a single gene. According to Mendel's laws, these disorders are inherited in either a recessive or dominant fashion. Autosomal-recessive disorders require a disease-causing variant on both alleles, and according to our current understanding, their pathogenicities are not influenced by each other. Here we present an autosomal-recessive disorder, nephrotic syndrome type 2 (MIM 600995), in which the pathogenicity of an NPHS2 allele encoding p.Arg229Gln depends on the trans-associated mutation. We show that, contrary to expectations, this allele leads to a disease phenotype only when it is associated specifically with certain 3' NPHS2 mutations because of an altered heterodimerization and mislocalization of the encoded p.Arg229Gln podocin. The disease-associated 3' mutations exert a dominant-negative effect on p.Arg229Gln podocin but behave as recessive alleles when associated with wild-type podocin. Therefore, the transmission rates for couples carrying the disease-associated mutations and p.Arg229Gln may be substantially different from those expected in autosomal-recessive disorders.Entities:
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Year: 2014 PMID: 24509478 DOI: 10.1038/ng.2898
Source DB: PubMed Journal: Nat Genet ISSN: 1061-4036 Impact factor: 38.330