| Literature DB >> 26499107 |
Stefania Zampieri1, Mirella Filocamo2, Annalisa Pianta1, Susanna Lualdi2, Laura Gort3, Maria Jose Coll3, Richard Sinnott4, Tarekegn Geberhiwot5, Bruno Bembi1, Andrea Dardis1.
Abstract
Niemann-Pick Types A and B (NPA/B) diseases are autosomal recessive lysosomal storage disorders caused by the deficient activity of acid sphingomyelinase (ASM) because of the mutations in the SMPD1 gene. Here, we provide a comprehensive updated review of already reported and newly identified SMPD1 variants. Among them, 185 have been found in NPA/B patients. Disease-causing variants are equally distributed along the SMPD1 gene; most of them are missense (65.4%) or frameshift (19%) mutations. The most frequently reported mutation worldwide is the p.R610del, clearly associated with an attenuated NP disease type B phenotype. The available information about the impact of 52 SMPD1 variants on ASM mRNA and/or enzymatic activity has been collected and whenever possible, phenotype/genotype correlations were established. In addition, we created a locus-specific database easily accessible at http://www.inpdr.org/genes that catalogs the 417 SMPD1 variants reported to date and provides data on their in silico predicted effects on ASM protein function or mRNA splicing. The information reviewed in this article, providing new insights into the genotype/phenotype correlation, is extremely valuable to facilitate diagnosis and genetic counseling of families affected by NPA/B.Entities:
Keywords: Niemann-Pick; SMPD1; acid sphingomyelinase; lysosomal storage disorder
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Year: 2015 PMID: 26499107 DOI: 10.1002/humu.22923
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878