ArticleJournal of human genetics2007
Genetic heterogeneity of megaloblastic anaemia type 1 in Tunisian patients.
Article in Journal of human genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Imerslund-Gräsbeck syndrome: a comprehensive review of reported cases.Orphanet journal of rare diseases · 2023Review
- Detailed investigations of proximal tubular function in Imerslund-Gräsbeck syndrome.BMC medical genetics · 2013Article
- Inherited cobalamin malabsorption. Mutations in three genes reveal functional and ethnic patterns.Orphanet journal of rare diseases · 2012Article
- Founder mutations in Tunisia: implications for diagnosis in North Africa and Middle East.Orphanet journal of rare diseases · 2012Article
- Ancient founder mutation is responsible for Imerslund-Gräsbeck Syndrome among diverse ethnicities.Orphanet journal of rare diseases · 2011Article
- Exome sequencing reveals cubilin mutation as a single-gene cause of proteinuria.Journal of the American Society of Nephrology : JASN · 2011Article
- Genetic analysis of hereditary multiple exostoses in Tunisian families: a novel frame-shift mutation in the EXT1 gene.Molecular biology reports · 2009Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Megaloblastic anaemia 1 (MGA1) is a rare autosomal recessive condition characterized by selective intestinal vitamin B12 malabsorption and proteinuria. More than 200 MGA1 patients have been identified worldwide, but the disease is relatively prevalent in Finland, Norway and several Eastern Mediterranean regions. MGA1 is genetically heterogeneous and can be caused by mutations in either the cubilin (CUBN) or the amnionless (AMN) gene. In the present study we investigated the molecular defect underlying MGA1 in nine Tunisian patients belonging to six unrelated consanguineous families. Haplotype and linkage analyses, using microsatellite markers surrounding both CUBN and AMN genes, indicated that four out of the six families were likely to be linked to the CUBN gene. Patients from these families were screened for the Finnish, Mediterranean and Arabian mutations already published. None of the screened mutations could be detected in our population. One family showed a linkage to AMN gene. Direct screening of the AMN gene allowed the identification of the c.208-2A>G mutation, previously described in a Jewish Israeli patient of Tunisian origin and in Turkish patients. This suggests that the c.208-2A>G mutation may derive from a single Mediterranean founder ancestor. For the last family, haplotype analysis excluded both CUBN and AMN genes, suggesting the existence of a third locus that may cause MGA1.
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