PubMed:16849419 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/16849419","sourcedb":"PubMed","sourceid":"16849419","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/16849419","text":"Intronic deletions in the SLC34A3 gene cause hereditary hypophosphatemic rickets with hypercalciuria.\nCONTEXT: Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a rare metabolic disorder, characterized by hypophosphatemia and rickets/osteomalacia with increased serum 1,25-dihydroxyvitamin D [1,25-(OH)(2)D] resulting in hypercalciuria.\nOBJECTIVE: Our objective was to determine whether mutations in the SLC34A3 gene, which encodes sodium-phosphate cotransporter type IIc, are responsible for the occurrence of HHRH.\nDESIGN AND SETTING: Mutation analysis of exons and adjacent introns in the SLC34A3 gene was conducted at an academic research laboratory and medical center.\nPATIENTS OR OTHER PARTICIPANTS: Members of two unrelated families with HHRH participated in the study.\nRESULTS: Two affected siblings in one family were homozygous for a 101-bp deletion in intron 9. Haplotype analysis of the SLC34A3 locus in the family showed that the two deletions are on different haplotypes. An unrelated individual with HHRH was a compound heterozygote for an 85-bp deletion in intron 10 and a G-to-A substitution at the last nucleotide in exon 7. The intron 9 deletion (and likely the other two mutations) identified in this study causes aberrant RNA splicing. Sequence analysis of the deleted regions revealed the presence of direct repeats of homologous sequences.\nCONCLUSION: HHRH is caused by biallelic mutations in the SLC34A3 gene. Haplotype analysis suggests that the two intron 9 deletions arose independently. The identification of three independent deletions in introns 9 and 10 suggests that the SLC34A3 gene may be susceptible to unequal crossing over because of sequence misalignment during 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