Novel compound heterozygous mutations in SLC5A2 are responsible for autosomal recessive renal glucosuria.

Article Details

Citation

Calado J, Soto K, Clemente C, Correia P, Rueff J

Novel compound heterozygous mutations in SLC5A2 are responsible for autosomal recessive renal glucosuria.

Hum Genet. 2004 Feb;114(3):314-6. Epub 2003 Nov 12.

PubMed ID
14614622 [ View in PubMed
]
Abstract

Familial renal glucosuria is an inherited renal tubular disorder. A homozygous nonsense mutation in the SLC5A2 gene, encoding the sodium/glucose co-transporter SGLT2, has recently been identified in an affected child of consanguineous parents. We now report novel compound heterozygous mutations in the son of non-consanguineous parents. One allele has a p.Q167fsX186 mutation, which is expected to produce a truncated protein, and the other a p.N654S mutation involving a highly conserved residue. These findings confirm that mutations in the SLC5A2 gene are responsible for recessive renal glucosuria.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Sodium/glucose cotransporter 2P31639Details