GO curators for mouse genes have assigned the following annotations to the gene product of Slc26a4. (This text reflects annotations as of Wednesday, January 23, 2013.) Summary from NCBI RefSeq
[Summary is not available for the mouse gene. This summary is for the human ortholog.] Mutations in this gene are associated with Pendred syndrome, the most common form of syndromic deafness, an autosomal-recessive disease. It is highly homologous to the SLC26A3 gene; they have similar genomic structures and this gene is located 3' of the SLC26A3 gene. The encoded protein has homology to sulfate transporters. [provided by RefSeq, Jul 2008]Summary text based on GO annotations supported by experimental evidence in mouse
Researchers have inferred from direct assay, that the gene product of Slc26a4
Dou H et al. (2004) Co-expression of pendrin, vacuolar H+-ATPase alpha4-subunit and carbonic anhydrase II in epithelial cells of the murine endolymphatic sac. J Histochem Cytochem, 52:1377-84. (PubMed:15385584)
Kim YH et al. (2005) Intercalated cell H+/OH- transporter expression is reduced in Slc26a4 null mice. Am J Physiol Renal Physiol, 289:F1262-72. (PubMed:16144965)
Verlander JW et al. (2003) Localization of the ammonium transporter proteins RhBG and RhCG in mouse kidney. Am J Physiol Renal Physiol, 284:F323-37. (PubMed:12388412)