The sulfate transporter is a solute carrier familyprotein that in humans is encoded by the SLC26A2gene.[5] SLC26A2 is also called the diastrophic dysplasia sulfate transporter (DTDST), and was first described by Hästbacka et al. in 1994.[5] A defect in sulfate activation described by Superti-Furga in achondrogenesis type 1B[6] was subsequently also found to be caused by genetic variants in the sulfate transporter gene.[7] This sulfate (SO42−) transporter also accepts chloride, hydroxyl ions (OH−), and oxalate as substrates.[8][9] SLC26A2 is expressed at high levels in developing and mature cartilage, as well as being expressed in lung, placenta, colon, kidney, pancreas and testis.[10][11]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ abHästbacka J, de la Chapelle A, Mahtani MM, Clines G, Reeve-Daly MP, Daly M, Hamilton BA, Kusumi K, Trivedi B, Weaver A (September 1994). "The diastrophic dysplasia gene encodes a novel sulfate transporter: positional cloning by fine-structure linkage disequilibrium mapping". Cell. 78 (6): 1073–87. doi:10.1016/0092-8674(94)90281-X. PMID7923357. S2CID36181375.
^Superti-Furga A, Hästbacka J, Wilcox WR, Cohn DH, van der Harten HJ, Rossi A, Blau N, Rimoin DL, Steinmann B, Lander ES, Gitzelmann R (January 1996). "Achondrogenesis type IB is caused by mutations in the diastrophic dysplasia sulphate transporter gene". Nature Genetics. 12 (1): 100–2. doi:10.1038/ng0196-100. PMID8528239. S2CID31143438.
