SLC26A2 encodes sulfate transporter with N-terminal cytoplasmic domain and C-terminal cytoplasmic STAS domains flanking a transmembrane domain, modeled to span the lipid bilayer 8 times. SLC26A2 is highly conserved among different vertebrate species and zebrafish SLC26A2 protein shares 87.6% identical amino acid sequence with human SLC26A2 protein, which consists chiefly of a sulphate transporter domain, the STAS domain, and the C terminal dimerization domain, which are key functional domains shared with the remaining Slc26 family members.
|Basic Information of SLC26A2|
|Protein Name||Sulfate transporter|
|Gene Name||SLC26A2, DTD, DTDST|
|Aliases||Diastrophic dysplasia protein, Solute carrier family 26 member 2|
|Organism||Homo sapiens (Human)|
SLC26A2 is ubiquitously expressed with particularly high levels in developing and mature cartilage as well as in epithelial tissues like pancreas, salivary glands, colon, bronchial glands, tracheal epithelium, and eccrine sweat glands. SLC26A2 is a transporter with an essential role in bone formation, which may also participate in chondrocyte volume expansion. SLC26A2 also functions as a SO42-/Cl-/OH- exchanger that is exquisitely regulated by extracellular Cl-. Mutations in SLC26A2 cause many forms of osteochondrodysplasia including achondrogenesis type 1B, diastrophic dysplasia, atelosteogenesis, and type IIrecessive multiple epiphyseal dysplasias. SLC26A2 was upregulated in Crohn's colitis and has been proposed as part of a diagnostic index distinguishing Crohn's from ulcerative colitis.
Fig.1 In silico model of the putative structure of the Slc26a2 TMDs. (Ohana E, 2012)
This article finds multiple roles for SLC26A2 in chondrocyte biology and emphasizes the importance of SLC26A2-mediated protein sulfation in cell signaling, which may account for the complex phenotype of DTD.
This article suggests that several children with rMED are caused by compound heterozygocity for previously described SLC26A2 mutations.
This article suggests that SLC26A2 regulating aldosterone secretion potentially plays a role in the pathogenesis of primary aldosteronism.
This article reveals that bioinformatics can predict new deafness genes and shows SLC26A2 is a critical otic gene whose dysfunction may induce hearing impairment.
This article suggests that SLC13A4 and SLC26A2 transporter play an important role in meeting the fetal needs for sulfate in late-gestation.
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