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FLASH GENE
Symbol SLC26A1 contributors: mct - updated : 01-07-2016
HGNC name solute carrier family 26 (sulfate transporter), member 1
HGNC id 10993
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • nine transmembrane segments
  • cytoplasmic N and C termini with a sulfate transporter family motif
  • an STAS domain (sulfate transporter and anti sigma antagonist)
    • conjugated GlycoP
    HOMOLOGY
    interspecies homolog to rattus Slc26a1 (78.5 pc)
    homolog to murine Slc26a1 (79.1 pc)
    Homologene
    FAMILY
  • sulfate/anion exchanger family
  • SLC26A/SulP transporter (TC 2.A.53) family
    • CATEGORY transport carrier
    SUBCELLULAR LOCALIZATION     plasma membrane
    text multi-pass membrane protein
    basic FUNCTION
  • involved in sulfate transport in exchange for HCO3 or oxalate
  • characterized as an anion exchanger that transports anions by mediating electroneutral sulfate-oxalate, sulfate-bicarbonate, or oxalate-bicarbonate exchange
  • mediates epithelial transport of oxalate and sulfate, and its localization in the kidney, liver, and intestine suggests that it may play a role in oxalate and sulfate homeostasis
  • regulates both oxalate and sulfate homeostasis and may be critical to the development of calcium oxalate urolithiasis and hepatotoxicity
  • is a basolateral membrane anion exchanger that mediates intestinal oxalate transport
  • SLC26A1, SLC26A6 and SLC26A7 are novel participants in the extracellular transport of bicarbonate during enamel maturation, and that their functional roles may be achieved by forming interaction units with CFTR (pMID: 26671068)
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS active transport
    text
  • Na+ independent sulfate transporter
  • Cl- transport
  • oxalate transport
    • PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
    cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s) NPHL3
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • Slc26a1-/- mice exhibit hyposulfatemia, hypersulfaturia, calcium oxalate urolithiasis, and nephrocalcinosis in the setting of hyperoxalemia and hyperoxaluria
  • Sat1-deficient mice also have a phenotype of hyperoxalemia, hyperoxaluria, and calcium oxalate stones
  • Slc36a1 loss in mice leads to hyperoxaluria and calcium oxalate renal stones
  • hyperoxalemia in Slc26a1-/- mice was most likely caused by reduced intestinal secretion of oxalate, based on reduced oxalate transport in basolateral membrane vesicles from the distal ileum, cecum, and proximal colon