Na+-sulfate cotransporter SLC13A1

Markovich, Daniel (2014) Na+-sulfate cotransporter SLC13A1. Pflugers Archiv European Journal of Physiology, 466 1: 131-137. doi:10.1007/s00424-013-1388-8

Author Markovich, Daniel
Title Na+-sulfate cotransporter SLC13A1
Formatted title
Na+-sulfate cotransporter SLC13A1
Journal name Pflugers Archiv European Journal of Physiology   Check publisher's open access policy
ISSN 0031-6768
Publication date 2014-01-01
Year available 2013
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1007/s00424-013-1388-8
Volume 466
Issue 1
Start page 131
End page 137
Total pages 7
Place of publication Heidelberg, Germany
Publisher Springer
Language eng
Formatted abstract
Sulfate is essential for normal physiology. The kidney plays a major role in sulfate homeostasis. Sulfate is freely filtered and strongly reabsorbed in the proximal tubule. The apical membrane Na+-sulfate cotransporter NaS1 (SLC13A1) mediates sulfate (re)absorption across renal proximal tubule and small intestinal epithelia. NaS1 encodes a 595-amino acid (≈66 kDa) protein with 13 putative transmembrane domains. Its substrate preferences are sodium and sulfate, thiosulfate, and selenate, and its activity is inhibited by molybdate, selenate, tungstate, thiosulfate, succinate, and citrate. NaS1 is primarily expressed in the kidney (proximal tubule) and intestine (duodenum to colon). NaS1 expression is down-regulated in the renal cortex by high sulfate diet, hypothyroidism, vitamin D depletion, glucocorticoids, hypokalemia, metabolic acidosis, and NSAIDs and up-regulated by low sulfate diet, thyroid hormone, vitamin D supplementation, growth hormone, chronic renal failure, and during post-natal growth. Disruption of murine NaS1 gene leads to hyposulfatemia and hypersulfaturia, as well as changes in metabolism, growth, fecundity, behavior, gut physiology, and liver detoxification. This suggests that NaS1 is an important sulfate transporter and its disruption leads to perturbed sulfate homeostasis, which contributes to numerous pathophysiological conditions.
Keyword Knock-out mouse
Renal reabsorption
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Official 2014 Collection
School of Biomedical Sciences Publications
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