ReviewPflugers Archiv : European journal of physiology2014
Na+-sulfate cotransporter SLC13A1.
Review in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Exome-wide association study reveals common and rare coding variants shaping chronic pain in 327,642 UK biobank participants.Genome medicine · 2026Article
- Functional role of a structural water in the elevator domain of dicarboxylate transporter VcINDY.PNAS nexus · 2026Article
- Liver-specific SLC13A3 modulation alleviates MASLD by regulating NADMolecular and cellular biochemistry · 2026Article
- Host genome regulation of the porcine gut microbiota and its impact on feed conversion efficiency.Animal microbiome · 2026Article
- Hookworm infection modulates lung and intestinal transcriptomic responses to SARS-CoV-2 in Syrian hamsters.Frontiers in immunology · 2025Article
- BiallelicGenetics in medicine open · 2025Article
- Key roles of two-component systems in intestinal signal sensing and virulence regulation in enterohemorrhagic Escherichia coli.FEMS microbiology reviews · 2024Review
- Structural basis for the reaction cycle and transport mechanism of human NaScience advances · 2024Article
- Cryo-EM structures of the human NaS1 and NaDC1 transporters revealed the elevator transport and allosteric regulation mechanism.Science advances · 2024Article
- The impact of solute carrier proteins on disrupting substance regulation in metabolic disorders: insights and clinical applications.Frontiers in pharmacology · 2024Review
- Sulfoconjugation of protein peptides and glycoproteins in physiology and diseases.Pharmacology & therapeutics · 2023Review
- Sulfur-Element containing metabolic pathways in human health and crosstalk with the microbiome.Biochemistry and biophysics reports · 2023Review
- The Profiles and Functions of RNA Editing Sites Associated with High-Altitude Adaptation in Goats.International journal of molecular sciences · 2023Article
- Biallelic variants in the SLC13A1 sulfate transporter gene cause hyposulfatemia with a mild spondylo-epi-metaphyseal dysplasia.Clinical genetics · 2023Article
- Understanding host-microbiota interactions in the commercial piglet around weaning.Scientific reports · 2021Article
- Renal cell markers: lighthouses for managing renal diseases.American journal of physiology. Renal physiology · 2021Article
- A guide to plasma membrane solute carrier proteins.The FEBS journal · 2021Review
- Follow-Up of Adefovir Dipivoxil Induced Osteomalacia: Clinical Characteristics and Genetic Predictors.Frontiers in pharmacology · 2021Article
- Skeletal Dysplasias Caused by Sulfation Defects.International journal of molecular sciences · 2020Review
- Structure and Mechanism of the Divalent Anion/Na⁺ Symporter.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.