The Mouse Sulfate Anion Transporter Gene<i>Sat1</i>(Slc26a1): Cloning, Tissue Distribution, Gene Structure, Functional Characterization, and Transcriptional Regulation Thyroid Hormone

Lee, Aven; Beck, Laurent; Markovich, Daniel

doi:10.1089/104454903321112460

Cited by 56 publications

(55 citation statements)

References 48 publications

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“…In addition to CFEX, other members of the Slc26 family are localized in the intestine. Sat-1 (Slc26a1) is usually associated with kidneys and liver, but recently its mRNA expression was also detected in mouse cecum (112) and human small intestine and colon (113). However, although it is presumed that Sat-1 is localized in the BLM of intestinal epithelial cells (114,115), in rats an anti-Sat-1 antibody clearly labeled the Sat-1 protein in specifi c membrane domains of hepatocytes and proximal tubules (116)(117)(118), whereas in the intestine, the same antibody stained intracellular organelles, possibly mitochondria, with (11,14).…”

Section: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 99%

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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Oxalate urolithiasis (nephrolithiasis) is the most frequent type of kidney stone disease. Epidemiological research has shown that urolithiasis is approximately twice as common in men as in women, but the underlying mechanism of this sex-related prevalence is unclear. Oxalate in the organism partially originate from food (exogenous oxalate) and largely as a metabolic end-product from numerous precursors generated mainly in the liver (endogenous oxalate). Oxalate concentrations in plasma and urine can be modifi ed by various foodstuffs, which can interact in positively or negatively by affecting oxalate absorption, excretion, and/or its metabolic pathways. Oxalate is mostly removed from blood by kidneys and partially via bile and intestinal excretion. In the kidneys, after reaching certain conditions, such as high tubular concentration and damaged integrity of the tubule epithelium, oxalate can precipitate and initiate the formation of stones. Recent studies have indicated the importance of the SoLute Carrier 26 (SLC26) family of membrane transporters for handling oxalate. Two members of this family [Sulfate Anion Transporter 1 (SAT-1; SLC26A1) and Chloride/Formate EXchanger (CFEX; SLC26A6)] may contribute to oxalate transport in the intestine, liver, and kidneys. Malfunction or absence of SAT-1 or CFEX has been associated with hyperoxaluria and urolithiasis. However, numerous questions regarding their roles in oxalate transport in the respective organs and male-prevalent urolithiasis, as well as the role of sex hormones in the expression of these transporters at the level of mRNA and protein, still remain to be answered.

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Section: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 99%

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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“…Toward this end, SLC26A1 (also know as SAT1, for sulfate anion transporters 1) (3,16,29) was fused in frame with GFP (see Materials and Methods) and expressed in MDCK cells in isotonic media at pH 7.4. As indicated in Figure 6A, SLC26A1 is expressed predominantly in the plasma membrane, with little expression in the cytoplasm (Z-line image).…”

Section: Expression Of Slc26a1 and Slc26a7/a1 Chimera In Mdck Cellsmentioning

confidence: 99%

Chloride/Bicarbonate Exchanger SLC26A7 Is Localized in Endosomes in Medullary Collecting Duct Cells and Is Targeted to the Basolateral Membrane in Hypertonicity and Potassium Depletion

Xu¹,

Worrell

Li³

et al. 2006

Journal of the American Society of Nephrology

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“…SLC26A1 encodes the SO 4 2Ϫ /HCO 3 Ϫ /oxalate exchanger (sat-1) identified in the BLM of mammalian renal proximal tubule cells (41) ( Table 2). In addition, SLC26A1 exhibits Cl Ϫ transport activity when expressed in Xenopus oocytes (45). SLC26A2 (DTDST), which appears to be expressed ubiquitously (32), has affinities for many anions, including SO 4 2Ϫ , HCO 3 Ϫ , Cl Ϫ , oxalate, and S 2 O 3 2Ϫ (79).…”

Section: Tubular Somentioning

confidence: 99%

Role of tubular secretion and carbonic anhydrase in vertebrate renal sulfate excretion

Pelis¹,

Renfro²

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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/HCO 3 Ϫ exchange at the brushborder membrane, tubular carbonic anhydrase (CA) activity, CAII protein, and a proportion of tubular SO 4 2Ϫ secretion that is CA dependent. CA activity is required for about one-half of this net SO 4 2Ϫ secretion but is also required for about one-half of the net reabsorption in bird proximal epithelium. A CA-SO 4 2Ϫ /anion exchanger metabolon arrangement is proposed that may speed both the secretory and reabsorptive processes. renal proximal tubule; transport metabolon INORGANIC SO 4 2Ϫ IS THE SECOND most abundant anion in the sea and one of the most abundant anions in vertebrate plasma, with concentrations varying among species from 0.3 to 1.8 mM. This large tetrahedral divalent anion can be obtained from the diet (83) or oxidation of the sulfur-containing amino acids cysteine and methionine (77). Sulfoconjugation reactions are the initial detoxification process for many endogenous (e.g., steroid hormones) and xenobiotic compounds and are required for the activation of numerous biological molecules (e.g., heparin, cholecystokinin, and gastrin) (59). SO 4 2Ϫ is a major component of glycosaminoglycans (dermatan sulfate, chondroitin sulfate, keratan sulfate, and heparan sulfate), which are structural components of numerous tissues, including cartilage, bone, myelin, and basal lamina (40 ]) in the renal tubule lumen reduces Ca 2ϩ and Mg 2ϩ reabsorption (66). RENAL SULFATE CLEARANCEThe kidneys are the major avenue for SO 4 2Ϫ excretion in vertebrates. Nearly all of plasma SO 4 2Ϫ is ultrafilterable in mammals (4), whereas 80% and 47% of plasma SO 4 2Ϫ are ultrafilterable in birds (71) and fish (75), respectively. Variation in the estimates of the ultrafilterable fraction of plasma SO 4 2Ϫ in vertebrates may arise from species differences or variations in method of determination. Urine content is determined by glomerular filtration, tubular reabsorption, and tubular secretion. This review will focus on the latter and will provide only a brief overview of tubular reabsorption because it has been described in detail elsewhere (2,51,52,57).Reabsorption of filtered SO 4 2Ϫ occurs primarily in the proximal tubule (35) secretion does not occur in these animals. SO 4 2Ϫ loading apparently has no effect on the saturable reabsorptive transport maximum for SO 4 2Ϫ (Tm SO 4 2Ϫ ) in the renal tubule of the human, dog, and frog (3,28,48). In contrast, Tm SO 4 2Ϫ in rats is reduced ϳ50% after plasma SO 4 2Ϫ loading, indicating that adaptive mechanisms are in place to depress reabsorption, thus increasing excretion (27). Similarly, in domestic fowl, Tm SO 4 2Ϫ decreases with plasma SO 4 2Ϫ loading, leading to the conclusion that a fraction of the excreted SO 4 2Ϫ is the result of tubular secretion (30). Thiosulfate, an inhibitor of SO 4 2Ϫ transporters,

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The Mouse Sulfate Anion Transporter GeneSat1(Slc26a1): Cloning, Tissue Distribution, Gene Structure, Functional Characterization, and Transcriptional Regulation Thyroid Hormone

Cited by 56 publications

References 48 publications

Oxalate: From the Environment to Kidney Stones

Oxalate: From the Environment to Kidney Stones

Chloride/Bicarbonate Exchanger SLC26A7 Is Localized in Endosomes in Medullary Collecting Duct Cells and Is Targeted to the Basolateral Membrane in Hypertonicity and Potassium Depletion

Role of tubular secretion and carbonic anhydrase in vertebrate renal sulfate excretion

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