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Solute carrier family 26, member 7

SLC26A7, sut-2
This gene is one member of a family of sulfate/anion transporter genes. Family members are well conserved in their genomic (number and size of exons) and protein (aa length among species) structures yet have markedly different tissue expression patterns. This gene has abundant and specific expression in the kidney. Splice variants that use both alternate transcription initiation and polyadenylation sites have been described for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, SLC26A6, PGD2, DTDST, DRA
Papers on SLC26A7
SLC26A Gene Family Participate in pH Regulation during Enamel Maturation.
Paine et al., Nanning, China. In Plos One, 2014
The bicarbonate transport activities of Slc26a1, Slc26a6 and Slc26a7 are essential to physiological processes in multiple organs.
Photophysical properties of open-framework germanates templated by nickel complexes.
Schwingenschlögl et al., Saudi Arabia. In Phys Chem Chem Phys, 2014
We investigate the optical and electronic features of these systems (SUT-1 and SUT-2) from first principles.
Genome-wide association study for calving traits in Holstein-Friesian dairy cattle.
Berry et al., Dublin, Ireland. In Animal, 2014
Morphological abnormalities are a known contributor to perinatal mortality and the most significantly associated SNP for perinatal mortality in the present study was located in a region in linkage disequilibrium with the gene SLC26A7.
Slc26a7 chloride channel activity and localization in mouse Reissner's membrane epithelium.
Marcus et al., Cincinnati, United States. In Plos One, 2013
A previous report pointed to SLC26A7 as a candidate gene important for cochlear function.
High-throughput screening of mouse gene knockouts identifies established and novel skeletal phenotypes.
Vogel et al., The Woodlands, United States. In Bone Res, 2013
Together, these screens identified multiple genes affecting bone mass: 23 previously reported genes (Calcr, Cebpb, Crtap, Dcstamp, Dkk1, Duoxa2, Enpp1, Fgf23, Kiss1/Kiss1r, Kl (Klotho), Lrp5, Mstn, Neo1, Npr2, Ostm1, Postn, Sfrp4, Slc30a5, Slc39a13, Sost, Sumf1, Src, Wnt10b), five novel genes extensively characterized (Cldn18, Fam20c, Lrrk1, Sgpl1, Wnt16), five novel genes with preliminary characterization (Agpat2, Rassf5, Slc10a7, Slc26a7, Slc30a10) and three novel undisclosed genes coding for potential osteoporosis drug targets.
SLC26 Cl-/HCO3- exchangers in the kidney: roles in health and disease.
Soleimani, Cincinnati, United States. In Kidney Int, 2013
Except for SLC26A5 (prestin), all can operate as multifunctional anion exchangers, with three members (SLC26A7, SLC26A9, and SLC26A11) also capable of functioning as chloride channels.
The SLC26 gene family of anion transporters and channels.
Sharma et al., Boston, United States. In Mol Aspects Med, 2013
Additional disease phenotypes evident only in mouse knockout models include oxalate urolithiasis for Slc26a6 and Slc26a1, non-syndromic deafness for Slc26a5, gastric hypochlorhydria for Slc26a7 and Slc26a9, distal renal tubular acidosis for Slc26a7, and male infertility for Slc26a8.
Placental, renal, and ileal sulfate transporter gene expression in mouse gestation.
Simmons et al., South Brisbane, Australia. In Biol Reprod, 2012
In the kidney, Slc13a1 and Slc26a1 were the most abundant sulfate transporter mRNAs, which increased by ≈2-fold at E4.5 or E6.5, whereas lower levels of Slc26a2, Slc26a6, and Slc26a7 mRNA increased by ≈3- to 6-fold from E4.5.
Anion transport by the cochlear motor protein prestin.
Fahlke et al., Hannover, Germany. In J Physiol, 2012
A comparison with a non-mammalian prestin from D. rerio - recently shown to function as Cl(-)/SO(4)(2-) antiporter - and an SLC26 anion channel, human SLC26A7, revealed that SCN(-) transport is conserved in these distinct members of the SLC26 family.
Genes linked to energy metabolism and immunoregulatory mechanisms are associated with subcutaneous adipose tissue distribution in HIV-infected men.
Arnett et al., Birmingham, United States. In Pharmacogenet Genomics, 2011
RESULTS: Loci (rs10504906, rs13267998, rs921231) in or near the anion exchanger solute carrier family 26, member 7 isoform a (SLC26A7) were strongly associated with the upper trunk and the arm SAT (9.8×10(-7) ≤P<7.8×10(-6)).
Two open-framework germanates with nickel complexes incorporated into the framework.
Sun et al., Stockholm, Sweden. In Inorg Chem, 2011
Two open-framework germanates, SUT-1 and SUT-2, have been synthesized under hydrothermal conditions using ethylenediamine (en, H(2)NCH(2)CH(2)NH(2)) as templates and Ni(NO(3))(2)·6H(2)O as the transition-metal source.
MSUT2 is a determinant of susceptibility to tau neurotoxicity.
Kraemer et al., Seattle, United States. In Hum Mol Genet, 2011
We previously identified sut-2 as a gene required for tau neurotoxicity in a transgenic Caenorhabditis elegans model of tauopathy.
The role of MSUT-2 in tau neurotoxicity: a target for neuroprotection in tauopathy?
Kraemer et al., Seattle, United States. In Biochem Soc Trans, 2010
We ultimately cloned the sut-2 (suppressor of tau pathology-2) gene, mutations in which alleviate tau neurotoxicity in C. elegans.
Deletion of the chloride transporter slc26a7 causes distal renal tubular acidosis and impairs gastric acid secretion.
Soleimani et al., Cincinnati, United States. In J Biol Chem, 2009
SLC26A7 dysfunction should be investigated as a potential cause of unexplained distal renal tubular acidosis
Diverse transport modes by the solute carrier 26 family of anion transporters.
Muallem et al., Dallas, United States. In J Physiol, 2009
SLC26A7 and SLC26A9 function exclusively as Cl- channels.
Decreased expression of Slc26a4 (Pendrin) and Slc26a7 in the kidneys of carbonic anhydrase II-deficient mice.
Petrovic et al., Cincinnati, United States. In Cell Physiol Biochem, 2007
CAII deficiency results in a significant decrease in the gene and protein expression of bicarbonate transport proteins from Slc26 gene family - Slc26a4 (pendrin) and Slc26a7.
Increased acid load and deletion of AE1 increase Slc26a7 expression.
Petrovic et al., Cincinnati, United States. In Nephron Physiol, 2007
Suggest that the increase in Slc26a7 expression caused by acid challenge represents an adaptive response, indicating that Slc26a7 contributes to the regulation of acid-base balance by the kidney.
SLC26A7 can function as a chloride-loading mechanism in parietal cells.
Geibel et al., New Haven, United States. In Pflugers Arch, 2007
SLC26A7 is a Cl(-) uptake system under histamine stimulation
Renal physiology of SLC26 anion exchangers.
Romero et al., Boston, United States. In Curr Opin Nephrol Hypertens, 2007
Slc26a4 (pendrin) and Slc26a7 are expressed in intercalated cells, and are involved in acid-base homeostasis and blood pressure regulation.
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.
Soleimani et al., Cincinnati, United States. In J Am Soc Nephrol, 2006
The trafficking to the cell surface suggests novel functional upregulation of SLC26A7 in states that are associated with hypokalemia or increased medullary tonicity.
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