Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
Mapping of five new putative anion transporter genes in human and characterization of SLC26A6, a candidate gene for pancreatic anion exchanger.
Cloning and characterization of SLC26A6, a novel member of the solute carrier 26 gene family.
Isoforms of SLC26A6 mediate anion transport and have functional PDZ interaction domains.
Functional comparison of mouse slc26a6 anion exchanger with human SLC26A6 polypeptide variants: differences in anion selectivity, regulation, and electrogenicity.
Metabolon disruption: a mechanism that regulates bicarbonate transport.
Characterization of the 5'-flanking region and regulation of expression of human anion exchanger SLC26A6.
Parsing apical oxalate exchange in Caco-2BBe1 monolayers: siRNA knockdown of SLC26A6 reveals the role and properties of PAT-1.
N-glycosylation critically regulates function of oxalate transporter SLC26A6.
Ex vivo quantification of intracellular pH in Drosophila Malpighian tubule reveals basolateral HCO(3) (-)/oxalate exchange through a novel oxalate transporter "Neat".
SLC26A3,6 exchange Cl- for HCO3-
SLC-mediated transport of inorganic anions
Calcium oxalate urolithiasis in mice lacking anion transporter Slc26a6.
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Slc26a6-null mice lack intestinal oxalate secretion, develop hyperoxaluria, hyperoxalemia and calcium oxalate urolithiasis.
"mice lacking Slc26a6 have a defect in intestinal oxalate secretion resulting in enhanced net absorption of oxalate"
Dominant negative mutation in oxalate transporter SLC26A6 associated with enteric hyperoxaluria and nephrolithiasis.
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A heterozygous dominant-negative SLC26A6 p.R507W variant reduces chloride-dependent oxalate transport and surface expression and cosegregates with hyperoxaluria.
"SLC26A6 inactivation can cause inherited enteric hyperoxaluria with calcium oxalate NL."
Phenotypic and functional analysis of human SLC26A6 variants in patients with familial hyperoxaluria and calcium oxalate nephrolithiasis.