Associated Papers
Dominant negative mutation in oxalate transporter SLC26A6 associated with enteric hyperoxaluria and nephrolithiasis.
Cornière N et al.
Journal of Medical Genetics, 2022
Novel Human Polymorphisms Define a Key Role for the SLC26A6-STAS Domain in Protection From Ca2+-Oxalate Lithogenesis.
Shimshilashvili L et al.
Frontiers in Pharmacology, 2020
Molecular analysis of human solute carrier SLC26 anion transporter disease-causing mutations using 3-dimensional homology modeling.
Rapp C et al.
Biochimica Et Biophysica Acta. Biomembranes, 2017
An association-adjusted consensus deleterious scheme to classify homozygous Mis-sense mutations for personal genome interpretation.
Preeprem T et al.
Biodata Mining, 2013
24365473 (PubMed )
Supplement: 1756-0381-6-24-S2.xlsx › Additional_Table_7
SNP-based large-scale identification of allele-specific gene expression in human B cells.
Song MY et al.
Gene, 2012
Analysis of the 206M polymorphic variant of the SLC26A6 gene encoding a Cl- oxalate transporter in patients with primary hyperparathyroidism.
Corbetta S et al.
European Journal of Endocrinology, 2009
Phenotypic and functional analysis of human SLC26A6 variants in patients with familial hyperoxaluria and calcium oxalate nephrolithiasis.
Monico CG et al.
American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation, 2008
The SLC26 gene family of anion transporters and channels.
Alper SL et al.
Molecular Aspects of Medicine, 0
Genetic analysis of the bicarbonate secreting anion exchanger SLC26A6 in chronic pancreatitis.
Balázs A et al.
Pancreatology : Official Journal of the International Association of Pancreatology (iap) ... [et Al.], 0
CFTR and/or pancreatitis susceptibility genes mutations as risk factors of pancreatitis in cystic fibrosis patients?
Gaitch N et al.
Pancreatology : Official Journal of the International Association of Pancreatology (iap) ... [et Al.], 0
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