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The protein encoded by SLC26A3 is a transmembrane glycoprotein that transports chloride ions across the cell membrane in exchange for bicarbonate ions. Zusätzlich bieten wir Ihnen SLC26A3 Antikörper (16) und SLC26A3 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
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This study confirms the molecular heterogeneity of sporadic congenital chloride diarrhea, adding 12 novel SLC26A3 mutations to the list of known pathogenic mutations.
Molecular analysis of human solute carrier SLC26A2, SLC26A3, and SLC26A4 (zeige SLC26A4 ELISA Kits) anion transporter disease-causing mutations using 3-dimensional homology modeling has been presented.
In intestinal cells, TNF (zeige TNF ELISA Kits) activates NF-kappaB (zeige NFKB1 ELISA Kits), which reduces expression of the Cl(-) / HCO3(-) exchanger SLC26A3, via direct binding to the promoter region.
Genetic variations of the SLC26A3 rs2108225 is associated with enhance the risk of ulcerative colitis.
We report the first Tunisian case of SLC26A3 gene mutation in congenital chloride diarrhea. Our patient was homozygous for G187X mutation. Both parents were heterozygous for the same mutation.
Expression of NHE3 and DRA was reduced with high tacrolimus levels and impaired renal function after intestinal transplantation.
A variety of mutations in SLC26A3 are responsible for CCD (zeige RUNX2 ELISA Kits). A total of 55 mutations in SLC26A3 have been reported
Data demonstrate an upregulation of SLC26A3 via activation of the ERK1/2 (zeige MAPK1/3 ELISA Kits) pathway that may underlie potential antidiarrheal effects of Bifidobacterium sp.
Efficacy of lactobacillus acidophilus or its secreted soluble factors in alleviating inflammation and inflammation-associated dysregulation of DRA activity could justify their therapeutic potential in inflammatory diarrheal diseases.
The SLC26A3-NHERF4 (zeige PDZD3 ELISA Kits) interaction was modulated by phosphorylation; serine 329 of NHERF4 (zeige PDZD3 ELISA Kits)-PDZ3 played a critical role in modulating binding selectivity.
This study showed that transepithelial sulfate fluxes across the mouse distal ileum demonstrating that DRA (and to a lesser extent, PAT1) secretes sulfate with significant implications for intestinal sulfate absorption and overall homeostasis.
DRA surface expression was reduced partly via an increase in DRA endocytosis and a decrease in exocytosis
Both PAT-1 and DRA significantly contribute to intestinal fluid absorption and enterocyte acid/base balance but are activated by different ion gradients.
Data indicate that solute carrier family 26, member 3 protein (Slc26a3) is expressed in male reproductive tract, and its expression pattern is related to the function.
Deletion of DRA results in severely reduced colonic HCO3 (-) secretory rate, a loss of colonic fluid absorption, a lack of a firmly adherent mucus layer and a severely reduced colonic mucosal resistance to dextran sodium sulphate damage.
DRA mediates a predominance of the apical uptake of oxalate and Cl(-) absorbed in the small and large intestine of mice under short-circuit conditions.
Endogenous and recombinant human/mouse Slc26a3 do not exhibit electrogenic 2Cl-/1HCO- exchange. Acute induction of Slc26a3 Cl-/HCO3- exchange is associated with secondary membrane potential changes representing homeostatic responses.
The protein encoded by this gene is a transmembrane glycoprotein that transports chloride ions across the cell membrane in exchange for bicarbonate ions. It is localized to the mucosa of the lower intestinal tract, particularly to the apical membrane of columnar epithelium and some goblet cells. The protein is essential for intestinal chloride absorption, and mutations in this gene have been associated with congenital chloride diarrhea.
chloride anion exchanger
, down-regulated in adenoma protein
, solute carrier family 26, member 3
, down-regulated in adenoma
, down-regulated in adenoma DRA
, solute carrier family 26 member 3
, chloride anion exchanger-like