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Slc26a9 is one member of a family of sulfate/anion transporter genes. Additionally we are shipping Slc26a9 Antibodies (9) and many more products for this protein.
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SLC26A9 single nucleotide polymorphisms modify prenatal exocrine pancreatic damage in cystic fibrosis (show S100A8 Proteins)
We have identified two SLC26A9 mutations decreasing Cl- channel transport in patients with a CF-like lung disease.
SLC26A9 is an epithelial chloride/bicarbonate channel that can interact with the CF transmembrane regulator (CFTR (show CFTR Proteins)), the protein mutated in CF
Several SNPs in the 3' UTR of SLC26A9 (rs12031234, rs2282429, rs2282430)were associ (show IL13 Proteins)ated with asthma in children with asthma.
SLC26A9 polymorphisms lead to several function modifications (increased activity, decreased activity, altered protein expression), which could lead to a spectrum of pathophysiologies.
Single nucleotide polymorphism in SLC26A9 gene is associated with cystic fibrosis (show S100A8 Proteins).
Report functional interaction between CFTR (show CFTR Proteins) and SLC26A9 in polarized airway epithelial cells and in non-polarized HEK293 cells.
the L683P mutation of SLC26A9 was found to reduce Cl(-) transport through SLC26A9 as well as the positive interaction exerted by SLC26A9 on CFTR (show CFTR Proteins) ion transport activity
The interactions between SLC26A9 and CFTR (show CFTR Proteins) were studied, and an alternative hypothesis to their known interactions is presented.
Functions as an anion conductance in the apical membranes of bronchial epithelium; contributes to transepithelial chloride currents under basal and cyclic AMP (show APRT Proteins)/protein kinase A-stimulated conditions.
The chloride channel (show CLCA1 Proteins)/transporter Slc26a9 regulates the systemic arterial pressure and renal chloride excretion.
SLC26A9 is activated in airway inflammation. Slc26a9-deficient mice exhibited IL-13 (show IL13 Proteins)-induced airway mucus obstruction. SLC26A9-mediated Cl- secretion is essential for preventing airway obstruction in allergic airway disease.
Cellular HCO(3)(-) secretion, likely through SLC26A9, is the dominant mechanism whereby gastric mucosal surface pH transiently increases in response to photodamage.
Slc26a9 functions as an electrogenic nCl (show NCL Proteins)-/HCO3- exchanger, suggesting a role in pulmonary and gastric HCO3- secretion and/or CO2 transport.
Slc26a9 plays an essential role in gastric acid secretion via effects on the viability of tubulovesicles/secretory canaliculi and by regulating chloride secretion in parietal cells.
Slc26a9 has three discrete physiological modes: nCl (show NCL Proteins)(-)-HCO(3)(-) exchanger, Cl(-) channel, and Na(+)-anion cotransporter.
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. The product of this gene is a highly selective chloride ion channel regulated by WNK kinases. Alternative splicing results in multiple transcript variants encoding differing isoforms.
anion transporter/exchanger protein 9
, anion transporter/exchanger-9
, solute carrier family 26 member 9
, solute carrier family 26, member 9
, SLC26A9 anion transporter/exchanger