Browse our anti-SLC26A7 (SLC26A7) Antibodies

Human Solute Carrier Family 26 (Sulfate Transporter), Member 7 (SLC26A7) interaction partners

1. SLC26A7 mutations appear to be associated with thyroid dyshormonogenesis.

2. the molecular cloning from human HEVEC of a 2.9-kb cDNA encoding SLC26A7, a novel member of the SLC26 (solute carrier 26) sulfate/anion exchanger family

3. In human kidney SLC26A6 and A7 have a distinct, partially overlapping expression in distal segments of nephrons. The distribution partly differs from that found previously in rodent kidneys.

4. The trafficking to the cell surface suggests novel functional upregulation of SLC26A7 in states that are associated with hypokalemia or increased medullary tonicity.

Mouse (Murine) Solute Carrier Family 26 (Sulfate Transporter), Member 7 (SLC26A7) interaction partners

1. Slc26a1, Slc26a6 and Slc26a7 are novel participants in the extracellular transport of bicarbonate during enamel maturation.

2. Slc26a7 chloride channel activity and localization in mouse Reissner's membrane epithelium

3. SLC26A7 is a basolateral Cl(-)/HCO(3)(-) exchanger in gastric parietal cells and possibly plays a major role in gastric acid secretion

4. findings reveal that SLC26A7 functions as a unique Cl(-) channel that is regulated by intracellular H(+)

5. Slc26a7 is expressed in the proximal tubule and thick ascending limb of the loop of Henle, and it may therefore contribute to anion transport in these nephron segments

6. 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.

7. Suggest that the increase in Slc26a7 expression caused by deletion of AE1 represents an adaptive response, indicating that Slc26a7 contributes to the regulation of acid-base balance by the kidney.

8. SLC26A7 dysfunction should be investigated as a potential cause of unexplained distal renal tubular acidosis