Background: Na-K-Cl cotransporters (NKCC) are channel proteins that aid in the transcellular movement of chloride across both secretory and absorptive epithelia. NKCC1 is expressed in muscle cells, neurons, and red blood cells. In the basolateral membrane of secretory epithelia, NKCC1 mediates active chloride secretion. The gene encoding human NKCC1 maps to chromosome 5q23.3. In mice, disruption of the NKCC1 gene leads to deafness and impaired balance. NKCC2 is specifically expressed in the kidney where it mediates active reabsorption of sodium chloride in the thick ascending limb of the loop of Henle. NKCC2 is sensitive to the clinically important diuretics furosemide and bumetanide. The gene encoding human NKCC2 maps to chromosome 15q15-q21 and mutations in this gene lead to Bartter’s syndrome, an inherited hypokalaemic alkalosis. NCCT is a thiazide-sensitive Na-Cl cotransporter that is primarily expressed in the distal convoluted tubule of the kidney where it accounts for a significant fraction of net renal sodium reabsorption. The gene for human NCCT map to chromosome 16q13. Mutations in the gene encoding NCCT cause Gitelman’s syndrome, a subset of Bartter’s syndrome.
Description: Rabbit polyclonal to NKCC1
Immunogen: KLH conjugated synthetic peptide derived from NKCC1
Specificity: ·Reacts with Human, Mouse, Pig, Dog and Rat.
·Isotype: IgG
Application: ·Western blotting: 1/100-500. Predicted Mol wt: 130 kDa;
·Immunohistochemistry (Paraffin/frozen tissue section): 1/50-200;
·Immunocytochemistry/Immunofluorescence: 1/100;
·Immunoprecipitation: 1/50;
·ELISA: 1/500;
·Optimal working dilutions must be determined by the end user.
