Because NCC is located at the apical membrane of the distal convoluted tubule of the nephron, it faces the lumen of the tubule and is in contact with the tubular fluid. Using the<unk>  gradient across the apical membrane of the cells in distal convoluted tubule, the<unk>  transports Na+ and Cl− from the tubular fluid into these cells. Afterward, the Na+ is pumped out of the cell and into the bloodstream by the Na+-K+ ATPase located at the basal membrane and the Cl− leaves the cells through the basolateral<unk>  channel ClC-Kb. The<unk>  accounts for the absorption of 5% of the salt filtered at the glomerulus. NCC activity is known to have two control mechanisms affecting protein trafficking to the plasma membrane and transporter kinetics by phosphorylation and de-phosphorylation of conserved serine/threonine residues. As NCC has to be at the plasma membrane to function, its activity can be regulated by increasing or decreasing the amount of protein at the plasma membrane. Some NCC modulators, such as the WNK3 and WNK4 kinases may regulate the amount of NCC at the cell surface by inducing the insertion or removal, respectively, of the protein from the plasma membrane. Furthermore, many residues of NCC can be phosphorylated or dephosphorylated to activate or inhibit NCC uptake of Na+ and Cl−. Other NCC modulators, including intracellular<unk>  depletion, angiotensin II, aldosterone and vasopressin, can regulate NCC activity by phosphorylating conserved serine/threonine residues. NCC activity can be inhibited by thiazides, which is why this<unk>  is also known as the thiazide-sensitive Na+-Cl− cotransporter.
Sodium-chloride symporter
Sulfate transporter
Thiamine transporter 1
Carboxylate transporter
Band 3 anion transport protein
Norepinephrine transporter
Zinc transporter 8
Phosphorylase kinase, alpha 1