[HTML][HTML] The Na+: Cl–cotransporter is activated and phosphorylated at the amino-terminal domain upon intracellular chloride depletion
D Pacheco-Alvarez, P San Cristóbal, P Meade… - Journal of Biological …, 2006 - ASBMB
The renal Na+: Cl–cotransporter rNCC is mutated in human disease, is the therapeutic
target of thiazide-type diuretics, and is clearly involved in arterial blood pressure regulation.
rNCC belongs to an electroneutral cation-coupled chloride cotransporter family (SLC12A)
that has two major branches with inverse physiological functions and regulation: sodium-
driven cotransporters (NCC and NKCC1/2) that mediate cellular Cl–influx are activated by
phosphorylation, whereas potassium-driven cotransporters (KCCs) that mediate cellular Cl …
target of thiazide-type diuretics, and is clearly involved in arterial blood pressure regulation.
rNCC belongs to an electroneutral cation-coupled chloride cotransporter family (SLC12A)
that has two major branches with inverse physiological functions and regulation: sodium-
driven cotransporters (NCC and NKCC1/2) that mediate cellular Cl–influx are activated by
phosphorylation, whereas potassium-driven cotransporters (KCCs) that mediate cellular Cl …