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WNK protein kinases modulate cellular Cl- flux by altering the phosphorylation state of the Na-K-Cl and K-Cl cotransporters Kahle KT; Rinehart J; Ring A; Gimenez I; Gamba G; Hebert SC; Lifton RPPhysiology (Bethesda) 2006[Oct]; 21 (ä): 326-35Precise control of cellular Cl(-) transport is necessary for many fundamental physiological processes. For example, the intracellular concentration of Cl(-), fine-tuned through the coordinated action of cellular Cl(-) influx and efflux mechanisms, determines whether a neuron's response to GABA is excitatory or inhibitory. In epithelia, synchrony between apical and basolateral Cl(-) flux, and transcellular and paracellular Cl(-) transport, is necessary for efficient transepithelial Cl(-) reabsorption or secretion. In cells throughout the body, coordination of Cl(-) entry and exit mechanisms help defend against changes in cell volume. The Na-K-Cl and K-Cl cotransporters of the SLC12 gene family are important molecular determinants of Cl(-) entry and exit, respectively, in these systems. The WNK serine-threonine kinase family, members of which are mutated in an inherited form of human hypertension, are components of a signaling pathway that coordinates Cl(-) influx and efflux through SLC12 cotransporters to dynamically regulate intracellular Cl(-) activity.|Biological Transport[MESH]|Chlorine/*metabolism[MESH]|Humans[MESH]|Intracellular Signaling Peptides and Proteins[MESH]|K Cl- Cotransporters[MESH]|Minor Histocompatibility Antigens[MESH]|Phosphorylation[MESH]|Protein Serine-Threonine Kinases/metabolism/*physiology[MESH]|Sodium-Potassium-Chloride Symporters/*metabolism[MESH]|Symporters/*metabolism[MESH]|WNK Lysine-Deficient Protein Kinase 1[MESH] |
