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. 2011 Oct 14;69(5):683–695. doi: 10.1007/s00018-011-0858-4

Table 1.

Renal aquaporins

Protein Localization Transport Physiology Regulated factorsa Pathophysiology from transgenic miceb Human gene mutations
Aquaporin-1 Apical and basolateral plasma membranes of proximal tubule cells, thin limb of Henle’s loop cells and descending vasa recta Water Urine concentration process, cell migration Unknown Polyuria and increased water intake defect in cell recovery after injury Mild urinary concentrating defect
Aquaporin-7 Apical plasma membrane of proximal tubule cells (s3) Water, anions and glicerol Water reabsorption, glycerol reabsorption Unknown Glyceroluria, defective glycerol metabolism, obesity, smaller islet cells Defective glycerol metabolism
Aquaporin-11 Endoplasmic reticulum of proximal tubules cells Water Organelle maintenance Unknown Polycystic kidney (fatal) No abnormalities reported
Aquaporin-2 Apical plasma membrane and intracellular vesicle of collecting duct principal cells Water Urine concentration process Vasopressin, prostaglandin E2, dopamine, aldosterone, PKA, cAMP, RhoA, intracellular calcium, RyR1, RapGEF-3, MLCK, AKAPs, phosphodiesterases, calcitonin, SNAREs, Spa-1, clathrin-mediated endocytosis, LIP5, TonEBP Diabetes insipidus Diabetes insipidus
Aquaporin-3 Basolateral plasma membrane of collecting duct principal cells Water, urea Urine concentration process Vasopressin, aldosterone, insulin, copper Polyuria and increased water intake No abnormalities reported
Aquaporin-4 Basolateral plasma membrane of collecting duct principal cells Water Urine concentration process PKC, dopamine Mild urinary concentration defect No abnormalities reported
Aquaporin-6 Intracellular vesicles of collecting duct intercalated cells Water, anions and glicerol Acid secretion Mercuric ion Not known No abnormalities reported

aSee text for details

bTransgenic mice with loss of transporter function