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REVIEW-ARTICLE
1Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland and ; 2Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania
Submitted March 30, 2009 ; accepted in final form May 15, 2009
The discovery of the renal outer medullary K+ channel (ROMK, Kir1.1), the founding member of the inward-rectifying K+ channel (Kir) family, by Ho and Hebert in 1993 revolutionized our understanding of potassium channel biology and renal potassium handling. Because of the central role that ROMK plays in the regulation of salt and potassium homeostasis, considerable efforts have been invested in understanding the underlying molecular mechanisms. Here we provide a comprehensive guide to ROMK, spanning from the physiology in the kidney to the organization and regulation by intracellular factors to the structural basis of its function at the atomic level.
Kir1.1; KCNJ; inward-rectifying potassium channel; Bartter's syndrome; pseudohypoaldosteronism type II; serine- and glucocorticoid-regulated kinase-1; WNK kinase; phosphatidylinositol 4,5-bisphosphate
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