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Soon after the WNKs were identified, mutations in genes encoding WNK1 and -4 were determined to cause the human disease familial hyperkalemic hypertension (also known as pseudohypoaldosteronism II, or Gordon's Syndrome). For this reason, a major focus of investigation has been to dissect the role of WNK kinases in renal regulation of ion transport. More recently, a different mutation in WNK1 was identified as the cause of hereditary sensory and autonomic neuropathy type II, an early-onset autosomal disease of peripheral sensory nerves. Thus the WNKs represent an important family of potential targets for the treatment of human disease, and further elucidation of their physiological actions outside of the kidney and brain is necessary. In this review, we describe the gene structure and mechanisms regulating expression and activity of the WNKs. Subsequently, we outline substrates and targets of WNKs as well as effects of WNKs on cellular physiology, both in the kidney and elsewhere. Next, consequences of these effects on integrated physiological function are outlined. Finally, we discuss the known and putative pathophysiological relevance of the WNKs.<\/jats:p>","DOI":"10.1152\/physrev.00017.2010","type":"journal-article","created":{"date-parts":[[2011,1,19]],"date-time":"2011-01-19T17:44:12Z","timestamp":1295459052000},"page":"177-219","source":"Crossref","is-referenced-by-count":260,"title":["The WNKs: Atypical Protein Kinases With Pleiotropic Actions"],"prefix":"10.1152","volume":"91","author":[{"given":"James A.","family":"McCormick","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Oregon Health and Science University and Veterans Affairs Medical Center, Portland, Oregon"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David H.","family":"Ellison","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Oregon Health and Science University and Veterans Affairs Medical Center, Portland, 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