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WNK lysine deficient protein kinase 4 (WNK4) is a kinase member of the serine/threonine protein kinase family.1,2 It is composed of an N-terminal kinase domain, a PF2-like autoinhibitory domain, a coiled-coiled domain, an acidic motif, an RFQV sequence, a second coil-coiled domain, and a C-termina ddl calmodulin-binding domain.1,3 WNK4 localizes to cell tight junctions and is primarily expressed in distal nephron epithelial cells.1 It regulates renal ion exchange by positively regulating kidney-specific Na-K-Cl cotransporter (NKCC2), Na-Cl symporter (NCC), and pendrin and negatively regulating epithelial sodium channel (ENac) and inward-rectifier potassium channel 1.1 (Kir1.1).1,3,4 Missense mutations in WNK4 lead to the development of familial hyperkalemic hypertension (FHHt), a syndrome characterized by hypertension and increased blood levels of potassium and chloride caused by disrupted kidney ion exchange.5 Cayman's WNK4 protein can be used for enzyme activity and Western blot (WB) applications. This protein consists of 441 amino acids and has a calculated molecular weight of 86 kDa.
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1. WNK4 kinase: From structure to physiology. Am. J. Physiol. Renal Physiol. 320(3), F378-F403 (2021).
2. WNK4-
3. An SGK1 site in WNK4 regulates Na+ channel and K+ channel activity and has implications for aldosterone signaling and K+ homeostasis. Proc. Natl. Acad. Sci. USA 104(10), 4025-4029 (2007).
4. With no lysine kinase 4 modulates sodium potassium 2 chloride cotransporter activity in vivo. Am. J. Physiol. Renal Physiol. 315(4), F781-F790 (2018).
5. Human hypertension caused by mutations in WNK kinases. Science 293(5532), 1107-1112 (2001).