WNK1 is a member of the WNK subfamily of serine/threonine protein kinases that is a key regulator of blood pressure by controlling the transport of sodium and chloride ions. Mutations in WNK1 have been associated with pseudohypoaldosteronism type II and hereditary sensory neuropathy type II. WNK1 is a regulator of blood pressure and deficiency of this protein in mice lowers the blood pressure. WNK1 can regulate the Ca(2+) sensing and the subsequent Ca(2+)-dependent interactions mediated by synaptotagmin C2 domains and WNK1 exhibits additive CFTR inhibition.
Proceedings of the National Academy of Sciences of the United States of America, 100(24), 14109-14114 (2003-11-12)
The availability of both the mouse and human genome sequences allows for the systematic discovery of human gene function through the use of the mouse as a model system. To accelerate the genetic determination of gene function, we have developed
WNK (with no lysine [K]) protein kinases were named for their unique active site organization. Mutations in WNK1 and WNK4 cause a familial form of hypertension by undefined mechanisms. Here, we report that WNK1 selectively binds to and phosphorylates synaptotagmin
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