Revisiting the NaCl cotransporter regulation by with-no-lysine kinases.

@article{BazaValenti2015RevisitingTN,
  title={Revisiting the NaCl cotransporter regulation by with-no-lysine kinases.},
  author={Silvana Baz{\'u}a-Valenti and Gerardo Gamba},
  journal={American journal of physiology. Cell physiology},
  year={2015},
  volume={308 10},
  pages={C779-91}
}
The renal thiazide-sensitive Na(+)-Cl(-) cotransporter (NCC) is the salt transporter in the distal convoluted tubule. Its activity is fundamental for defining blood pressure levels. Decreased NCC activity is associated with salt-remediable arterial hypotension with hypokalemia (Gitelman disease), while increased activity results in salt-sensitive arterial hypertension with hyperkalemia (pseudohypoaldosteronism type II; PHAII). The discovery of four different genes causing PHAII revealed a… CONTINUE READING
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References

Publications referenced by this paper.
Showing 1-10 of 94 references

Renal and brain isoforms of WNK3 have opposite effects on NCCT expression.

Journal of the American Society of Nephrology : JASN • 2009
View 4 Excerpts
Highly Influenced

WNK1-related Familial Hyperkalemic Hypertension results from an increased expression of L-WNK1 specifically in the distal nephron.

Proceedings of the National Academy of Sciences of the United States of America • 2013
View 4 Excerpts
Highly Influenced

Angiotensin II signaling via protein kinase C phosphorylates Kelch-like 3, preventing WNK4 degradation.

Proceedings of the National Academy of Sciences of the United States of America • 2014
View 1 Excerpt

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