pseudohypoaldosteronism/phosphatase

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NakalaMajaribio ya klinikiHati miliki

Chagua aina ya aina

3 matokeo

C-terminally truncated, kidney-specific variants of the WNK4 kinase lack several sites that regulate its activity.

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Ingia / Ingia

WNK lysine-deficient protein kinase 4 (WNK4) is an important regulator of renal salt handling. Mutations in its gene cause pseudohypoaldosteronism type II, mainly arising from overactivation of the renal Na+/Cl- cotransporter (NCC). In addition to full-length WNK4, we have observed faster migrating

WNK4 kinase is a negative regulator of K+-Cl- cotransporters.

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Ingia / Ingia

WNK kinases [with no lysine (K) kinase] are emerging as regulators of several membrane transport proteins in which WNKs act as molecular switches that coordinate the activity of several players. Members of the cation-coupled chloride cotransporters family (solute carrier family number 12) are one of

Exploring the intricate regulatory network controlling the thiazide-sensitive NaCl cotransporter (NCC).

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Ingia / Ingia

The thiazide-sensitive NaCl cotransporter (NCC) plays key roles in renal electrolyte transport and blood pressure maintenance. Regulation of this cotransporter has received increased attention recently, prompted by the discovery that mutations in the with-no-lysine (WNK) kinases are the molecular

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Herbal & Natural Medicine

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