| http://purl.uniprot.org/citations/33498219 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/33498219 | http://www.w3.org/2000/01/rdf-schema#comment | "K+ loading inhibits NKCC2 (Na-K-Cl cotransporter) and NCC (Na-Cl cotransporter) in the early distal tubules, resulting in Na+ delivery to the late distal convoluted tubules (DCTs). In the DCTs, Na+ entry through ENaC (epithelial Na channel) drives K+ secretion through ROMK (renal outer medullary potassium channel). WNK4 (with-no-lysine 4) regulates the NCC/NKCC2 through SAPK (Ste20-related proline-alanine-rich kinase)/OSR1 (oxidative stress responsive). K+ loading increases intracellular Cl-, which binds to the WNK4, thereby inhibiting autophosphorylation and downstream signals. Acute K+ loading-deactivated NCC was not observed in Cl--insensitive WNK4 mice, indicating that WNK4 was involved in K+ loading-inhibited NCC activity. However, chronic K+ loading deactivated NCC in Cl--insensitive WNK4 mice, indicating that other mechanisms may be involved. We previously reported that mammalian Ste20-like protein kinase 3 (MST3/STK24) was expressed mainly in the medullary TAL (thick ascending tubule) and at lower levels in the DCTs. MST3 -/- mice exhibited higher ENaC activity, causing hypernatremia and hypertension. To investigate MST3 function in maintaining Na+/K+ homeostasis in kidneys, mice were fed diets containing various concentrations of Na+ and K+. The 2% KCl diets induced less MST3 expression in MST3 -/- mice than that in wild-type (WT) mice. The MST3 -/- mice had higher WNK4, NKCC2-S130 phosphorylation, and ENaC expression, resulting in lower urinary Na+ and K+ excretion than those of WT mice. Lower urinary Na+ excretion was associated with elevated plasma [Na+] and hypertension. These results suggest that MST3 maintains Na+/K+ homeostasis in response to K+ loading by regulation of WNK4 expression and NKCC2 and ENaC activity."xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.org/dc/terms/identifier | "doi:10.3390/ijms22030999"xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/author | "Chan C.H."xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/author | "Li H.W."xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/author | "Bao B.Y."xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/author | "Lu T.L."xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/author | "Wu S.N."xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/date | "2021"xsd:gYear |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/name | "Int J Mol Sci"xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/pages | "999"xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/title | "MST3 Involvement in Na+ and K+ Homeostasis with Increasing Dietary Potassium Intake."xsd:string |
| http://purl.uniprot.org/citations/33498219 | http://purl.uniprot.org/core/volume | "22"xsd:string |
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