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10.1152/ajprenal.00002.2016 http://scihub22266oqcxt.onion/10.1152/ajprenal.00002.2016 27009335!5005279!27009335     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27009335&cmd=llinks): Failed to open stream: HTTP request failed! 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Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC |pdf=|usr=}}{{27009335}} gab.com Text Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27009335 #FOAvip The stimulation of postprandial K(+) clearance involves aldosterone-independent and -dependent mechanisms. In this context, serum- and glucocorticoid-induced kinase (SGK)1, a ubiquitously expressed kinase, is one of the primary aldosterone-induced proteins in the aldosterone-sensitive distal nephron. Germline inactivation of SGK1 suggests that this kinase is fundamental for K(+) excretion under conditions of K(+) load, but the specific role of renal SGK1 remains elusive. To avoid compensatory mechanisms that may occur during nephrogenesis, we used inducible, nephron-specific Sgk1(Pax8/LC1) mice to assess the role of renal tubular SGK1 in K(+) regulation. Under a standard diet, these animals exhibited normal K(+) handling. When challenged by a high-K(+) diet, they developed severe hyperkalemia accompanied by a defect in K(+) excretion. Molecular analysis revealed reduced neural precursor cell expressed developmentally downregulated protein (NEDD)4-2 phosphorylation and total expression. gamma-Epithelial Na(+) channel (ENaC) expression and alpha/gammaENaC proteolytic processing were also decreased in mutant mice. Moreover, with no lysine kinase (WNK)1, which displayed in control mice punctuate staining in the distal convoluted tubule and diffuse distribution in the connecting tubule/cortical colleting duct, was diffused in the distal convoluted tubule and less expressed in the connecting tubule/collecting duct of Sgk(Pax8/LC1) mice. Moreover, Ste20-related proline/alanine-rich kinase phosphorylation, and Na(+)-Cl(-) cotransporter phosphorylation/apical localization were reduced in mutant mice. Consistent with the altered WNK1 expression, increased renal outer medullary K(+) channel apical localization was observed. In conclusion, our data suggest that renal tubular SGK1 is important in the regulation of K(+) excretion via the control of NEDD4-2, WNK1, and ENaC. Twit Text FOAVip Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27009335 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27009335 #FOAvip English Wikipedia <ref>{{Cite pmid|27009335}}</ref> Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC #MMPMID27009335 Al-Qusairi L; Basquin D; Roy A; Stifanelli M; Rajaram RD; Debonneville A; Nita I; Maillard M; Loffing J; Subramanya AR; Staub O Am J Physiol Renal Physiol 2016[Aug]; 311 (2): F330-42 PMID27009335show ga The stimulation of postprandial K(+) clearance involves aldosterone-independent and -dependent mechanisms. In this context, serum- and glucocorticoid-induced kinase (SGK)1, a ubiquitously expressed kinase, is one of the primary aldosterone-induced proteins in the aldosterone-sensitive distal nephron. Germline inactivation of SGK1 suggests that this kinase is fundamental for K(+) excretion under conditions of K(+) load, but the specific role of renal SGK1 remains elusive. To avoid compensatory mechanisms that may occur during nephrogenesis, we used inducible, nephron-specific Sgk1(Pax8/LC1) mice to assess the role of renal tubular SGK1 in K(+) regulation. Under a standard diet, these animals exhibited normal K(+) handling. When challenged by a high-K(+) diet, they developed severe hyperkalemia accompanied by a defect in K(+) excretion. Molecular analysis revealed reduced neural precursor cell expressed developmentally downregulated protein (NEDD)4-2 phosphorylation and total expression. gamma-Epithelial Na(+) channel (ENaC) expression and alpha/gammaENaC proteolytic processing were also decreased in mutant mice. Moreover, with no lysine kinase (WNK)1, which displayed in control mice punctuate staining in the distal convoluted tubule and diffuse distribution in the connecting tubule/cortical colleting duct, was diffused in the distal convoluted tubule and less expressed in the connecting tubule/collecting duct of Sgk(Pax8/LC1) mice. Moreover, Ste20-related proline/alanine-rich kinase phosphorylation, and Na(+)-Cl(-) cotransporter phosphorylation/apical localization were reduced in mutant mice. Consistent with the altered WNK1 expression, increased renal outer medullary K(+) channel apical localization was observed. In conclusion, our data suggest that renal tubular SGK1 is important in the regulation of K(+) excretion via the control of NEDD4-2, WNK1, and ENaC. |Amino Acid Sequence[MESH] |Animals[MESH] |Antibodies, Blocking/pharmacology[MESH] |Diet[MESH] |Endosomal Sorting Complexes Required for Transport/*metabolism[MESH] |Epithelial Sodium Channels/*metabolism[MESH] |Gene Expression Regulation[MESH] |Immediate-Early Proteins/*deficiency/*genetics[MESH] |Kidney Tubules/metabolism[MESH] |Male[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Minor Histocompatibility Antigens/*metabolism[MESH] |Nedd4 Ubiquitin Protein Ligases[MESH] |Potassium Channels, Inwardly Rectifying/antagonists & inhibitors/immunology[MESH] |Potassium, Dietary/pharmacology[MESH] |Potassium/*urine[MESH] |Protein Serine-Threonine Kinases/*deficiency/*genetics/*metabolism[MESH] |Ubiquitin-Protein Ligases/*metabolism[MESH]Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of(epmc).pdf DeepDyve Pubget Overpricing