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10.1016/j.bbrc.2016.10.127 http://scihub22266oqcxt.onion/10.1016/j.bbrc.2016.10.127 27942049!5144580!27942049     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochem+Biophys+Res+Commun 2016 ; 480 (4): 745-751 Nephropedia Template TP {{tp|p=27942049|t=2016. Potassium depletion stimulates Na-Cl cotransporter via phosphorylation and inactivation of the ubiquitin ligase Kelch-like 3 |pdf=|usr=}}{{27942049}} gab.com Text Potassium depletion stimulates Na-Cl cotransporter via phosphorylation and inactivation of the ubiquitin ligase Kelch-like 3 JO: Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=27942049 #FOAvip Kelch-like 3 (KLHL3) is a component of an E3 ubiquitin ligase complex that regulates blood pressure by targeting With-No-Lysine (WNK) kinases for degradation. Mutations in KLHL3 cause constitutively increased renal salt reabsorption and impaired K(+) secretion, resulting in hypertension and hyperkalemia. Although clinical studies have shown that dietary K(+) intake affects blood pressure, the mechanisms have been obscure. In this study, we demonstrate that the KLHL3 ubiquitin ligase complex is involved in the low-K(+)-mediated activation of Na-Cl cotransporter (NCC) in the kidney. In the distal convoluted tubules of mice eating a low-K(+) diet, we found increased KLHL3 phosphorylation at S433 (KLHL3(S433-P)), a modification that impairs WNK binding, and also reduced total KLHL3 levels. These changes are accompanied by the accumulation of the target substrate WNK4, and activation of the downstream kinases SPAK (STE20/SPS1-related proline-alanine-rich protein kinase) and OSR1 (oxidative stress-responsive 1), resulting in NCC phosphorylation and its accumulation at the plasma membrane. Increased phosphorylation of S433 was explained by increased levels of active, phosphorylated protein kinase C (but not protein kinase A), which directly phosphorylates S433. Moreover, in HEK cells expressing KLHL3 and WNK4, we showed that the activation of protein kinase C by phorbol 12-myristate 13-acetate induces KLHL3(S433-P) and increases WNK4 levels by abrogating its ubiquitination. These data demonstrate the role of KLHL3 in low-K(+)-mediated induction of NCC; this physiologic adaptation reduces distal electrogenic Na(+) reabsorption, preventing further renal K(+) loss but promoting increased blood pressure. Twit Text FOAVip Potassium depletion stimulates Na-Cl cotransporter via phosphorylation and inactivation of the ubiquitin ligase Kelch-like 3 ????Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=27942049 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27942049 #FOAvip English Wikipedia <ref>{{Cite pmid|27942049}}</ref> Potassium depletion stimulates Na-Cl cotransporter via phosphorylation and inactivation of the ubiquitin ligase Kelch-like 3 #MMPMID27942049 Ishizawa K; Xu N; Loffing J; Lifton RP; Fujita T; Uchida S; Shibata S Biochem Biophys Res Commun 2016[Nov]; 480 (4): 745-751 PMID27942049show ga Kelch-like 3 (KLHL3) is a component of an E3 ubiquitin ligase complex that regulates blood pressure by targeting With-No-Lysine (WNK) kinases for degradation. Mutations in KLHL3 cause constitutively increased renal salt reabsorption and impaired K(+) secretion, resulting in hypertension and hyperkalemia. Although clinical studies have shown that dietary K(+) intake affects blood pressure, the mechanisms have been obscure. In this study, we demonstrate that the KLHL3 ubiquitin ligase complex is involved in the low-K(+)-mediated activation of Na-Cl cotransporter (NCC) in the kidney. In the distal convoluted tubules of mice eating a low-K(+) diet, we found increased KLHL3 phosphorylation at S433 (KLHL3(S433-P)), a modification that impairs WNK binding, and also reduced total KLHL3 levels. These changes are accompanied by the accumulation of the target substrate WNK4, and activation of the downstream kinases SPAK (STE20/SPS1-related proline-alanine-rich protein kinase) and OSR1 (oxidative stress-responsive 1), resulting in NCC phosphorylation and its accumulation at the plasma membrane. Increased phosphorylation of S433 was explained by increased levels of active, phosphorylated protein kinase C (but not protein kinase A), which directly phosphorylates S433. Moreover, in HEK cells expressing KLHL3 and WNK4, we showed that the activation of protein kinase C by phorbol 12-myristate 13-acetate induces KLHL3(S433-P) and increases WNK4 levels by abrogating its ubiquitination. These data demonstrate the role of KLHL3 in low-K(+)-mediated induction of NCC; this physiologic adaptation reduces distal electrogenic Na(+) reabsorption, preventing further renal K(+) loss but promoting increased blood pressure. |Adaptor Proteins, Signal Transducing[MESH] |Animals[MESH] |Diet[MESH] |Gene Expression Regulation[MESH] |HEK293 Cells[MESH] |Humans[MESH] |Hypertension/*genetics/metabolism/pathology[MESH] |Hypokalemia/*genetics/metabolism/pathology[MESH] |Kidney/metabolism/pathology[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Microfilament Proteins/*genetics/metabolism[MESH] |Minor Histocompatibility Antigens/genetics/metabolism[MESH] |Phosphorylation[MESH] |Potassium Deficiency/*genetics/metabolism/pathology[MESH] |Potassium, Dietary/administration & dosage/*metabolism[MESH] |Protein Kinase C/genetics/metabolism[MESH] |Protein Serine-Threonine Kinases/genetics/metabolism[MESH] |Signal Transduction[MESH] |Sodium/metabolism[MESH] |Solute Carrier Family 12, Member 3/genetics/metabolism[MESH]Potassium depletion stimulates Na-Cl cotransporter via phosphorylation(epmc).pdf DeepDyve Pubget Overpricing