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10.1681/ASN.2014050470 http://scihub22266oqcxt.onion/10.1681/ASN.2014050470 25542968!4520168!25542968     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2015 ; 26 (8): 1781-6 Nephropedia Template TP {{tp|p=25542968|t=2015. The Effect of WNK4 on the Na+-Cl- Cotransporter Is Modulated by Intracellular Chloride |pdf=|usr=}}{{25542968}} gab.com Text The Effect of WNK4 on the Na+-Cl- Cotransporter Is Modulated by Intracellular Chloride JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25542968 #FOAvip It is widely recognized that the phenotype of familial hyperkalemic hypertension is mainly a consequence of increased activity of the renal Na(+)-Cl(-) cotransporter (NCC) because of altered regulation by with no-lysine-kinase 1 (WNK1) or WNK4. The effect of WNK4 on NCC, however, has been controversial because both inhibition and activation have been reported. It has been recently shown that the long isoform of WNK1 (L-WNK1) is a chloride-sensitive kinase activated by a low Cl(-) concentration. Therefore, we hypothesized that WNK4 effects on NCC could be modulated by intracellular chloride concentration ([Cl(-)]i), and we tested this hypothesis in oocytes injected with NCC cRNA with or without WNK4 cRNA. At baseline in oocytes, [Cl(-)]i was near 50 mM, autophosphorylation of WNK4 was undetectable, and NCC activity was either decreased or unaffected by WNK4. A reduction of [Cl(-)]i, either by low chloride hypotonic stress or coinjection of oocytes with the solute carrier family 26 (anion exchanger)-member 9 (SLC26A9) cRNA, promoted WNK4 autophosphorylation and increased NCC-dependent Na(+) transport in a WNK4-dependent manner. Substitution of the leucine with phenylalanine at residue 322 of WNK4, homologous to the chloride-binding pocket in L-WNK1, converted WNK4 into a constitutively autophosphorylated kinase that activated NCC, even without chloride depletion. Elimination of the catalytic activity (D321A or D321K-K186D) or the autophosphorylation site (S335A) in mutant WNK4-L322F abrogated the positive effect on NCC. These observations suggest that WNK4 can exert differential effects on NCC, depending on the intracellular chloride concentration. Twit Text FOAVip The Effect of WNK4 on the Na+-Cl- Cotransporter Is Modulated by Intracellular Chloride ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25542968 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25542968 #FOAvip English Wikipedia <ref>{{Cite pmid|25542968}}</ref> The Effect of WNK4 on the Na+-Cl- Cotransporter Is Modulated by Intracellular Chloride #MMPMID25542968 Bazua-Valenti S; Chavez-Canales M; Rojas-Vega L; Gonzalez-Rodriguez X; Vazquez N; Rodriguez-Gama A; Argaiz ER; Melo Z; Plata C; Ellison DH; Garcia-Valdes J; Hadchouel J; Gamba G J Am Soc Nephrol 2015[Aug]; 26 (8): 1781-6 PMID25542968show ga It is widely recognized that the phenotype of familial hyperkalemic hypertension is mainly a consequence of increased activity of the renal Na(+)-Cl(-) cotransporter (NCC) because of altered regulation by with no-lysine-kinase 1 (WNK1) or WNK4. The effect of WNK4 on NCC, however, has been controversial because both inhibition and activation have been reported. It has been recently shown that the long isoform of WNK1 (L-WNK1) is a chloride-sensitive kinase activated by a low Cl(-) concentration. Therefore, we hypothesized that WNK4 effects on NCC could be modulated by intracellular chloride concentration ([Cl(-)]i), and we tested this hypothesis in oocytes injected with NCC cRNA with or without WNK4 cRNA. At baseline in oocytes, [Cl(-)]i was near 50 mM, autophosphorylation of WNK4 was undetectable, and NCC activity was either decreased or unaffected by WNK4. A reduction of [Cl(-)]i, either by low chloride hypotonic stress or coinjection of oocytes with the solute carrier family 26 (anion exchanger)-member 9 (SLC26A9) cRNA, promoted WNK4 autophosphorylation and increased NCC-dependent Na(+) transport in a WNK4-dependent manner. Substitution of the leucine with phenylalanine at residue 322 of WNK4, homologous to the chloride-binding pocket in L-WNK1, converted WNK4 into a constitutively autophosphorylated kinase that activated NCC, even without chloride depletion. Elimination of the catalytic activity (D321A or D321K-K186D) or the autophosphorylation site (S335A) in mutant WNK4-L322F abrogated the positive effect on NCC. These observations suggest that WNK4 can exert differential effects on NCC, depending on the intracellular chloride concentration. |Animals[MESH] |Chlorides/*metabolism[MESH] |Humans[MESH] |Mice[MESH] |Protein Serine-Threonine Kinases/*metabolism[MESH] |Sodium Chloride Symporters/*metabolism[MESH] |Xenopus Proteins/*metabolism[MESH]The Effect of WNK4 on the Na+-Cl- Cotransporter Is Modulated by Intrac(epmc).pdf DeepDyve Pubget Overpricing