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10.1152/ajpcell.00193.2015 http://scihub22266oqcxt.onion/10.1152/ajpcell.00193.2015 C4967140!4967140!27170636     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Cell+Physiol 2016 ; 311 (1): C54-66 Nephropedia Template TP {{tp|p=27170636|t=2016. With no lysine L-WNK1 isoforms are negative regulators of the K+-Cl? cotransporters |pdf=|usr=}}{{27170636}} gab.com Text With no lysine L-WNK1 isoforms are negative regulators of the K+-Cl cotransporters JO: Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27170636 #FOAvip The K+-Cl? cotransporters (KCC1-KCC4) encompass a branch of the SLC12 family of electroneutral cation-coupled chloride cotransporters that translocate ions out of the cell to regulate various factors, including cell volume and intracellular chloride concentration, among others. L-WNK1 is an ubiquitously expressed kinase that is activated in response to osmotic stress and intracellular chloride depletion, and it is implicated in two distinct hereditary syndromes: the renal disease pseudohypoaldosteronism type II (PHAII) and the neurological disease hereditary sensory neuropathy 2 (HSN2). The effect of L-WNK1 on KCC activity is unknown. Using Xenopus laevis oocytes and HEK-293 cells, we show that the activation of KCCs by cell swelling was prevented by L-WNK1 coexpression. In contrast, the activity of the Na+-K+-2Cl? cotransporter NKCC1 was remarkably increased with L-WNK1 coexpression. The negative effect of L-WNK1 on the KCCs is kinase dependent. Elimination of the STE20 proline-alanine rich kinase (SPAK)/oxidative stress-responsive kinase (OSR1) binding site or the HQ motif required for the WNK-WNK interaction prevented the effect of L-WNK1 on KCCs, suggesting a required interaction between L-WNK1 molecules and SPAK. Together, our data support that NKCC1 and KCCs are coordinately regulated by L-WNK1 isoforms. Twit Text FOAVip With no lysine L-WNK1 isoforms are negative regulators of the K+-Cl cotransporters ????Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27170636 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27170636 #FOAvip English Wikipedia <ref>{{Cite pmid|27170636}}</ref> With no lysine L-WNK1 isoforms are negative regulators of the K+-Cl? cotransporters #MMPMID27170636 Mercado A; de los Heros P; Melo Z; Chávez-Canales M; Murillo-de-Ozores AR; Moreno E; Bazúa-Valenti S; Vázquez N; Hadchouel J; Gamba G Am J Physiol Cell Physiol 2016[Jul]; 311 (1): C54-66 PMID27170636show ga The K+-Cl? cotransporters (KCC1-KCC4) encompass a branch of the SLC12 family of electroneutral cation-coupled chloride cotransporters that translocate ions out of the cell to regulate various factors, including cell volume and intracellular chloride concentration, among others. L-WNK1 is an ubiquitously expressed kinase that is activated in response to osmotic stress and intracellular chloride depletion, and it is implicated in two distinct hereditary syndromes: the renal disease pseudohypoaldosteronism type II (PHAII) and the neurological disease hereditary sensory neuropathy 2 (HSN2). The effect of L-WNK1 on KCC activity is unknown. Using Xenopus laevis oocytes and HEK-293 cells, we show that the activation of KCCs by cell swelling was prevented by L-WNK1 coexpression. In contrast, the activity of the Na+-K+-2Cl? cotransporter NKCC1 was remarkably increased with L-WNK1 coexpression. The negative effect of L-WNK1 on the KCCs is kinase dependent. Elimination of the STE20 proline-alanine rich kinase (SPAK)/oxidative stress-responsive kinase (OSR1) binding site or the HQ motif required for the WNK-WNK interaction prevented the effect of L-WNK1 on KCCs, suggesting a required interaction between L-WNK1 molecules and SPAK. Together, our data support that NKCC1 and KCCs are coordinately regulated by L-WNK1 isoforms. äWith no lysine L-WNK1 isoforms are negative regulators of the K+-Cl? c(epmc).pdf DeepDyve Pubget Overpricing