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10.1016/j.bbadis.2010.07.009 http://scihub22266oqcxt.onion/10.1016/j.bbadis.2010.07.009 20637866!3529164!20637866     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochim+Biophys+Acta 2010 ; 1802 (12): 1150-8 Nephropedia Template TP {{tp|p=20637866|t=2010. Phosphoregulation of the Na-K-2Cl and K-Cl cotransporters by the WNK kinases |pdf=|usr=}}{{20637866}} gab.com Text Phosphoregulation of the Na-K-2Cl and K-Cl cotransporters by the WNK kinases JO: Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=20637866 #FOAvip Precise regulation of the intracellular concentration of chloride [Cl-]i is necessary for proper cell volume regulation, transepithelial transport, and GABA neurotransmission. The Na-K-2Cl (NKCCs) and K-Cl (KCCs) cotransporters, related SLC12A transporters mediating cellular chloride influx and efflux, respectively, are key determinants of [Cl-]i in numerous cell types, including red blood cells, epithelial cells, and neurons. A common "chloride/volume-sensitive kinase", or related system of kinases, has long been hypothesized to mediate the reciprocal but coordinated phosphoregulation of the NKCCs and the KCCs, but the identity of these kinase(s) has remained unknown. Recent evidence suggests that the WNK (with no lysine = K) serine-threonine kinases directly or indirectly via the downstream Ste20-type kinases SPAK/OSR1, are critical components of this signaling pathway. Hypertonic stress (cell shrinkage), and possibly decreased [Cl-]i, triggers the phosphorylation and activation of specific WNKs, promoting NKCC activation and KCC inhibition via net transporter phosphorylation. Silencing WNK kinase activity can promote NKCC inhibition and KCC activation via net transporter dephosphorylation, revealing a dynamic ability of the WNKs to modulate [Cl-]. This pathway is essential for the defense of cell volume during osmotic perturbation, coordination of epithelial transport, and gating of sensory information in the peripheral system. Commiserate with their importance in serving these critical roles in humans, mutations in WNKs underlie two different Mendelian diseases, pseudohypoaldosteronism type II (an inherited form of salt-sensitive hypertension), and hereditary sensory and autonomic neuropathy type 2. WNKs also regulate ion transport in lower multicellular organisms, including Caenorhabditis elegans, suggesting that their functions are evolutionarily-conserved. An increased understanding of how the WNKs regulate the Na-K-2Cl and K-Cl cotransporters may provide novel opportunities for the selective modulation of these transporters, with ramifications for common human diseases like hypertension, sickle cell disease, neuropathic pain, and epilepsy. Twit Text FOAVip Phosphoregulation of the Na-K-2Cl and K-Cl cotransporters by the WNK kinases ????Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=20637866 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20637866 #FOAvip English Wikipedia <ref>{{Cite pmid|20637866}}</ref> Phosphoregulation of the Na-K-2Cl and K-Cl cotransporters by the WNK kinases #MMPMID20637866 Kahle KT; Rinehart J; Lifton RP Biochim Biophys Acta 2010[Dec]; 1802 (12): 1150-8 PMID20637866show ga Precise regulation of the intracellular concentration of chloride [Cl-]i is necessary for proper cell volume regulation, transepithelial transport, and GABA neurotransmission. The Na-K-2Cl (NKCCs) and K-Cl (KCCs) cotransporters, related SLC12A transporters mediating cellular chloride influx and efflux, respectively, are key determinants of [Cl-]i in numerous cell types, including red blood cells, epithelial cells, and neurons. A common "chloride/volume-sensitive kinase", or related system of kinases, has long been hypothesized to mediate the reciprocal but coordinated phosphoregulation of the NKCCs and the KCCs, but the identity of these kinase(s) has remained unknown. Recent evidence suggests that the WNK (with no lysine = K) serine-threonine kinases directly or indirectly via the downstream Ste20-type kinases SPAK/OSR1, are critical components of this signaling pathway. Hypertonic stress (cell shrinkage), and possibly decreased [Cl-]i, triggers the phosphorylation and activation of specific WNKs, promoting NKCC activation and KCC inhibition via net transporter phosphorylation. Silencing WNK kinase activity can promote NKCC inhibition and KCC activation via net transporter dephosphorylation, revealing a dynamic ability of the WNKs to modulate [Cl-]. This pathway is essential for the defense of cell volume during osmotic perturbation, coordination of epithelial transport, and gating of sensory information in the peripheral system. Commiserate with their importance in serving these critical roles in humans, mutations in WNKs underlie two different Mendelian diseases, pseudohypoaldosteronism type II (an inherited form of salt-sensitive hypertension), and hereditary sensory and autonomic neuropathy type 2. WNKs also regulate ion transport in lower multicellular organisms, including Caenorhabditis elegans, suggesting that their functions are evolutionarily-conserved. An increased understanding of how the WNKs regulate the Na-K-2Cl and K-Cl cotransporters may provide novel opportunities for the selective modulation of these transporters, with ramifications for common human diseases like hypertension, sickle cell disease, neuropathic pain, and epilepsy. |Anemia, Sickle Cell/genetics/metabolism[MESH] |Animals[MESH] |Caenorhabditis/genetics/metabolism[MESH] |Chlorides/*metabolism[MESH] |Enzyme Activation/genetics[MESH] |Epilepsy/genetics/metabolism[MESH] |Humans[MESH] |Hypertension/genetics/metabolism[MESH] |Ion Transport/genetics[MESH] |Mutation[MESH] |Neuralgia/genetics/metabolism[MESH] |Osmotic Pressure[MESH] |Phosphorylation/genetics[MESH] |Protein Serine-Threonine Kinases/genetics/*metabolism[MESH] |Pseudohypoaldosteronism/genetics/metabolism[MESH] |Sodium-Potassium-Chloride Symporters/genetics/*metabolism[MESH]Phosphoregulation of the Na-K-2Cl and K-Cl cotransporters by the WNK k(epmc).pdf DeepDyve Pubget Overpricing