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10.1113/jphysiol.2007.135855 http://scihub22266oqcxt.onion/10.1113/jphysiol.2007.135855 17673510!2277069!17673510     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Physiol 2007 ; 584 (Pt 1): 333-45 Nephropedia Template TP {{tp|p=17673510|t=2007. SLC26A9 is a Cl(-) channel regulated by the WNK kinases |pdf=|usr=}}{{17673510}} gab.com Text SLC26A9 is a Cl(-) channel regulated by the WNK kinases JO: J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=17673510 #FOAvip SLC26A9 is a member of the SLC26 family of anion transporters, which is expressed at high levels in airway and gastric surface epithelial cells. The transport properties and regulation of SLC26A9, and thus its physiological function, are not known. Here we report that SLC26A9 is a highly selective Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability that is regulated by the WNK kinases. Expression in Xenopus oocytes and simultaneous measurement of membrane potential or current, intracellular pH (pH(i)) and intracellular Cl(-) (Cl(-)(i)) revealed that expression of SLC26A9 resulted in a large Cl(-) current. SLC26A9 displays a selectivity sequence of I(-) > Br(-) > NO(3)(-) > Cl(-) > Glu(-), but it conducts Br(-) > Cl(-) > I(-) > NO(3)(-) > Glu(-), with NO(3)(-) and I(-) inhibiting the Cl(-) conductance. Similarly, expression of SLC26A9 in HEK cells resulted in a large Cl(-) current. Although detectable, OH(-) and HCO(3)(-) fluxes in oocytes expressing SLC26A9 were very small. Moreover, HCO(3)(-) had no discernable effect on the Cl(-) current, the reversal potential in the presence or absence of Cl(-)(o) and, importantly, HCO(3)(-) had no effect on Cl(-) fluxes. These findings indicate that SLC26A9 is a Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability. Co-expression of SLC26A9 with the WNK kinases WNK1, WNK3 or WNK4 inhibited SLC26A9 activity, and the inhibition was independent of WNK kinase activity. Immunolocalization in oocytes and cell surface biotinylation in HEK cells indicated that the WNK-mediated inhibition of SLC26A9 activity is caused by reduced SLC26A9 surface expression. Expression of SLC26A9 in the airway and the response of the WNKs to homeostatic stress raise the possibility that SLC26A9 serves to mediate the response of the airway to stress. Twit Text FOAVip SLC26A9 is a Cl(-) channel regulated by the WNK kinases ????J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=17673510 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17673510 #FOAvip English Wikipedia <ref>{{Cite pmid|17673510}}</ref> SLC26A9 is a Cl(-) channel regulated by the WNK kinases #MMPMID17673510 Dorwart MR; Shcheynikov N; Wang Y; Stippec S; Muallem S J Physiol 2007[Oct]; 584 (Pt 1): 333-45 PMID17673510show ga SLC26A9 is a member of the SLC26 family of anion transporters, which is expressed at high levels in airway and gastric surface epithelial cells. The transport properties and regulation of SLC26A9, and thus its physiological function, are not known. Here we report that SLC26A9 is a highly selective Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability that is regulated by the WNK kinases. Expression in Xenopus oocytes and simultaneous measurement of membrane potential or current, intracellular pH (pH(i)) and intracellular Cl(-) (Cl(-)(i)) revealed that expression of SLC26A9 resulted in a large Cl(-) current. SLC26A9 displays a selectivity sequence of I(-) > Br(-) > NO(3)(-) > Cl(-) > Glu(-), but it conducts Br(-) > Cl(-) > I(-) > NO(3)(-) > Glu(-), with NO(3)(-) and I(-) inhibiting the Cl(-) conductance. Similarly, expression of SLC26A9 in HEK cells resulted in a large Cl(-) current. Although detectable, OH(-) and HCO(3)(-) fluxes in oocytes expressing SLC26A9 were very small. Moreover, HCO(3)(-) had no discernable effect on the Cl(-) current, the reversal potential in the presence or absence of Cl(-)(o) and, importantly, HCO(3)(-) had no effect on Cl(-) fluxes. These findings indicate that SLC26A9 is a Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability. Co-expression of SLC26A9 with the WNK kinases WNK1, WNK3 or WNK4 inhibited SLC26A9 activity, and the inhibition was independent of WNK kinase activity. Immunolocalization in oocytes and cell surface biotinylation in HEK cells indicated that the WNK-mediated inhibition of SLC26A9 activity is caused by reduced SLC26A9 surface expression. Expression of SLC26A9 in the airway and the response of the WNKs to homeostatic stress raise the possibility that SLC26A9 serves to mediate the response of the airway to stress. |Animals[MESH] |Antiporters/*metabolism[MESH] |Bicarbonates/metabolism[MESH] |Cell Line[MESH] |Chlorides/*metabolism[MESH] |Cystic Fibrosis/metabolism[MESH] |Epithelial Cells/metabolism[MESH] |Female[MESH] |Humans[MESH] |Protein Serine-Threonine Kinases/*metabolism[MESH] |Stress, Physiological/metabolism[MESH] |Sulfate Transporters[MESH]SLC26A9 is a Cl(-) channel regulated by the WNK kinases (epmc).pdf DeepDyve Pubget Overpricing