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10.1038/s41598-017-03510-5 http://scihub22266oqcxt.onion/10.1038/s41598-017-03510-5 28646163!5482882!28646163     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (1): 4149 Nephropedia Template TP {{tp|p=28646163|t=2017. Aldosterone Modulates the Association between NCC and ENaC |pdf=|usr=}}{{28646163}} gab.com Text Aldosterone Modulates the Association between NCC and ENaC JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28646163 #FOAvip Distal sodium transport is a final step in the regulation of blood pressure. As such, understanding how the two main sodium transport proteins, the thiazide-sensitive sodium chloride cotransporter (NCC) and the epithelial sodium channel (ENaC), are regulated is paramount. Both are expressed in the late distal nephron; however, no evidence has suggested that these two sodium transport proteins interact. Recently, we established that these two sodium transport proteins functionally interact in the second part of the distal nephron (DCT2). Given their co-localization within the DCT2, we hypothesized that NCC and ENaC interactions might be modulated by aldosterone (Aldo). Aldo treatment increased NCC and alphaENaC colocalization (electron microscopy) and interaction (coimmunoprecipitation). Finally, with co-expression of the Aldo-induced protein serum- and glucocorticoid-inducible kinase 1 (SGK1), NCC and alphaENaC interactions were increased. These data demonstrate that Aldo promotes increased interaction of NCC and ENaC, within the DCT2 revealing a novel method of regulation for distal sodium reabsorption. Twit Text FOAVip Aldosterone Modulates the Association between NCC and ENaC ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28646163 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28646163 #FOAvip English Wikipedia <ref>{{Cite pmid|28646163}}</ref> Aldosterone Modulates the Association between NCC and ENaC #MMPMID28646163 Wynne BM; Mistry AC; Al-Khalili O; Mallick R; Theilig F; Eaton DC; Hoover RS Sci Rep 2017[Jun]; 7 (1): 4149 PMID28646163show ga Distal sodium transport is a final step in the regulation of blood pressure. As such, understanding how the two main sodium transport proteins, the thiazide-sensitive sodium chloride cotransporter (NCC) and the epithelial sodium channel (ENaC), are regulated is paramount. Both are expressed in the late distal nephron; however, no evidence has suggested that these two sodium transport proteins interact. Recently, we established that these two sodium transport proteins functionally interact in the second part of the distal nephron (DCT2). Given their co-localization within the DCT2, we hypothesized that NCC and ENaC interactions might be modulated by aldosterone (Aldo). Aldo treatment increased NCC and alphaENaC colocalization (electron microscopy) and interaction (coimmunoprecipitation). Finally, with co-expression of the Aldo-induced protein serum- and glucocorticoid-inducible kinase 1 (SGK1), NCC and alphaENaC interactions were increased. These data demonstrate that Aldo promotes increased interaction of NCC and ENaC, within the DCT2 revealing a novel method of regulation for distal sodium reabsorption. |Aldosterone/*pharmacology[MESH] |Animals[MESH] |Cell Line[MESH] |Epithelial Sodium Channels/*metabolism/ultrastructure[MESH] |Kidney Cortex/metabolism/ultrastructure[MESH] |Mice[MESH] |Protein Subunits/metabolism[MESH]Aldosterone Modulates the Association between NCC and ENaC (epmc).pdf DeepDyve Pubget Overpricing