Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1172/JCI73935 http://scihub22266oqcxt.onion/10.1172/JCI73935 25415435!4382226!25415435     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       J+Clin+Invest 2015 ; 125 (1): 117-28 Nephropedia Template TP {{tp|p=25415435|t=2015. mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity |pdf=|usr=}}{{25415435}} gab.com Text mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25415435 #FOAvip The epithelial Na+ channel (ENaC) is essential for Na+ homeostasis, and dysregulation of this channel underlies many forms of hypertension. Recent studies suggest that mTOR regulates phosphorylation and activation of serum/glucocorticoid regulated kinase 1 (SGK1), which is known to inhibit ENaC internalization and degradation; however, it is not clear whether mTOR contributes to the regulation of renal tubule ion transport. Here, we evaluated the effect of selective mTOR inhibitors on kidney tubule Na+ and K+ transport in WT and Sgk1-/- mice, as well as in isolated collecting tubules. We found that 2 structurally distinct competitive inhibitors (PP242 and AZD8055), both of which prevent all mTOR-dependent phosphorylation, including that of SGK1, caused substantial natriuresis, but not kaliuresis, in WT mice, which indicates that mTOR preferentially influences ENaC function. PP242 also substantially inhibited Na+ currents in isolated perfused cortical collecting tubules. Accordingly, patch clamp studies on cortical tubule apical membranes revealed that mTOR inhibition markedly reduces ENaC activity, but does not alter activity of K+ inwardly rectifying channels (ROMK channels). Together, these results demonstrate that mTOR regulates kidney tubule ion handling and suggest that mTOR regulates Na+ homeostasis through SGK1-dependent modulation of ENaC activity. Twit Text FOAVip mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25415435 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25415435 #FOAvip English Wikipedia <ref>{{Cite pmid|25415435}}</ref> mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity #MMPMID25415435 Gleason CE; Frindt G; Cheng CJ; Ng M; Kidwai A; Rashmi P; Lang F; Baum M; Palmer LG; Pearce D J Clin Invest 2015[Jan]; 125 (1): 117-28 PMID25415435show ga The epithelial Na+ channel (ENaC) is essential for Na+ homeostasis, and dysregulation of this channel underlies many forms of hypertension. Recent studies suggest that mTOR regulates phosphorylation and activation of serum/glucocorticoid regulated kinase 1 (SGK1), which is known to inhibit ENaC internalization and degradation; however, it is not clear whether mTOR contributes to the regulation of renal tubule ion transport. Here, we evaluated the effect of selective mTOR inhibitors on kidney tubule Na+ and K+ transport in WT and Sgk1-/- mice, as well as in isolated collecting tubules. We found that 2 structurally distinct competitive inhibitors (PP242 and AZD8055), both of which prevent all mTOR-dependent phosphorylation, including that of SGK1, caused substantial natriuresis, but not kaliuresis, in WT mice, which indicates that mTOR preferentially influences ENaC function. PP242 also substantially inhibited Na+ currents in isolated perfused cortical collecting tubules. Accordingly, patch clamp studies on cortical tubule apical membranes revealed that mTOR inhibition markedly reduces ENaC activity, but does not alter activity of K+ inwardly rectifying channels (ROMK channels). Together, these results demonstrate that mTOR regulates kidney tubule ion handling and suggest that mTOR regulates Na+ homeostasis through SGK1-dependent modulation of ENaC activity. |Amiloride/pharmacology[MESH] |Animals[MESH] |Biological Transport[MESH] |Endosomal Sorting Complexes Required for Transport/metabolism[MESH] |Epithelial Sodium Channels/*metabolism[MESH] |Female[MESH] |Immediate-Early Proteins/metabolism[MESH] |Indoles/pharmacology[MESH] |Kidney Tubules, Distal/*metabolism[MESH] |Male[MESH] |Mechanistic Target of Rapamycin Complex 2[MESH] |Membrane Potentials[MESH] |Mice, 129 Strain[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Multiprotein Complexes/*physiology[MESH] |Nedd4 Ubiquitin Protein Ligases[MESH] |Patch-Clamp Techniques[MESH] |Phosphorylation[MESH] |Protein Processing, Post-Translational[MESH] |Protein Serine-Threonine Kinases/metabolism[MESH] |Purines/pharmacology[MESH] |Rats, Sprague-Dawley[MESH] |Sirolimus/pharmacology[MESH] |Sodium/*metabolism[MESH] |TOR Serine-Threonine Kinases/metabolism/*physiology[MESH]mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity(epmc).pdf DeepDyve Pubget Overpricing