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10.1093/ndt/gfv270 http://scihub22266oqcxt.onion/10.1093/ndt/gfv270 26163195!6281043!26163195     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 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26163195.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nephrol+Dial+Transplant 2016 ; 31 (2): 200-5 Nephropedia Template TP {{tp|p=26163195|t=2016. Regulation of the epithelial Na+ channel by the mTORC2/SGK1 pathway |pdf=|usr=}}{{26163195}} gab.com Text Regulation of the epithelial Na+ channel by the mTORC2/SGK1 pathway JO: Nephrol Dial Transplant http://www.kidney.de/pget.php?&tw=1&pmid=26163195 #FOAvip The epithelial Na(+) channel (ENaC) is decisive for sodium reabsorption by the aldosterone-sensitive distal nephron (ASDN) of the kidney. ENaC is regulated by the serum- and glucocorticoid-inducible kinase 1 (SGK1), a kinase genomically upregulated by several hormones including glucocorticoids and mineralocorticoids. SGK1 is activated by the serine/threonine kinase mammalian target of rapamycin (mTOR) isoform mTORC2. SGK1 knockout (sgk1(-/-) mice) impairs renal Na(+) retention during salt depletion. The mTOR catalytic site inhibitor, PP242, but not mTORC1 inhibitor rapamycin, inhibits ENaC, decreases Na(+) flux in isolated perfused tubules and induces natriuresis in wild-type mice. PP242 does not lead to further impairment of Na(+) reabsorption in sgk1(-/-) mice. The mTORC2/SGK1 sensitive renal Na(+) retention leads to extracellular volume expansion with increase of blood pressure. A SGK1 gene variant (prevalence approximately 3-5% in Caucasians, approximately 10% in Africans) predisposes to hypertension, stroke, obesity and type 2 diabetes. Future studies will be required to define the role of mTORC2 in the regulation of further SGK1 sensitive transport proteins, such as further ion channels, carriers and the Na(+)/K(+)-ATPase. Moreover, studies are required disclosing the impact of mTORC2 on SGK1 sensitive disorders, such as hypertension, obesity, diabetes, thrombosis, stroke, inflammation, autoimmune disease, fibrosis and tumour growth. Twit Text FOAVip Regulation of the epithelial Na+ channel by the mTORC2/SGK1 pathway ????Nephrol Dial Transplant http://www.kidney.de/pget.php?&tw=1&pmid=26163195 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26163195 #FOAvip English Wikipedia <ref>{{Cite pmid|26163195}}</ref> Regulation of the epithelial Na+ channel by the mTORC2/SGK1 pathway #MMPMID26163195 Lang F; Pearce D Nephrol Dial Transplant 2016[Feb]; 31 (2): 200-5 PMID26163195show ga The epithelial Na(+) channel (ENaC) is decisive for sodium reabsorption by the aldosterone-sensitive distal nephron (ASDN) of the kidney. ENaC is regulated by the serum- and glucocorticoid-inducible kinase 1 (SGK1), a kinase genomically upregulated by several hormones including glucocorticoids and mineralocorticoids. SGK1 is activated by the serine/threonine kinase mammalian target of rapamycin (mTOR) isoform mTORC2. SGK1 knockout (sgk1(-/-) mice) impairs renal Na(+) retention during salt depletion. The mTOR catalytic site inhibitor, PP242, but not mTORC1 inhibitor rapamycin, inhibits ENaC, decreases Na(+) flux in isolated perfused tubules and induces natriuresis in wild-type mice. PP242 does not lead to further impairment of Na(+) reabsorption in sgk1(-/-) mice. The mTORC2/SGK1 sensitive renal Na(+) retention leads to extracellular volume expansion with increase of blood pressure. A SGK1 gene variant (prevalence approximately 3-5% in Caucasians, approximately 10% in Africans) predisposes to hypertension, stroke, obesity and type 2 diabetes. Future studies will be required to define the role of mTORC2 in the regulation of further SGK1 sensitive transport proteins, such as further ion channels, carriers and the Na(+)/K(+)-ATPase. Moreover, studies are required disclosing the impact of mTORC2 on SGK1 sensitive disorders, such as hypertension, obesity, diabetes, thrombosis, stroke, inflammation, autoimmune disease, fibrosis and tumour growth. |*Gene Expression Regulation[MESH] |Animals[MESH] |Epithelial Sodium Channels/*metabolism[MESH] |Humans[MESH] |Immediate-Early Proteins/biosynthesis/*genetics[MESH] |Kidney/*metabolism/pathology[MESH] |Mechanistic Target of Rapamycin Complex 1[MESH] |Multiprotein Complexes/biosynthesis/*genetics[MESH] |Nephrons/*metabolism[MESH] |Nuclear Proteins[MESH] |Protein Serine-Threonine Kinases/biosynthesis/*genetics[MESH] |TOR Serine-Threonine Kinases/biosynthesis/*genetics[MESH]Regulation of the epithelial Na+ channel by the mTORC2/SGK1 pathway (epmc).pdf DeepDyve Pubget Overpricing