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10.1042/CS20171525 http://scihub22266oqcxt.onion/10.1042/CS20171525 29352074!5817097!29352074     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29352074.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Clin+Sci+(Lond) 2018 ; 132 (2): 173-183 Nephropedia Template TP {{tp|p=29352074|t=2018. Aldosterone, SGK1, and ion channels in the kidney |pdf=|usr=}}{{29352074}} gab.com Text Aldosterone, SGK1, and ion channels in the kidney JO: Clin Sci (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=29352074 #FOAvip Hyperaldosteronism, a common cause of hypertension, is strongly connected to Na(+), K(+), and Mg(2+) dysregulation. Owing to its steroidal structure, aldosterone is an active transcriptional modifier when bound to the mineralocorticoid receptor (MR) in cells expressing the enzyme 11beta-hydroxysteroid dehydrogenase 2, such as those comprising the aldosterone-sensitive distal nephron (ASDN). One such up-regulated protein, the ubiquitous serum and glucocorticoid regulated kinase 1 (SGK1), has the capacity to modulate the surface expression and function of many classes of renal ion channels, including those that transport Na(+) (ENaC), K(+) (ROMK/BK), Ca(2+) (TRPV4/5/6), Mg(2+) (TRPM7/6), and Cl(-) (ClC-K, CFTR). Here, we discuss the mechanisms by which ASDN expressed channels are up-regulated by SGK1, while highlighting newly discovered pathways connecting aldosterone to nonselective cation channels that are permeable to Mg(2+) (TRPM7) or Ca(2+) (TRPV4). Twit Text FOAVip Aldosterone, SGK1, and ion channels in the kidney ????Clin Sci (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=29352074 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29352074 #FOAvip English Wikipedia <ref>{{Cite pmid|29352074}}</ref> Aldosterone, SGK1, and ion channels in the kidney #MMPMID29352074 Valinsky WC; Touyz RM; Shrier A Clin Sci (Lond) 2018[Jan]; 132 (2): 173-183 PMID29352074show ga Hyperaldosteronism, a common cause of hypertension, is strongly connected to Na(+), K(+), and Mg(2+) dysregulation. Owing to its steroidal structure, aldosterone is an active transcriptional modifier when bound to the mineralocorticoid receptor (MR) in cells expressing the enzyme 11beta-hydroxysteroid dehydrogenase 2, such as those comprising the aldosterone-sensitive distal nephron (ASDN). One such up-regulated protein, the ubiquitous serum and glucocorticoid regulated kinase 1 (SGK1), has the capacity to modulate the surface expression and function of many classes of renal ion channels, including those that transport Na(+) (ENaC), K(+) (ROMK/BK), Ca(2+) (TRPV4/5/6), Mg(2+) (TRPM7/6), and Cl(-) (ClC-K, CFTR). Here, we discuss the mechanisms by which ASDN expressed channels are up-regulated by SGK1, while highlighting newly discovered pathways connecting aldosterone to nonselective cation channels that are permeable to Mg(2+) (TRPM7) or Ca(2+) (TRPV4). |Aldosterone/*metabolism[MESH] |Animals[MESH] |Humans[MESH] |Immediate-Early Proteins/*metabolism[MESH] |Ion Channels/*metabolism[MESH] |Kidney/*metabolism[MESH] |Nephrons/metabolism[MESH] |Protein Serine-Threonine Kinases/*metabolism[MESH] |Signal Transduction[MESH]Aldosterone, SGK1, and ion channels in the kidney (epmc).pdf DeepDyve Pubget Overpricing