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/JCI33004 http://scihub22266oqcxt.onion/10.1172/JCI33004 C1934592!1934592!17671646     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\17671646.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Clin+Invest 2007 ; 117 (8): 2086-9 Nephropedia Template TP {{tp|p=17671646|t=2007. When EGF is offside, magnesium is wasted |pdf=|usr=}}{{17671646}} gab.com Text When EGF is offside, magnesium is wasted JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=17671646 #FOAvip Our understanding of magnesium (Mg2+) regulation has recently been catapulted forward by the discovery of several disease loci for monogenic disorders of Mg2+ homeostasis. In this issue of the JCI, Groenestege et al. report that their study of a rare inherited Mg2+ wasting disorder in consanguineous kindred shows that EGF acts as an autocrine/paracrine magnesiotropic hormone (see the related article beginning on page 2260). EGF stimulates Mg2+ reabsorption in the renal distal convoluted tubule (DCT) via engagement of its receptor on the basolateral membrane of DCT cells and activation of the Mg2+ channel TRPM6 (transient receptor potential cation channel, subfamily M, member 6) in the apical membrane. These authors show that a point mutation in pro-EGF retains EGF secretion to the apical but not the basolateral membrane, disrupting this cascade and causing renal Mg2+ wasting. This work is another seminal example of the power of the study of monogenic disorders in the quest to understand human physiology. Twit Text FOAVip When EGF is offside, magnesium is wasted ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=17671646 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17671646 #FOAvip English Wikipedia <ref>{{Cite pmid|17671646}}</ref> When EGF is offside, magnesium is wasted #MMPMID17671646 Muallem S; Moe OW J Clin Invest 2007[Aug]; 117 (8): 2086-9 PMID17671646show ga Our understanding of magnesium (Mg2+) regulation has recently been catapulted forward by the discovery of several disease loci for monogenic disorders of Mg2+ homeostasis. In this issue of the JCI, Groenestege et al. report that their study of a rare inherited Mg2+ wasting disorder in consanguineous kindred shows that EGF acts as an autocrine/paracrine magnesiotropic hormone (see the related article beginning on page 2260). EGF stimulates Mg2+ reabsorption in the renal distal convoluted tubule (DCT) via engagement of its receptor on the basolateral membrane of DCT cells and activation of the Mg2+ channel TRPM6 (transient receptor potential cation channel, subfamily M, member 6) in the apical membrane. These authors show that a point mutation in pro-EGF retains EGF secretion to the apical but not the basolateral membrane, disrupting this cascade and causing renal Mg2+ wasting. This work is another seminal example of the power of the study of monogenic disorders in the quest to understand human physiology. äWhen EGF is offside, magnesium is wasted (epmc).pdf DeepDyve Pubget Overpricing