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10.1684/mrh.2011.0286 http://scihub22266oqcxt.onion/10.1684/mrh.2011.0286 21983175!3732466!21983175     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21983175&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Magnes+Res 2011 ; 24 (3): S109-14 Nephropedia Template TP {{tp|p=21983175|t=2011. Loss of MAGT1 abrogates the Mg2+ flux required for T cell signaling and leads to a novel human primary immunodeficiency |pdf=|usr=}}{{21983175}} gab.com Text Loss of MAGT1 abrogates the Mg2+ flux required for T cell signaling and leads to a novel human primary immunodeficiency JO: Magnes Res http://www.kidney.de/pget.php?&tw=1&pmid=21983175 #FOAvip Although Mg(2+) has a well-recognized role as an essential cofactor for all ATP-binding enzymes, its role as a signaling ion, like Ca(2+), has been controversial. A requirement for Mg(2+)for optimal T lymphocyte stimulation was demonstrated more than 30 years ago, but the mechanism of its synergistic effect with Ca(2+)in T cell activation remains elusive. Here, we summarize our recent discovery of a signaling role for Mg(2+)in the T cell antigen receptor (TCR) signaling pathway from the study of a novel primary immunodeficiency, now named X-linked immunodeficiency with Mg(2+)defect, EBV infection and neoplasia (XMEN). XMEN patients were found to have a deficiency in magnesium transporter 1 (MAGT1), an Mg(2+)-specific transporter, which leads to the absence of a TCR-stimulated Mg(2+)flux and an attenuation of T cell activation. We further showed that this Mg(2+)flux is required proximally for the temporal orchestration of phospholipase C-gamma1 (PLCgamma1) activation. Thus, our study not only provides a second messenger role for Mg(2+)to explain its synergism with calcium in T cell signaling, it also identifies a potential extracellular therapeutic target for T cell-specific immunomodulation. Twit Text FOAVip Loss of MAGT1 abrogates the Mg2+ flux required for T cell signaling and leads to a novel human primary immunodeficiency ????Magnes Res http://www.kidney.de/pget.php?&tw=1&pmid=21983175 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21983175 #FOAvip English Wikipedia <ref>{{Cite pmid|21983175}}</ref> Loss of MAGT1 abrogates the Mg2+ flux required for T cell signaling and leads to a novel human primary immunodeficiency #MMPMID21983175 Li FY; Lenardo MJ; Chaigne-Delalande B Magnes Res 2011[Sep]; 24 (3): S109-14 PMID21983175show ga Although Mg(2+) has a well-recognized role as an essential cofactor for all ATP-binding enzymes, its role as a signaling ion, like Ca(2+), has been controversial. A requirement for Mg(2+)for optimal T lymphocyte stimulation was demonstrated more than 30 years ago, but the mechanism of its synergistic effect with Ca(2+)in T cell activation remains elusive. Here, we summarize our recent discovery of a signaling role for Mg(2+)in the T cell antigen receptor (TCR) signaling pathway from the study of a novel primary immunodeficiency, now named X-linked immunodeficiency with Mg(2+)defect, EBV infection and neoplasia (XMEN). XMEN patients were found to have a deficiency in magnesium transporter 1 (MAGT1), an Mg(2+)-specific transporter, which leads to the absence of a TCR-stimulated Mg(2+)flux and an attenuation of T cell activation. We further showed that this Mg(2+)flux is required proximally for the temporal orchestration of phospholipase C-gamma1 (PLCgamma1) activation. Thus, our study not only provides a second messenger role for Mg(2+)to explain its synergism with calcium in T cell signaling, it also identifies a potential extracellular therapeutic target for T cell-specific immunomodulation. |Calcium/metabolism[MESH] |Cation Transport Proteins/*deficiency/metabolism[MESH] |Humans[MESH] |Immunologic Deficiency Syndromes/*immunology[MESH] |Magnesium/*metabolism[MESH] |Primary Immunodeficiency Diseases[MESH] |Signal Transduction/*immunology[MESH]Loss of MAGT1 abrogates the Mg2+ flux required for T cell signaling an(epmc).pdf DeepDyve Pubget Overpricing