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10.1152/ajprenal.00634.2017 http://scihub22266oqcxt.onion/10.1152/ajprenal.00634.2017 29412701!ä!29412701 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29412701&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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29412701.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Physiol+Renal+Physiol 2018 ; 314 (6): F1027-F1033 Nephropedia Template TP {{tp|p=29412701|t=2018. The rise and fall of novel renal magnesium transporters |pdf=|usr=}}{{29412701}} gab.com Text The rise and fall of novel renal magnesium transporters JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=29412701 #FOAvip Body Mg(2+) balance is finely regulated in the distal convoluted tubule (DCT), where a tight interplay among transcellular reabsorption, mitochondrial exchange, and basolateral extrusion takes place. In the last decades, several research groups have aimed to identify the molecular players in these processes. A multitude of proteins have been proposed to function as Mg(2+) transporter in eukaryotes based on phylogenetic analysis, differential gene expression, and overexpression studies. However, functional evidence for many of these proteins is lacking. The aim of this review is, therefore, to critically reconsider all putative Mg(2+) transporters and put their presumed function in context of the renal handling of Mg(2+). Sufficient experimental evidence exists to acknowledge transient receptor potential melastatin (TRPM) 6 and TRPM7, solute carrier family 41 (SLC41) A1 and SLC41A3, and mitochondrial RNA splicing 2 (MRS2) as Mg(2+) transporters. TRPM6/7 facilitate Mg(2+) influx, SLC41A1 mediates Mg(2+) extrusion, and MRS2 and SLC41A3 are implicated in mitochondrial Mg(2+) homeostasis. These proteins are highly expressed in the DCT. The function of cyclin M (CNNM) proteins is still under debate. For the other proposed Mg(2+) transporters including Mg(2+) transporter subtype 1 (MagT1), nonimprinted in Prader-Willi/Angelman syndrome (NIPA), membrane Mg(2+) transport (MMgT), Huntingtin-interacting protein 14 (HIP14), and ATP13A4, functional evidence is limited, or functions alternative to Mg(2+) transport have been suggested. Additional characterization of their Mg(2+) transport proficiency should be provided before further claims about their role as Mg(2+) transporter can be made. Twit Text FOAVip The rise and fall of novel renal magnesium transporters ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=29412701 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29412701 #FOAvip English Wikipedia <ref>{{Cite pmid|29412701}}</ref> The rise and fall of novel renal magnesium transporters #MMPMID29412701 Schaffers OJM; Hoenderop JGJ; Bindels RJM; de Baaij JHF Am J Physiol Renal Physiol 2018[Jun]; 314 (6): F1027-F1033 PMID29412701show ga Body Mg(2+) balance is finely regulated in the distal convoluted tubule (DCT), where a tight interplay among transcellular reabsorption, mitochondrial exchange, and basolateral extrusion takes place. In the last decades, several research groups have aimed to identify the molecular players in these processes. A multitude of proteins have been proposed to function as Mg(2+) transporter in eukaryotes based on phylogenetic analysis, differential gene expression, and overexpression studies. However, functional evidence for many of these proteins is lacking. The aim of this review is, therefore, to critically reconsider all putative Mg(2+) transporters and put their presumed function in context of the renal handling of Mg(2+). Sufficient experimental evidence exists to acknowledge transient receptor potential melastatin (TRPM) 6 and TRPM7, solute carrier family 41 (SLC41) A1 and SLC41A3, and mitochondrial RNA splicing 2 (MRS2) as Mg(2+) transporters. TRPM6/7 facilitate Mg(2+) influx, SLC41A1 mediates Mg(2+) extrusion, and MRS2 and SLC41A3 are implicated in mitochondrial Mg(2+) homeostasis. These proteins are highly expressed in the DCT. The function of cyclin M (CNNM) proteins is still under debate. For the other proposed Mg(2+) transporters including Mg(2+) transporter subtype 1 (MagT1), nonimprinted in Prader-Willi/Angelman syndrome (NIPA), membrane Mg(2+) transport (MMgT), Huntingtin-interacting protein 14 (HIP14), and ATP13A4, functional evidence is limited, or functions alternative to Mg(2+) transport have been suggested. Additional characterization of their Mg(2+) transport proficiency should be provided before further claims about their role as Mg(2+) transporter can be made. |*Renal Elimination[MESH] |*Renal Reabsorption[MESH] |Animals[MESH] |Cation Transport Proteins/*metabolism[MESH] |Homeostasis[MESH] |Humans[MESH] |Ion Channels/*metabolism[MESH] |Ion Transport[MESH] |Kidney Tubules/*metabolism[MESH]The rise and fall of novel renal magnesium transporters (epmc).pdf DeepDyve Pubget Overpricing