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10.1016/j.gde.2016.02.004 http://scihub22266oqcxt.onion/10.1016/j.gde.2016.02.004 C5035716!5035716 !27026139     free     free     free Deprecated: Implicit conversion from float 211.6 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\27026139 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Opin+Genet+Dev 2016 ; 38 (ä): 31-37 Nephropedia Template TP {{tp|p=27026139 |t=2016. Mitochondrial iron overload: causes and consequences |pdf=|usr=}}{{27026139 }} gab.com Text Mitochondrial iron overload: causes and consequences JO: Curr Opin Genet Dev http://www.kidney.de/pget.php?&tw=1&pmid=27026139 #FOAvip Pathological overload of iron in the mitochondrial matrix has been observed in numerous diseases, including sideroblastic anemias, which have many causes, and in genetic diseases that affect iron-sulfur cluster biogenesis, heme synthesis, and mitochondrial protein translation and its products. Although high expression of the mitochondrial iron importer, mitoferrin, appears to be an underlying common feature, it is unclear what drives high mitoferrin expression and what other proteins are involved in trapping excess toxic iron in the mitochondrial matrix. Numerous examples of human diseases and model systems suggest that mitochondrial iron homeostasis is coordinated through transcriptional remodeling. A cytosolic/nuclear molecule may affect a transcriptional factor to coordinate the events that lead to iron accumulation, but no candidates for this role have yet been identified. Twit Text FOAVip Mitochondrial iron overload: causes and consequences ????Curr Opin Genet Dev http://www.kidney.de/pget.php?&tw=1&pmid=27026139 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27026139 #FOAvip English Wikipedia <ref>{{Cite pmid|27026139 }}</ref> Mitochondrial iron overload: causes and consequences #MMPMID27026139 Rouault TA Curr Opin Genet Dev 2016[Jun]; 38 (ä): 31-37 PMID27026139 show ga Pathological overload of iron in the mitochondrial matrix has been observed in numerous diseases, including sideroblastic anemias, which have many causes, and in genetic diseases that affect iron-sulfur cluster biogenesis, heme synthesis, and mitochondrial protein translation and its products. Although high expression of the mitochondrial iron importer, mitoferrin, appears to be an underlying common feature, it is unclear what drives high mitoferrin expression and what other proteins are involved in trapping excess toxic iron in the mitochondrial matrix. Numerous examples of human diseases and model systems suggest that mitochondrial iron homeostasis is coordinated through transcriptional remodeling. A cytosolic/nuclear molecule may affect a transcriptional factor to coordinate the events that lead to iron accumulation, but no candidates for this role have yet been identified. |Anemia, Sideroblastic/*genetics/metabolism/pathology [MESH] |Cytosol/metabolism [MESH] |Homeostasis/genetics [MESH] |Humans [MESH] |Iron Overload/*genetics/metabolism/pathology [MESH] |Iron/*metabolism [MESH] |Mitochondria/*genetics/metabolism/pathology [MESH]Mitochondrial iron overload: causes and consequences (epmc).pdf DeepDyve Pubget Overpricing