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10.1038/s41467-018-05387-y http://scihub22266oqcxt.onion/10.1038/s41467-018-05387-y C6063938!6063938!30054480     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=30054480|t=2018. Neutrophil extracellular trap formation requires OPA1-dependent glycolytic ATP production |pdf=|usr=}}{{30054480}} gab.com Text Neutrophil extracellular trap formation requires OPA1-dependent glycolytic ATP production JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=30054480 #FOAvip Optic atrophy 1 (OPA1) is a mitochondrial inner membrane protein that has an important role in mitochondrial fusion and structural integrity. Dysfunctional OPA1 mutations cause atrophy of the optic nerve leading to blindness. Here, we show that OPA1 has an important role in the innate immune system. Using conditional knockout mice lacking Opa1 in neutrophils (Opa1N?), we report that lack of OPA1 reduces the activity of mitochondrial electron transport complex I in neutrophils. This then causes a decline in adenosine-triphosphate (ATP) production through glycolysis due to lowered NAD+ availability. Additionally, we show that OPA1-dependent ATP production in these cells is required for microtubule network assembly and for the formation of neutrophil extracellular traps. Finally, we show that Opa1N? mice exhibit a reduced antibacterial defense capability against Pseudomonas aeruginosa. Twit Text FOAVip Neutrophil extracellular trap formation requires OPA1-dependent glycolytic ATP production ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=30054480 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30054480 #FOAvip English Wikipedia <ref>{{Cite pmid|30054480}}</ref> Neutrophil extracellular trap formation requires OPA1-dependent glycolytic ATP production #MMPMID30054480 Amini P; Stojkov D; Felser A; Jackson CB; Courage C; Schaller A; Gelman L; Soriano ME; Nuoffer JM; Scorrano L; Benarafa C; Yousefi S; Simon HU Nat Commun 2018[]; 9 (ä): ä PMID30054480show ga Optic atrophy 1 (OPA1) is a mitochondrial inner membrane protein that has an important role in mitochondrial fusion and structural integrity. Dysfunctional OPA1 mutations cause atrophy of the optic nerve leading to blindness. Here, we show that OPA1 has an important role in the innate immune system. Using conditional knockout mice lacking Opa1 in neutrophils (Opa1N?), we report that lack of OPA1 reduces the activity of mitochondrial electron transport complex I in neutrophils. This then causes a decline in adenosine-triphosphate (ATP) production through glycolysis due to lowered NAD+ availability. Additionally, we show that OPA1-dependent ATP production in these cells is required for microtubule network assembly and for the formation of neutrophil extracellular traps. Finally, we show that Opa1N? mice exhibit a reduced antibacterial defense capability against Pseudomonas aeruginosa. äNeutrophil extracellular trap formation requires OPA1-dependent glycol(epmc).pdf DeepDyve Pubget Overpricing