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10.1016/j.celrep.2018.02.051 http://scihub22266oqcxt.onion/10.1016/j.celrep.2018.02.051 C5909989!5909989!29514094     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2018 ; 22 (10): 2654-66 Nephropedia Template TP {{tp|p=29514094|t=2018. An Essential Role for ECSIT in Mitochondrial Complex I Assembly and Mitophagy in Macrophages |pdf=|usr=}}{{29514094}} gab.com Text An Essential Role for ECSIT in Mitochondrial Complex I Assembly and Mitophagy in Macrophages JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=29514094 #FOAvip ECSIT is a mitochondrial complex I (CI)-associated protein that has been shown to regulate the production of mitochondrial reactive oxygen species (mROS) following engagement of Toll-like receptors (TLRs). We have generated an Ecsit conditional knockout (CKO) mouse strain to study the in vivo role of ECSIT. ECSIT deletion results in profound alteration of macrophage metabolism, leading to a striking shift to reliance on glycolysis, complete disruption of CI activity, and loss of the CI holoenzyme and multiple subassemblies. An increase in constitutive mROS production in ECSIT-deleted macrophages prevents further TLR-induced mROS production. Surprisingly, ECSIT-deleted cells accumulate damaged mitochondria because of defective mitophagy. ECSIT associates with the mitophagy regulator PINK1 and exhibits Parkin-dependent ubiquitination. However, upon ECSIT deletion, we observed increased mitochondrial Parkin without the expected increase in mitophagy. Taken together, these results demonstrate a key role of ECSIT in CI function, mROS production, and mitophagy-dependent mitochondrial quality control. Twit Text FOAVip An Essential Role for ECSIT in Mitochondrial Complex I Assembly and Mitophagy in Macrophages ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=29514094 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29514094 #FOAvip English Wikipedia <ref>{{Cite pmid|29514094}}</ref> An Essential Role for ECSIT in Mitochondrial Complex I Assembly and Mitophagy in Macrophages #MMPMID29514094 Carneiro FR; Lepelley A; Seeley JJ; Hayden MS; Ghosh S Cell Rep 2018[Mar]; 22 (10): 2654-66 PMID29514094show ga ECSIT is a mitochondrial complex I (CI)-associated protein that has been shown to regulate the production of mitochondrial reactive oxygen species (mROS) following engagement of Toll-like receptors (TLRs). We have generated an Ecsit conditional knockout (CKO) mouse strain to study the in vivo role of ECSIT. ECSIT deletion results in profound alteration of macrophage metabolism, leading to a striking shift to reliance on glycolysis, complete disruption of CI activity, and loss of the CI holoenzyme and multiple subassemblies. An increase in constitutive mROS production in ECSIT-deleted macrophages prevents further TLR-induced mROS production. Surprisingly, ECSIT-deleted cells accumulate damaged mitochondria because of defective mitophagy. ECSIT associates with the mitophagy regulator PINK1 and exhibits Parkin-dependent ubiquitination. However, upon ECSIT deletion, we observed increased mitochondrial Parkin without the expected increase in mitophagy. Taken together, these results demonstrate a key role of ECSIT in CI function, mROS production, and mitophagy-dependent mitochondrial quality control. äAn Essential Role for ECSIT in Mitochondrial Complex I Assembly and Mi(epmc).pdf DeepDyve Pubget Overpricing