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10.1016/j.cell.2014.11.037 http://scihub22266oqcxt.onion/10.1016/j.cell.2014.11.037 C4272443!4272443!25525875     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2014 ; 159 (7): 1563-77 Nephropedia Template TP {{tp|p=25525875|t=2014. Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA |pdf=|usr=}}{{25525875}} gab.com Text Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=25525875 #FOAvip The mechanism by which cells undergo death determines whether dying cells trigger inflammatory responses or remain immunologically silent. Mitochondria play a central role in the induction of cell death, as well as in immune signaling pathways. Here, we identify of a mechanism by which mitochondria and downstream pro-apoptotic caspases regulate the activation of antiviral immunity. In the absence of active caspases, mitochondrial outer membrane permeabilization by Bax and Bak results in the expression of type I interferons (IFNs). This induction is mediated by mitochondrial DNA-dependent activation of the cGAS/STING pathway and results in the establishment of a potent state of viral resistance. Our results show that mitochondria have the capacity to simultaneously expose a cell-intrinsic inducer of the IFN response, and to inactivate this response in a caspase-dependent manner. This mechanism provides a dual control, which determines whether mitochondria initiate an immunologically silent or a pro-inflammatory type of cell death. Twit Text FOAVip Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=25525875 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25525875 #FOAvip English Wikipedia <ref>{{Cite pmid|25525875}}</ref> Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA #MMPMID25525875 Rongvaux A; Jackson R; Harman CC; Li T; West AP; de Zoete MR; Wu Y; Yordy B; Lakhani SA; Kuan CY; Taniguchi T; Shadel GS; Chen ZJ; Iwasaki A; Flavell RA Cell 2014[Dec]; 159 (7): 1563-77 PMID25525875show ga The mechanism by which cells undergo death determines whether dying cells trigger inflammatory responses or remain immunologically silent. Mitochondria play a central role in the induction of cell death, as well as in immune signaling pathways. Here, we identify of a mechanism by which mitochondria and downstream pro-apoptotic caspases regulate the activation of antiviral immunity. In the absence of active caspases, mitochondrial outer membrane permeabilization by Bax and Bak results in the expression of type I interferons (IFNs). This induction is mediated by mitochondrial DNA-dependent activation of the cGAS/STING pathway and results in the establishment of a potent state of viral resistance. Our results show that mitochondria have the capacity to simultaneously expose a cell-intrinsic inducer of the IFN response, and to inactivate this response in a caspase-dependent manner. This mechanism provides a dual control, which determines whether mitochondria initiate an immunologically silent or a pro-inflammatory type of cell death. äApoptotic caspases prevent the induction of type I interferons by mito(epmc).pdf DeepDyve Pubget Overpricing