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10.1038/ni.3118 http://scihub22266oqcxt.onion/10.1038/ni.3118 C4406811!4406811!25774715     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 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 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Immunol 2015 ; 16 (5): 467-75 Nephropedia Template TP {{tp|p=25774715|t=2015. The transcription factor IRF1 and guanylate-binding proteins target AIM2 inflammasome activation by Francisella infection |pdf=|usr=}}{{25774715}} gab.com Text The transcription factor IRF1 and guanylate-binding proteins target AIM2 inflammasome activation by Francisella infection JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25774715 #FOAvip Inflammasomes are critical for mounting host defense against pathogens. The molecular mechanisms controlling activation of the AIM2 inflammasome in response to different cytosolic pathogens is unclear. Here, we show that the transcription factor IRF1 is the upstream molecule leading to AIM2 inflammasome activation during Francisella novicida infection, whereas engagement of the AIM2 inflammasome by mouse cytomegalovirus or transfected dsDNA did not require IRF1. F. novicida infection detected by the cGAS-STING pathway induces type I interferon-dependent expression of IRF1, which drives the expression of guanylate-binding proteins (GBPs) leading to intracellular bacterial killing and DNA release. These results reveal a specific requirement for IRF1 and GBPs in the liberation of DNA for AIM2 sensing depending on the pathogen encountered by the cell. Twit Text FOAVip The transcription factor IRF1 and guanylate-binding proteins target AIM2 inflammasome activation by Francisella infection ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25774715 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25774715 #FOAvip English Wikipedia <ref>{{Cite pmid|25774715}}</ref> The transcription factor IRF1 and guanylate-binding proteins target AIM2 inflammasome activation by Francisella infection #MMPMID25774715 Man SM; Karki R; Malireddi RS; Neale G; Vogel P; Yamamoto M; Lamkanfi M; Kanneganti TD Nat Immunol 2015[May]; 16 (5): 467-75 PMID25774715show ga Inflammasomes are critical for mounting host defense against pathogens. The molecular mechanisms controlling activation of the AIM2 inflammasome in response to different cytosolic pathogens is unclear. Here, we show that the transcription factor IRF1 is the upstream molecule leading to AIM2 inflammasome activation during Francisella novicida infection, whereas engagement of the AIM2 inflammasome by mouse cytomegalovirus or transfected dsDNA did not require IRF1. F. novicida infection detected by the cGAS-STING pathway induces type I interferon-dependent expression of IRF1, which drives the expression of guanylate-binding proteins (GBPs) leading to intracellular bacterial killing and DNA release. These results reveal a specific requirement for IRF1 and GBPs in the liberation of DNA for AIM2 sensing depending on the pathogen encountered by the cell. äThe transcription factor IRF1 and guanylate-binding proteins target AI(epmc).pdf DeepDyve Pubget Overpricing