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10.1016/j.celrep.2015.03.069 http://scihub22266oqcxt.onion/10.1016/j.celrep.2015.03.069 C4426031!4426031!25921537     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       Cell+Rep 2015 ; 11 (5): 785-97 Nephropedia Template TP {{tp|p=25921537|t=2015. DNA damage-induced type I interferon promotes senescence and inhibits stem cell function |pdf=|usr=}}{{25921537}} gab.com Text DNA damage-induced type I interferon promotes senescence and inhibits stem cell function JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=25921537 #FOAvip Expression of type I interferons (IFN) can be induced by DNA damaging agents but the mechanisms and significance of this regulation are not completely understood. We found that the transcription factor IRF3, activated in an ATM-IKK?/? dependent manner, stimulates cell-autonomous IFN? expression in response to double-stranded DNA breaks. Cells and tissues with accumulating DNA damage produce endogenous IFN? and stimulate IFN signaling in vitro and in vivo. In turn, IFN acts to amplify DNA damage responses, activate the p53 pathway, promote senescence and inhibit stem cells function in response to telomere shortening. Inactivation of the IFN pathway abrogates the development of diverse progeric phenotypes and extends the life span of Terc knockout mice. These data identify DNA damage response-induced IFN signaling as a critical mechanism that links accumulating DNA damage with senescence and premature aging. Twit Text FOAVip DNA damage-induced type I interferon promotes senescence and inhibits stem cell function ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=25921537 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25921537 #FOAvip English Wikipedia <ref>{{Cite pmid|25921537}}</ref> DNA damage-induced type I interferon promotes senescence and inhibits stem cell function #MMPMID25921537 Yu Q; Katlinskaya YV; Carbone CJ; Zhao B; Katlinski KV; Zheng H; Guha M; Li N; Chen Q; Yang T; Lengner CJ; Greenberg RA; Johnson FB; Fuchs SY Cell Rep 2015[May]; 11 (5): 785-97 PMID25921537show ga Expression of type I interferons (IFN) can be induced by DNA damaging agents but the mechanisms and significance of this regulation are not completely understood. We found that the transcription factor IRF3, activated in an ATM-IKK?/? dependent manner, stimulates cell-autonomous IFN? expression in response to double-stranded DNA breaks. Cells and tissues with accumulating DNA damage produce endogenous IFN? and stimulate IFN signaling in vitro and in vivo. In turn, IFN acts to amplify DNA damage responses, activate the p53 pathway, promote senescence and inhibit stem cells function in response to telomere shortening. Inactivation of the IFN pathway abrogates the development of diverse progeric phenotypes and extends the life span of Terc knockout mice. These data identify DNA damage response-induced IFN signaling as a critical mechanism that links accumulating DNA damage with senescence and premature aging. äDNA damage-induced type I interferon promotes senescence and inhibits (epmc).pdf DeepDyve Pubget Overpricing