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10.1016/j.chom.2013.04.015 http://scihub22266oqcxt.onion/10.1016/j.chom.2013.04.015 C3688842!3688842!23768494     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Host+Microbe 2013 ; 13 (6): 701-10 Nephropedia Template TP {{tp|p=23768494|t=2013. Cross-talk between the Type 1 interferon and Nuclear Factor Kappa B pathways confers resistance to a lethal virus infection |pdf=|usr=}}{{23768494}} gab.com Text Cross-talk between the Type 1 interferon and Nuclear Factor Kappa B pathways confers resistance to a lethal virus infection JO: Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=23768494 #FOAvip Nuclear factor kappaB (NF-?B) and Type 1 interferon (T1-IFN) signaling are innate immune mechanisms activated upon viral infection. However, the role of NF-?B and its interplay with TI-IFN in antiviral immunity is poorly understood. We show that NF-?B is essential for resistance to ectromelia virus (ECTV), a mouse orthopoxvirus related to the virus causing human smallpox. Additionally, an ECTV mutant lacking an NF-?B inhibitor activates NF-?B more effectively in vivo, resulting in increased pro-inflammatory molecule transcription in uninfected cells and organs and decreased viral replication. Unexpectedly, NF-?B activation compensates for genetic defects in the T1-IFN pathway, such as a deficiency in the IRF7 transcription factor, resulting in virus control. Thus, overlap between the T1-IFN and NF-?B pathways allows the host to overcome genetic or pathogen-induced deficiencies in T1-IFN and survive an otherwise lethal poxvirus infection. These findings may also explain why some pathogens target both pathways to cause disease. Twit Text FOAVip Cross-talk between the Type 1 interferon and Nuclear Factor Kappa B pathways confers resistance to a lethal virus infection ????Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=23768494 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23768494 #FOAvip English Wikipedia <ref>{{Cite pmid|23768494}}</ref> Cross-talk between the Type 1 interferon and Nuclear Factor Kappa B pathways confers resistance to a lethal virus infection #MMPMID23768494 Rubio D; Xu RH; Remakus S; Krouse TE; Truckenmiller ME; Thapa RJ; Balachandran S; Alcamí A; Norbury CC; Sigal LJ Cell Host Microbe 2013[Jun]; 13 (6): 701-10 PMID23768494show ga Nuclear factor kappaB (NF-?B) and Type 1 interferon (T1-IFN) signaling are innate immune mechanisms activated upon viral infection. However, the role of NF-?B and its interplay with TI-IFN in antiviral immunity is poorly understood. We show that NF-?B is essential for resistance to ectromelia virus (ECTV), a mouse orthopoxvirus related to the virus causing human smallpox. Additionally, an ECTV mutant lacking an NF-?B inhibitor activates NF-?B more effectively in vivo, resulting in increased pro-inflammatory molecule transcription in uninfected cells and organs and decreased viral replication. Unexpectedly, NF-?B activation compensates for genetic defects in the T1-IFN pathway, such as a deficiency in the IRF7 transcription factor, resulting in virus control. Thus, overlap between the T1-IFN and NF-?B pathways allows the host to overcome genetic or pathogen-induced deficiencies in T1-IFN and survive an otherwise lethal poxvirus infection. These findings may also explain why some pathogens target both pathways to cause disease. äCross-talk between the Type 1 interferon and Nuclear Factor Kappa B pa(epmc).pdf DeepDyve Pubget Overpricing