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10.3389/fimmu.2017.00350 http://scihub22266oqcxt.onion/10.3389/fimmu.2017.00350 C5364133!5364133!28392790     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       Front+Immunol 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28392790|t=2017. HIST1H1C Regulates Interferon-? and Inhibits Influenza Virus Replication by Interacting with IRF3 |pdf=|usr=}}{{28392790}} gab.com Text HIST1H1C Regulates Interferon- and Inhibits Influenza Virus Replication by Interacting with IRF3 JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28392790 #FOAvip Influenza virus NS2 is well known for its role in viral ribonucleoprotein nuclear export; however, its function has not been fully understood. A recent study showed that NS2 might interact with HIST1H1C (H1C, H1.2). Histones have been found to affect influenza virus replication, such as the H2A, H2B, H3, and H4, but H1 has not been detected. Here, we found that H1C interacts with NS2 via its C-terminal in the nucleus and that H1C affects influenza virus replication. The H1N1 influenza virus replicates better in H1C knockout A549 cells compared to wild-type A549 cells, primarily because of the regulation of H1C on interferon-? (IFN-?). Further studies showed that the H1C phosphorylation mutant (T146A) decreases IFN-?, while H1C methylation mutants (K34A, K187A) increases IFN-? by releasing the nucleosome and promoting IRF3 binding to the IFN-? promoter. Interestingly, NS2 interacts with H1C, which reduces H1C?IRF3 interaction and results in the inhibition of IFN-? enhanced by H1C. In summary, our study reveals a novel function of H1C to regulate IFN-? and uncovers an underlying mechanism, which suggests H1C plays a role in epigenetic regulation. Moreover, our results suggest a novel mechanism for the influenza virus to antagonize the innate immune response by NS2. Twit Text FOAVip HIST1H1C Regulates Interferon- and Inhibits Influenza Virus Replication by Interacting with IRF3 ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28392790 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28392790 #FOAvip English Wikipedia <ref>{{Cite pmid|28392790}}</ref> HIST1H1C Regulates Interferon-? and Inhibits Influenza Virus Replication by Interacting with IRF3 #MMPMID28392790 Liu X; Yang C; Hu Y; Lei E; Lin X; Zhao L; Zou Z; Zhang A; Zhou H; Chen H; Qian P; Jin M Front Immunol 2017[]; 8 (ä): ä PMID28392790show ga Influenza virus NS2 is well known for its role in viral ribonucleoprotein nuclear export; however, its function has not been fully understood. A recent study showed that NS2 might interact with HIST1H1C (H1C, H1.2). Histones have been found to affect influenza virus replication, such as the H2A, H2B, H3, and H4, but H1 has not been detected. Here, we found that H1C interacts with NS2 via its C-terminal in the nucleus and that H1C affects influenza virus replication. The H1N1 influenza virus replicates better in H1C knockout A549 cells compared to wild-type A549 cells, primarily because of the regulation of H1C on interferon-? (IFN-?). Further studies showed that the H1C phosphorylation mutant (T146A) decreases IFN-?, while H1C methylation mutants (K34A, K187A) increases IFN-? by releasing the nucleosome and promoting IRF3 binding to the IFN-? promoter. Interestingly, NS2 interacts with H1C, which reduces H1C?IRF3 interaction and results in the inhibition of IFN-? enhanced by H1C. In summary, our study reveals a novel function of H1C to regulate IFN-? and uncovers an underlying mechanism, which suggests H1C plays a role in epigenetic regulation. Moreover, our results suggest a novel mechanism for the influenza virus to antagonize the innate immune response by NS2. äHIST1H1C Regulates Interferon-? and Inhibits Influenza Virus Replicati(epmc).pdf DeepDyve Pubget Overpricing