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10.1002/2211-5463.12490 http://scihub22266oqcxt.onion/10.1002/2211-5463.12490 30186747!6120239!30186747     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       FEBS+Open+Bio 2018 ; 8 (9): 1457-1470 Nephropedia Template TP {{tp|p=30186747|t=2018. MicroR-9-5p suppresses EV71 replication through targeting NFkappaB of the RIG-I-mediated innate immune response |pdf=|usr=}}{{30186747}} gab.com Text MicroR-9-5p suppresses EV71 replication through targeting NFkappaB of the RIG-I-mediated innate immune response JO: FEBS Open Bio http://www.kidney.de/pget.php?&tw=1&pmid=30186747 #FOAvip Accumulating evidence demonstrates that there is a causative link between hsa-microRNA-9-5p (miR-9) and pathophysiological processes. Enterovirus 71 (EV71) has been found to contribute to numerous severe clinical symptoms which result in death. The exact mechanism by which EV71 influences miR-9 expression is unknown, and the relationship between miR-9 and EV71 is still unclear. Here, miR-9 expression was found to be impaired upon EV71 infection in several cell lines and in an EV71 infection mouse model. Additionally, we confirmed that EV71 infection induces robust expression of pro-inflammatory cytokines (TNF-alpha, IL-6, and IL-1) and interferons (IFN-alpha and IFN-beta). Overexpression of miR-9 attenuated EV71 proliferation and reduced protein and gene expressions of virion protein 1 (VP1) of EV71. Furthermore, we observed that the inflammation caused by EV71 infection was restored to a moderate level via miR-9 overexpression. Nuclear factor kappa B (NFkappaB) in the retinoic acid-induced gene 1 (RIG-I) signaling pathway, but not interferon regulating factor 3 (IRF3), was significantly decreased and inactivated by ectopic miR-9 expression. Moreover, in mouse infection experiments, administration of miR-9 agomirs caused a significant decrease in VP1 levels and pro-inflammatory cytokine production after viral inoculation. Taken together, the present data demonstrate that miR-9 exerts an anti-EV71 effect in cells and a mouse model via mediating NFkappaB activity of the RIG-I signal pathway, thereby suggesting a new candidate for antiviral drug development. Twit Text FOAVip MicroR-9-5p suppresses EV71 replication through targeting NFkappaB of the RIG-I-mediated innate immune response ????FEBS Open Bio http://www.kidney.de/pget.php?&tw=1&pmid=30186747 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30186747 #FOAvip English Wikipedia <ref>{{Cite pmid|30186747}}</ref> MicroR-9-5p suppresses EV71 replication through targeting NFkappaB of the RIG-I-mediated innate immune response #MMPMID30186747 Li B; Zheng J FEBS Open Bio 2018[Sep]; 8 (9): 1457-1470 PMID30186747show ga Accumulating evidence demonstrates that there is a causative link between hsa-microRNA-9-5p (miR-9) and pathophysiological processes. Enterovirus 71 (EV71) has been found to contribute to numerous severe clinical symptoms which result in death. The exact mechanism by which EV71 influences miR-9 expression is unknown, and the relationship between miR-9 and EV71 is still unclear. Here, miR-9 expression was found to be impaired upon EV71 infection in several cell lines and in an EV71 infection mouse model. Additionally, we confirmed that EV71 infection induces robust expression of pro-inflammatory cytokines (TNF-alpha, IL-6, and IL-1) and interferons (IFN-alpha and IFN-beta). Overexpression of miR-9 attenuated EV71 proliferation and reduced protein and gene expressions of virion protein 1 (VP1) of EV71. Furthermore, we observed that the inflammation caused by EV71 infection was restored to a moderate level via miR-9 overexpression. Nuclear factor kappa B (NFkappaB) in the retinoic acid-induced gene 1 (RIG-I) signaling pathway, but not interferon regulating factor 3 (IRF3), was significantly decreased and inactivated by ectopic miR-9 expression. Moreover, in mouse infection experiments, administration of miR-9 agomirs caused a significant decrease in VP1 levels and pro-inflammatory cytokine production after viral inoculation. Taken together, the present data demonstrate that miR-9 exerts an anti-EV71 effect in cells and a mouse model via mediating NFkappaB activity of the RIG-I signal pathway, thereby suggesting a new candidate for antiviral drug development. äMicroR-9-5p suppresses EV71 replication through targeting NFkappaB of (epmc).pdf DeepDyve Pubget Overpricing