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10.1038/cmi.2017.1 http://scihub22266oqcxt.onion/10.1038/cmi.2017.1 C5520414!5520414!28392573     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Mol+Immunol 2017 ; 14 (7): 607-20 Nephropedia Template TP {{tp|p=28392573|t=2017. Inducible Rubicon facilitates viral replication by antagonizing interferon production |pdf=|usr=}}{{28392573}} gab.com Text Inducible Rubicon facilitates viral replication by antagonizing interferon production JO: Cell Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28392573 #FOAvip The RUN domain Beclin-1-interacting cysteine-rich-containing (Rubicon) protein is involved in the maturation step of autophagy and the endocytic pathway as a Beclin-1-binding partner, but little is known regarding the role of Rubicon during viral infection. Here, we performed functional studies of the identified target in interferon (IFN) signaling pathways associated with Rubicon to elucidate the mechanisms of viral resistance to IFN. The Rubicon protein levels were elevated in peripheral blood mononuclear cells, sera and liver tissues from patients with hepatitis B virus (HBV) infection relative to those in healthy individuals. Assays of the overexpression and knockdown of Rubicon showed that Rubicon significantly promoted HBV replication. In addition, Rubicon knockdown resulted in the inhibition of enterovirus 71, influenza A virus and vesicular stomatitis virus. The expression o0f Rubicon led to the suppression of virus-induced type-I interferon (IFN-? and IFN-?) and type-III interferon (IFN-?1). Translocation of activated IRF3 and IRF7 from the cytoplasm to the nucleus was involved in this process, and the NF-?B essential modulator (NEMO), a key factor in the IFN pathway, was the target with which Rubicon interacted. Our results reveal a previously unrecognized function of Rubicon as a virus-induced protein that binds to NEMO, leading to the inhibition of type-I interferon production. Rubicon thus functions as an important negative regulator of the innate immune response, enhances viral replication and may play a role in viral immune evasion. Twit Text FOAVip Inducible Rubicon facilitates viral replication by antagonizing interferon production ????Cell Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28392573 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28392573 #FOAvip English Wikipedia <ref>{{Cite pmid|28392573}}</ref> Inducible Rubicon facilitates viral replication by antagonizing interferon production #MMPMID28392573 Wan Y; Cao W; Han T; Ren S; Feng J; Chen T; Wang J; Broering R; Lu M; Zhu Y Cell Mol Immunol 2017[Jul]; 14 (7): 607-20 PMID28392573show ga The RUN domain Beclin-1-interacting cysteine-rich-containing (Rubicon) protein is involved in the maturation step of autophagy and the endocytic pathway as a Beclin-1-binding partner, but little is known regarding the role of Rubicon during viral infection. Here, we performed functional studies of the identified target in interferon (IFN) signaling pathways associated with Rubicon to elucidate the mechanisms of viral resistance to IFN. The Rubicon protein levels were elevated in peripheral blood mononuclear cells, sera and liver tissues from patients with hepatitis B virus (HBV) infection relative to those in healthy individuals. Assays of the overexpression and knockdown of Rubicon showed that Rubicon significantly promoted HBV replication. In addition, Rubicon knockdown resulted in the inhibition of enterovirus 71, influenza A virus and vesicular stomatitis virus. The expression o0f Rubicon led to the suppression of virus-induced type-I interferon (IFN-? and IFN-?) and type-III interferon (IFN-?1). Translocation of activated IRF3 and IRF7 from the cytoplasm to the nucleus was involved in this process, and the NF-?B essential modulator (NEMO), a key factor in the IFN pathway, was the target with which Rubicon interacted. Our results reveal a previously unrecognized function of Rubicon as a virus-induced protein that binds to NEMO, leading to the inhibition of type-I interferon production. Rubicon thus functions as an important negative regulator of the innate immune response, enhances viral replication and may play a role in viral immune evasion. äInducible Rubicon facilitates viral replication by antagonizing interf(epmc).pdf DeepDyve Pubget Overpricing