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10.1128/JVI.05942-11 http://scihub22266oqcxt.onion/10.1128/JVI.05942-11 C3233149!3233149!21994456     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Virol 2011 ; 85 (24): 13019-26 Nephropedia Template TP {{tp|p=21994456|t=2011. Measles Virus V Protein Inhibits NLRP3 Inflammasome-Mediated Interleukin-1? Secretion? |pdf=|usr=}}{{21994456}} gab.com Text Measles Virus V Protein Inhibits NLRP3 Inflammasome-Mediated Interleukin-1 Secretion JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=21994456 #FOAvip Inflammasomes are cytosolic protein complexes that stimulate the activation of caspase-1, which in turn induces the secretion of the inflammatory cytokines Interleukin-1? (IL-1?) and IL-18. Recent studies have indicated that the inflammasome known as the NOD-like-receptor-family, pyrin domain-containing 3 (NLRP3) inflammasome recognizes several RNA viruses, including the influenza and encephalomyocarditis viruses, whereas the retinoic acid-inducible gene I (RIG-I) inflammasome may detect vesicular stomatitis virus. We demonstrate that measles virus (MV) infection induces caspase-1-dependent IL-1? secretion in the human macrophage-like cell line THP-1. Gene knockdown experiments indicated that IL-1? secretion in MV-infected THP-1 cells was mediated by the NLRP3 inflammasome but not the RIG-I inflammasome. MV produces the nonstructural V protein, which has been shown to antagonize host innate immune responses. The recombinant MV lacking the V protein induced more IL-1? than the parental virus. THP-1 cells stably expressing the V protein suppressed NLRP3 inflammasome-mediated IL-1? secretion. Furthermore, coimmunoprecipitation assays revealed that the V protein interacts with NLRP3 through its carboxyl-terminal domain. NLRP3 was located in cytoplasmic granular structures in THP-1 cells stably expressing the V protein, but upon inflammasome activation, NLRP3 was redistributed to the perinuclear region, where it colocalized with the V protein. These results indicate that the V protein of MV suppresses NLRP3 inflammasome-mediated IL-1? secretion by directly or indirectly interacting with NLRP3. Twit Text FOAVip Measles Virus V Protein Inhibits NLRP3 Inflammasome-Mediated Interleukin-1 Secretion ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=21994456 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21994456 #FOAvip English Wikipedia <ref>{{Cite pmid|21994456}}</ref> Measles Virus V Protein Inhibits NLRP3 Inflammasome-Mediated Interleukin-1? Secretion? #MMPMID21994456 Komune N; Ichinohe T; Ito M; Yanagi Y J Virol 2011[Dec]; 85 (24): 13019-26 PMID21994456show ga Inflammasomes are cytosolic protein complexes that stimulate the activation of caspase-1, which in turn induces the secretion of the inflammatory cytokines Interleukin-1? (IL-1?) and IL-18. Recent studies have indicated that the inflammasome known as the NOD-like-receptor-family, pyrin domain-containing 3 (NLRP3) inflammasome recognizes several RNA viruses, including the influenza and encephalomyocarditis viruses, whereas the retinoic acid-inducible gene I (RIG-I) inflammasome may detect vesicular stomatitis virus. We demonstrate that measles virus (MV) infection induces caspase-1-dependent IL-1? secretion in the human macrophage-like cell line THP-1. Gene knockdown experiments indicated that IL-1? secretion in MV-infected THP-1 cells was mediated by the NLRP3 inflammasome but not the RIG-I inflammasome. MV produces the nonstructural V protein, which has been shown to antagonize host innate immune responses. The recombinant MV lacking the V protein induced more IL-1? than the parental virus. THP-1 cells stably expressing the V protein suppressed NLRP3 inflammasome-mediated IL-1? secretion. Furthermore, coimmunoprecipitation assays revealed that the V protein interacts with NLRP3 through its carboxyl-terminal domain. NLRP3 was located in cytoplasmic granular structures in THP-1 cells stably expressing the V protein, but upon inflammasome activation, NLRP3 was redistributed to the perinuclear region, where it colocalized with the V protein. These results indicate that the V protein of MV suppresses NLRP3 inflammasome-mediated IL-1? secretion by directly or indirectly interacting with NLRP3. äMeasles Virus V Protein Inhibits NLRP3 Inflammasome-Mediated Interleuk(epmc).pdf DeepDyve Pubget Overpricing