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10.1080/2162402X.2016.1196309 http://scihub22266oqcxt.onion/10.1080/2162402X.2016.1196309 C5007953!5007953!27622065     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       Oncoimmunology 2016 ; 5 (8): ä Nephropedia Template TP {{tp|p=27622065|t=2016. Interferon alpha bioactivity critically depends on Scavenger receptor class B type I function |pdf=|usr=}}{{27622065}} gab.com Text Interferon alpha bioactivity critically depends on Scavenger receptor class B type I function JO: Oncoimmunology http://www.kidney.de/pget.php?&tw=1&pmid=27622065 #FOAvip Scavenger receptor class B type I (SR-B1) binds pathogen-associated molecular patterns participating in the regulation of the inflammatory reaction but there is no information regarding potential interactions between SR-B1 and the interferon system. Herein, we report that SR-B1 ligands strongly regulate the transcriptional response to interferon ? (IFN?) and enhance its antiviral and antitumor activity. This effect was mediated by the activation of TLR2 and TLR4 as it was annulled by the addition of anti-TLR2 or anti-TLR4 blocking antibodies. In vivo, we maximized the antitumor activity of IFN? co-expressing in the liver a SR-B1 ligand and IFN? by adeno-associated viruses. This gene therapy strategy eradicated liver metastases from colon cancer with reduced toxicity. On the other hand, genetic and pharmacological inhibition of SR-B1 blocks the clathrin-dependent interferon receptor recycling pathway with a concomitant reduction in IFN? signaling and bioactivity. This effect can be applied to enhance cancer immunotherapy with oncolytic viruses. Indeed, SR-B1 antagonists facilitate replication of oncolytic viruses amplifying their tumoricidal potential. In conclusion, SR-B1 agonists behave as IFN? enhancers while SR-B1 inhibitors dampen IFN? activity. These results demonstrate that SR-B1 is a suitable pharmacology target to enhance cancer immunotherapy based on IFN? and oncolytic viruses. Twit Text FOAVip Interferon alpha bioactivity critically depends on Scavenger receptor class B type I function ????Oncoimmunology http://www.kidney.de/pget.php?&tw=1&pmid=27622065 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27622065 #FOAvip English Wikipedia <ref>{{Cite pmid|27622065}}</ref> Interferon alpha bioactivity critically depends on Scavenger receptor class B type I function #MMPMID27622065 Vasquez M; Fioravanti J; Aranda F; Paredes V; Gomar C; Ardaiz N; Fernandez-Ruiz V; Méndez M; Nistal-Villan E; Larrea E; Gao Q; Gonzalez-Aseguinolaza G; Prieto J; Berraondo P Oncoimmunology 2016[Aug]; 5 (8): ä PMID27622065show ga Scavenger receptor class B type I (SR-B1) binds pathogen-associated molecular patterns participating in the regulation of the inflammatory reaction but there is no information regarding potential interactions between SR-B1 and the interferon system. Herein, we report that SR-B1 ligands strongly regulate the transcriptional response to interferon ? (IFN?) and enhance its antiviral and antitumor activity. This effect was mediated by the activation of TLR2 and TLR4 as it was annulled by the addition of anti-TLR2 or anti-TLR4 blocking antibodies. In vivo, we maximized the antitumor activity of IFN? co-expressing in the liver a SR-B1 ligand and IFN? by adeno-associated viruses. This gene therapy strategy eradicated liver metastases from colon cancer with reduced toxicity. On the other hand, genetic and pharmacological inhibition of SR-B1 blocks the clathrin-dependent interferon receptor recycling pathway with a concomitant reduction in IFN? signaling and bioactivity. This effect can be applied to enhance cancer immunotherapy with oncolytic viruses. Indeed, SR-B1 antagonists facilitate replication of oncolytic viruses amplifying their tumoricidal potential. In conclusion, SR-B1 agonists behave as IFN? enhancers while SR-B1 inhibitors dampen IFN? activity. These results demonstrate that SR-B1 is a suitable pharmacology target to enhance cancer immunotherapy based on IFN? and oncolytic viruses. äInterferon alpha bioactivity critically depends on Scavenger receptor (epmc).pdf DeepDyve Pubget Overpricing