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10.1186/s12929-017-0347-7 http://scihub22266oqcxt.onion/10.1186/s12929-017-0347-7 C5477258!5477258!28629361     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Biomed+Sci 2017 ; 24 (ä): ä Nephropedia Template TP {{tp|p=28629361|t=2017. Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions |pdf=|usr=}}{{28629361}} gab.com Text Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions JO: J Biomed Sci http://www.kidney.de/pget.php?&tw=1&pmid=28629361 #FOAvip Decoy receptor 3 (DcR3), also known as tumor necrosis factor receptor (TNFR) superfamily member 6b (TNFRSF6B), is a soluble decoy receptor which can neutralize the biological functions of three members of tumor necrosis factor superfamily (TNFSF): Fas ligand (FasL), LIGHT, and TL1A. In addition to ?decoy? function, recombinant DcR3.Fc is able to modulate the activation and differentiation of dendritic cells (DCs) and macrophages via ?non-decoy? action. DcR3-treated DCs skew T cell differentiation into Th2 phenotype, while DcR3-treated macrophages behave M2 phenotype. DcR3 is upregulated in various cancer cells and several inflammatory tissues, and is regarded as a potential biomarker to predict inflammatory disease progression and cancer metastasis. However, whether DcR3 is a pathogenic factor or a suppressor to attenuate inflammatory reactions, has not been discussed comprehensively yet. Because mouse genome does not have DcR3, it is not feasible to investigate its physiological functions by gene-knockout approach. However, DcR3-mediated effects in vitro are determined via overexpressing DcR3 or addition of recombinant DcR3.Fc fusion protein. Moreover, CD68-driven DcR3 transgenic mice are used to investigate DcR3-mediated systemic effects in vivo. Upregulation of DcR3 during inflammatory reactions exerts negative-feedback to suppress inflammation, while tumor cells hijack DcR3 to prevent apoptosis and promote tumor growth and invasion. Thus, ?switch-on? of DcR3 expression may be feasible for the treatment of inflammatory diseases and enhance tissue repairing, while ?switch-off? of DcR3 expression can enhance tumor apoptosis and suppress tumor growth in vivo. Twit Text FOAVip Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions ????J Biomed Sci http://www.kidney.de/pget.php?&tw=1&pmid=28629361 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28629361 #FOAvip English Wikipedia <ref>{{Cite pmid|28629361}}</ref> Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions #MMPMID28629361 Hsieh SL; Lin WW J Biomed Sci 2017[]; 24 (ä): ä PMID28629361show ga Decoy receptor 3 (DcR3), also known as tumor necrosis factor receptor (TNFR) superfamily member 6b (TNFRSF6B), is a soluble decoy receptor which can neutralize the biological functions of three members of tumor necrosis factor superfamily (TNFSF): Fas ligand (FasL), LIGHT, and TL1A. In addition to ?decoy? function, recombinant DcR3.Fc is able to modulate the activation and differentiation of dendritic cells (DCs) and macrophages via ?non-decoy? action. DcR3-treated DCs skew T cell differentiation into Th2 phenotype, while DcR3-treated macrophages behave M2 phenotype. DcR3 is upregulated in various cancer cells and several inflammatory tissues, and is regarded as a potential biomarker to predict inflammatory disease progression and cancer metastasis. However, whether DcR3 is a pathogenic factor or a suppressor to attenuate inflammatory reactions, has not been discussed comprehensively yet. Because mouse genome does not have DcR3, it is not feasible to investigate its physiological functions by gene-knockout approach. However, DcR3-mediated effects in vitro are determined via overexpressing DcR3 or addition of recombinant DcR3.Fc fusion protein. Moreover, CD68-driven DcR3 transgenic mice are used to investigate DcR3-mediated systemic effects in vivo. Upregulation of DcR3 during inflammatory reactions exerts negative-feedback to suppress inflammation, while tumor cells hijack DcR3 to prevent apoptosis and promote tumor growth and invasion. Thus, ?switch-on? of DcR3 expression may be feasible for the treatment of inflammatory diseases and enhance tissue repairing, while ?switch-off? of DcR3 expression can enhance tumor apoptosis and suppress tumor growth in vivo. äDecoy receptor 3: an endogenous immunomodulator in cancer growth and i(epmc).pdf DeepDyve Pubget Overpricing