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10.1038/srep24921 http://scihub22266oqcxt.onion/10.1038/srep24921 C4847014!4847014!27118681     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       Sci+Rep 2016 ; 6 (ä): ä Nephropedia Template TP {{tp|p=27118681|t=2016. LPS-induced NF?B enhanceosome requires TonEBP/NFAT5 without DNA binding |pdf=|usr=}}{{27118681}} gab.com Text LPS-induced NF B enhanceosome requires TonEBP/NFAT5 without DNA binding JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27118681 #FOAvip NF?B is a central mediator of inflammation. Present inhibitors of NF?B are mostly based on inhibition of essential machinery such as proteasome and protein kinases, or activation of nuclear receptors; as such, they are of limited therapeutic use due to severe toxicity. Here we report an LPS-induced NF?B enhanceosome in which TonEBP is required for the recruitment of p300. Increased expression of TonEBP enhances the NF?B activity and reduced TonEBP expression lowers it. Recombinant TonEBP molecules incapable of recruiting p300 do not stimulate NF?B. Myeloid-specific deletion of TonEBP results in milder inflammation and sepsis. We discover that a natural small molecule cerulenin specifically disrupts the enhanceosome without affecting the activation of NF?B itself. Cerulenin suppresses the pro-inflammatory activation of macrophages and sepsis without detectable toxicity. Thus, the NF?B enhanceosome offers a promising target for useful anti-inflammatory agents. Twit Text FOAVip LPS-induced NF B enhanceosome requires TonEBP/NFAT5 without DNA binding ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27118681 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27118681 #FOAvip English Wikipedia <ref>{{Cite pmid|27118681}}</ref> LPS-induced NF?B enhanceosome requires TonEBP/NFAT5 without DNA binding #MMPMID27118681 Lee HH; Sanada S; An SM; Ye BJ; Lee JH; Seo YK; Lee C; Lee-Kwon W; Küper C; Neuhofer W; Choi SY; Kwon HM Sci Rep 2016[]; 6 (ä): ä PMID27118681show ga NF?B is a central mediator of inflammation. Present inhibitors of NF?B are mostly based on inhibition of essential machinery such as proteasome and protein kinases, or activation of nuclear receptors; as such, they are of limited therapeutic use due to severe toxicity. Here we report an LPS-induced NF?B enhanceosome in which TonEBP is required for the recruitment of p300. Increased expression of TonEBP enhances the NF?B activity and reduced TonEBP expression lowers it. Recombinant TonEBP molecules incapable of recruiting p300 do not stimulate NF?B. Myeloid-specific deletion of TonEBP results in milder inflammation and sepsis. We discover that a natural small molecule cerulenin specifically disrupts the enhanceosome without affecting the activation of NF?B itself. Cerulenin suppresses the pro-inflammatory activation of macrophages and sepsis without detectable toxicity. Thus, the NF?B enhanceosome offers a promising target for useful anti-inflammatory agents. äLPS-induced NF?B enhanceosome requires TonEBP/NFAT5 without DNA bindin(epmc).pdf DeepDyve Pubget Overpricing