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10.1038/s41598-018-25123-2 http://scihub22266oqcxt.onion/10.1038/s41598-018-25123-2 C5928092!5928092!29712950     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2018 ; 8 (ä): ä Nephropedia Template TP {{tp|p=29712950|t=2018. Hsp90 inhibition as a means to inhibit activation of the NLRP3 inflammasome |pdf=|usr=}}{{29712950}} gab.com Text Hsp90 inhibition as a means to inhibit activation of the NLRP3 inflammasome JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29712950 #FOAvip Once activated, the intracellular receptor NLRP3 assembles an inflammasome protein complex that facilitates the caspase-1-mediated maturation of IL-1? and IL-18. Inactive NLRP3 is guarded by a protein complex containing Hsp90. In response to stress stimuli, Hsp90 is released, and NLRP3 can be activated to promote inflammation. In this study, we blocked Hsp90 with geldanamycin and studied the fate of NLRP3 in human retinal pigment epithelial (RPE) cells. RPE cells play a central role in the development of age-related macular degeneration (AMD), a progressive eye disease causing severe vision loss in the elderly. IL-1?-primed ARPE-19 cells, human embryonal stem cell (hESC)-derived RPE cells, and primary human RPE cells were exposed to MG-132 and bafilomycin A to activate NLRP3 via the inhibition of proteasomes and autophagy, respectively. Additionally, RPE cells were treated with geldanamycin at different time points and the levels of NLRP3 and IL-1? were determined. Caspase-1 activity was measured using a commercial assay. Geldanamycin prevented the activation of the inflammasome in human RPE cells. NLRP3 released from its protective complex became degraded by autophagy or secreted from the cells. Controlled destruction of NLRP3 is a potential way to regulate the inflammation associated with chronic diseases, such as AMD. Twit Text FOAVip Hsp90 inhibition as a means to inhibit activation of the NLRP3 inflammasome ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29712950 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29712950 #FOAvip English Wikipedia <ref>{{Cite pmid|29712950}}</ref> Hsp90 inhibition as a means to inhibit activation of the NLRP3 inflammasome #MMPMID29712950 Piippo N; Korhonen E; Hytti M; Skottman H; Kinnunen K; Josifovska N; Petrovski G; Kaarniranta K; Kauppinen A Sci Rep 2018[]; 8 (ä): ä PMID29712950show ga Once activated, the intracellular receptor NLRP3 assembles an inflammasome protein complex that facilitates the caspase-1-mediated maturation of IL-1? and IL-18. Inactive NLRP3 is guarded by a protein complex containing Hsp90. In response to stress stimuli, Hsp90 is released, and NLRP3 can be activated to promote inflammation. In this study, we blocked Hsp90 with geldanamycin and studied the fate of NLRP3 in human retinal pigment epithelial (RPE) cells. RPE cells play a central role in the development of age-related macular degeneration (AMD), a progressive eye disease causing severe vision loss in the elderly. IL-1?-primed ARPE-19 cells, human embryonal stem cell (hESC)-derived RPE cells, and primary human RPE cells were exposed to MG-132 and bafilomycin A to activate NLRP3 via the inhibition of proteasomes and autophagy, respectively. Additionally, RPE cells were treated with geldanamycin at different time points and the levels of NLRP3 and IL-1? were determined. Caspase-1 activity was measured using a commercial assay. Geldanamycin prevented the activation of the inflammasome in human RPE cells. NLRP3 released from its protective complex became degraded by autophagy or secreted from the cells. Controlled destruction of NLRP3 is a potential way to regulate the inflammation associated with chronic diseases, such as AMD. äHsp90 inhibition as a means to inhibit activation of the NLRP3 inflamm(epmc).pdf DeepDyve Pubget Overpricing