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10.1016/j.bcp.2020.114227 http://scihub22266oqcxt.onion/10.1016/j.bcp.2020.114227 32966814!7502229!32966814     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       Biochem+Pharmacol 2020 ; 182 (ä): 114227 Nephropedia Template TP {{tp|p=32966814|t=2020. AR12 (OSU-03012) suppresses GRP78 expression and inhibits SARS-CoV-2 replication |pdf=|usr=}}{{32966814}} gab.com Text AR12 (OSU-03012) suppresses GRP78 expression and inhibits SARS-CoV-2 replication JO: Biochem Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=32966814 #FOAvip AR12 is a derivative of celecoxib which no-longer acts against COX2 but instead inhibits the ATPase activity of multiple chaperone proteins, in particular GRP78. GRP78 acts as a sensor of endoplasmic reticulum stress and is an essential chaperone required for the life cycle of all mammalian viruses. We and others previously demonstrated in vitro and in vivo that AR12 increases autophagosome formation and autophagic flux, enhances virus protein degradation, preventing virus reproduction, and prolonging the survival of infected animals. In this report, we determined whether AR12 could act against SARS-CoV-2. In a dose-dependent fashion AR12 inhibited SARS-CoV-2 spike protein expression in transfected or infected cells. AR12 suppressed the production of infectious virions via autophagosome formation, which was also associated with degradation of GRP78. After AR12 exposure, the colocalization of GRP78 with spike protein was reduced. Knock down of eIF2alpha prevented AR12-induced spike degradation and knock down of Beclin1 or ATG5 caused the spike protein to localize in LAMP2+ vesicles without apparent degradation. HCT116 cells expressing ATG16L1 T300, found in the majority of persons of non-European descent, particularly from Africa, expressed greater amounts of GRP78 and SARS-CoV-2 receptor angiotensin converting enzyme 2 compared to ATG16L1 A300, predominantly found in Europeans, suggestive that ATG16L1 T300 expression may be associated with a greater ability to be infected and to reproduce SARS-CoV-2. In conclusion, our findings demonstrate that AR12 represents a clinically relevant anti-viral drug for the treatment of SARS-CoV-2. Twit Text FOAVip AR12 (OSU-03012) suppresses GRP78 expression and inhibits SARS-CoV-2 replication ????Biochem Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=32966814 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32966814 #FOAvip English Wikipedia <ref>{{Cite pmid|32966814}}</ref> AR12 (OSU-03012) suppresses GRP78 expression and inhibits SARS-CoV-2 replication #MMPMID32966814 Rayner JO; Roberts RA; Kim J; Poklepovic A; Roberts JL; Booth L; Dent P Biochem Pharmacol 2020[Dec]; 182 (ä): 114227 PMID32966814show ga AR12 is a derivative of celecoxib which no-longer acts against COX2 but instead inhibits the ATPase activity of multiple chaperone proteins, in particular GRP78. GRP78 acts as a sensor of endoplasmic reticulum stress and is an essential chaperone required for the life cycle of all mammalian viruses. We and others previously demonstrated in vitro and in vivo that AR12 increases autophagosome formation and autophagic flux, enhances virus protein degradation, preventing virus reproduction, and prolonging the survival of infected animals. In this report, we determined whether AR12 could act against SARS-CoV-2. In a dose-dependent fashion AR12 inhibited SARS-CoV-2 spike protein expression in transfected or infected cells. AR12 suppressed the production of infectious virions via autophagosome formation, which was also associated with degradation of GRP78. After AR12 exposure, the colocalization of GRP78 with spike protein was reduced. Knock down of eIF2alpha prevented AR12-induced spike degradation and knock down of Beclin1 or ATG5 caused the spike protein to localize in LAMP2+ vesicles without apparent degradation. HCT116 cells expressing ATG16L1 T300, found in the majority of persons of non-European descent, particularly from Africa, expressed greater amounts of GRP78 and SARS-CoV-2 receptor angiotensin converting enzyme 2 compared to ATG16L1 A300, predominantly found in Europeans, suggestive that ATG16L1 T300 expression may be associated with a greater ability to be infected and to reproduce SARS-CoV-2. In conclusion, our findings demonstrate that AR12 represents a clinically relevant anti-viral drug for the treatment of SARS-CoV-2. |Animals[MESH] |Antiviral Agents/*pharmacology[MESH] |COVID-19 Drug Treatment[MESH] |Cell Line, Tumor[MESH] |Chlorocebus aethiops[MESH] |Endoplasmic Reticulum Chaperone BiP[MESH] |Female[MESH] |Heat-Shock Proteins/*antagonists & inhibitors[MESH] |Humans[MESH] |Pyrazoles/*pharmacology[MESH] |SARS-CoV-2/*drug effects[MESH] |Spike Glycoprotein, Coronavirus/biosynthesis[MESH] |Sulfonamides/*pharmacology[MESH] |Vero Cells[MESH]AR12 (OSU-03012) suppresses GRP78 expression and inhibits SARS-CoV-2 r(epmc).pdf DeepDyve Pubget Overpricing