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10.1371/journal.ppat.1009599 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1009599 34043740!8189496!34043740     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2021 ; 17 (5): e1009599 Nephropedia Template TP {{tp|p=34043740|t=2021. TMEM41B is a host factor required for the replication of diverse coronaviruses including SARS-CoV-2 |pdf=|usr=}}{{34043740}} gab.com Text TMEM41B is a host factor required for the replication of diverse coronaviruses including SARS-CoV-2 JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=34043740 #FOAvip Antiviral therapeutics are a front-line defense against virally induced diseases. Because viruses frequently mutate to escape direct inhibition of viral proteins, there is interest in targeting the host proteins that the virus must co-opt to complete its replication cycle. However, a detailed understanding of the interactions between the virus and the host cell is necessary in order to facilitate development of host-directed therapeutics. As a first step, we performed a genome-wide loss of function screen using the alphacoronavirus HCoV-229E to better define the interactions between coronaviruses and host factors. We report the identification and validation of an ER-resident host protein, TMEM41B, as an essential host factor for not only HCoV-229E but also genetically distinct coronaviruses including the pandemic betacoronavirus SARS-CoV-2. We show that the protein is required at an early, but post-receptor engagement, stage of the viral lifecycle. Further, mechanistic studies revealed that although the protein was not enriched at replication complexes, it likely contributes to viral replication complex formation via mobilization of cholesterol and other lipids to facilitate host membrane expansion and curvature. Continued study of TMEM41B and the development of approaches to prevent its function may lead to broad spectrum anti-coronavirus therapeutics. Twit Text FOAVip TMEM41B is a host factor required for the replication of diverse coronaviruses including SARS-CoV-2 ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=34043740 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34043740 #FOAvip English Wikipedia <ref>{{Cite pmid|34043740}}</ref> TMEM41B is a host factor required for the replication of diverse coronaviruses including SARS-CoV-2 #MMPMID34043740 Trimarco JD; Heaton BE; Chaparian RR; Burke KN; Binder RA; Gray GC; Smith CM; Menachery VD; Heaton NS PLoS Pathog 2021[May]; 17 (5): e1009599 PMID34043740show ga Antiviral therapeutics are a front-line defense against virally induced diseases. Because viruses frequently mutate to escape direct inhibition of viral proteins, there is interest in targeting the host proteins that the virus must co-opt to complete its replication cycle. However, a detailed understanding of the interactions between the virus and the host cell is necessary in order to facilitate development of host-directed therapeutics. As a first step, we performed a genome-wide loss of function screen using the alphacoronavirus HCoV-229E to better define the interactions between coronaviruses and host factors. We report the identification and validation of an ER-resident host protein, TMEM41B, as an essential host factor for not only HCoV-229E but also genetically distinct coronaviruses including the pandemic betacoronavirus SARS-CoV-2. We show that the protein is required at an early, but post-receptor engagement, stage of the viral lifecycle. Further, mechanistic studies revealed that although the protein was not enriched at replication complexes, it likely contributes to viral replication complex formation via mobilization of cholesterol and other lipids to facilitate host membrane expansion and curvature. Continued study of TMEM41B and the development of approaches to prevent its function may lead to broad spectrum anti-coronavirus therapeutics. |Animals[MESH] |Antiviral Agents/pharmacology[MESH] |COVID-19/metabolism[MESH] |Cell Line[MESH] |Chlorocebus aethiops[MESH] |Coronavirus 229E, Human/*drug effects/physiology[MESH] |Endoplasmic Reticulum/metabolism/virology[MESH] |Host Microbial Interactions/genetics/*physiology[MESH] |Humans[MESH] |Membrane Proteins/*metabolism/physiology[MESH] |SARS-CoV-2/drug effects/metabolism/pathogenicity[MESH] |Vero Cells[MESH]TMEM41B is a host factor required for the replication of diverse coron(epmc).pdf DeepDyve Pubget Overpricing