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10.1016/j.cell.2020.12.004 http://scihub22266oqcxt.onion/10.1016/j.cell.2020.12.004 33333024!7723770!33333024     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\33333024.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell 2021 ; 184 (1): 106-119.e14 Nephropedia Template TP {{tp|p=33333024|t=2021. Genetic Screens Identify Host Factors for SARS-CoV-2 and Common Cold Coronaviruses |pdf=|usr=}}{{33333024}} gab.com Text Genetic Screens Identify Host Factors for SARS-CoV-2 and Common Cold Coronaviruses JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=33333024 #FOAvip The Coronaviridae are a family of viruses that cause disease in humans ranging from mild respiratory infection to potentially lethal acute respiratory distress syndrome. Finding host factors common to multiple coronaviruses could facilitate the development of therapies to combat current and future coronavirus pandemics. Here, we conducted genome-wide CRISPR screens in cells infected by SARS-CoV-2 as well as two seasonally circulating common cold coronaviruses, OC43 and 229E. This approach correctly identified the distinct viral entry factors ACE2 (for SARS-CoV-2), aminopeptidase N (for 229E), and glycosaminoglycans (for OC43). Additionally, we identified phosphatidylinositol phosphate biosynthesis and cholesterol homeostasis as critical host pathways supporting infection by all three coronaviruses. By contrast, the lysosomal protein TMEM106B appeared unique to SARS-CoV-2 infection. Pharmacological inhibition of phosphatidylinositol kinases and cholesterol homeostasis reduced replication of all three coronaviruses. These findings offer important insights for the understanding of the coronavirus life cycle and the development of host-directed therapies. Twit Text FOAVip Genetic Screens Identify Host Factors for SARS-CoV-2 and Common Cold Coronaviruses ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=33333024 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33333024 #FOAvip English Wikipedia <ref>{{Cite pmid|33333024}}</ref> Genetic Screens Identify Host Factors for SARS-CoV-2 and Common Cold Coronaviruses #MMPMID33333024 Wang R; Simoneau CR; Kulsuptrakul J; Bouhaddou M; Travisano KA; Hayashi JM; Carlson-Stevermer J; Zengel JR; Richards CM; Fozouni P; Oki J; Rodriguez L; Joehnk B; Walcott K; Holden K; Sil A; Carette JE; Krogan NJ; Ott M; Puschnik AS Cell 2021[Jan]; 184 (1): 106-119.e14 PMID33333024show ga The Coronaviridae are a family of viruses that cause disease in humans ranging from mild respiratory infection to potentially lethal acute respiratory distress syndrome. Finding host factors common to multiple coronaviruses could facilitate the development of therapies to combat current and future coronavirus pandemics. Here, we conducted genome-wide CRISPR screens in cells infected by SARS-CoV-2 as well as two seasonally circulating common cold coronaviruses, OC43 and 229E. This approach correctly identified the distinct viral entry factors ACE2 (for SARS-CoV-2), aminopeptidase N (for 229E), and glycosaminoglycans (for OC43). Additionally, we identified phosphatidylinositol phosphate biosynthesis and cholesterol homeostasis as critical host pathways supporting infection by all three coronaviruses. By contrast, the lysosomal protein TMEM106B appeared unique to SARS-CoV-2 infection. Pharmacological inhibition of phosphatidylinositol kinases and cholesterol homeostasis reduced replication of all three coronaviruses. These findings offer important insights for the understanding of the coronavirus life cycle and the development of host-directed therapies. |*Genome-Wide Association Study[MESH] |*Host-Pathogen Interactions/drug effects[MESH] |A549 Cells[MESH] |Animals[MESH] |Biosynthetic Pathways/drug effects[MESH] |COVID-19/*genetics/virology[MESH] |Cell Line[MESH] |Chlorocebus aethiops[MESH] |Cholesterol/biosynthesis/metabolism[MESH] |Cluster Analysis[MESH] |Clustered Regularly Interspaced Short Palindromic Repeats[MESH] |Common Cold/genetics/virology[MESH] |Coronavirus Infections/*genetics/virology[MESH] |Coronavirus/classification/*physiology[MESH] |Gene Knockout Techniques[MESH] |Humans[MESH] |Mice[MESH] |Phosphatidylinositols/biosynthesis[MESH] |SARS-CoV-2/*physiology[MESH] |Vero Cells[MESH] |Virus Internalization/drug effects[MESH]Genetic Screens Identify Host Factors for SARS-CoV-2 and Common Cold (epmc).pdf DeepDyve Pubget Overpricing