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10.1101/gad.348320.121 http://scihub22266oqcxt.onion/10.1101/gad.348320.121 34168039!8247602!34168039     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       Genes+Dev 2021 ; 35 (13-14): 1005-1019 Nephropedia Template TP {{tp|p=34168039|t=2021. Targeting the m(6)A RNA modification pathway blocks SARS-CoV-2 and HCoV-OC43 replication |pdf=|usr=}}{{34168039}} gab.com Text Targeting the m(6)A RNA modification pathway blocks SARS-CoV-2 and HCoV-OC43 replication JO: Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=34168039 #FOAvip N(6)-methyladenosine (m(6)A) is an abundant internal RNA modification, influencing transcript fate and function in uninfected and virus-infected cells. Installation of m(6)A by the nuclear RNA methyltransferase METTL3 occurs cotranscriptionally; however, the genomes of some cytoplasmic RNA viruses are also m(6)A-modified. How the cellular m(6)A modification machinery impacts coronavirus replication, which occurs exclusively in the cytoplasm, is unknown. Here we show that replication of SARS-CoV-2, the agent responsible for the COVID-19 pandemic, and a seasonal human beta-coronavirus HCoV-OC43, can be suppressed by depletion of METTL3 or cytoplasmic m(6)A reader proteins YTHDF1 and YTHDF3 and by a highly specific small molecule METTL3 inhibitor. Reduction of infectious titer correlates with decreased synthesis of viral RNAs and the essential nucleocapsid (N) protein. Sites of m(6)A modification on genomic and subgenomic RNAs of both viruses were mapped by methylated RNA immunoprecipitation sequencing (meRIP-seq). Levels of host factors involved in m(6)A installation, removal, and recognition were unchanged by HCoV-OC43 infection; however, nuclear localization of METTL3 and cytoplasmic m(6)A readers YTHDF1 and YTHDF2 increased. This establishes that coronavirus RNAs are m(6)A-modified and host m(6)A pathway components control beta-coronavirus replication. Moreover, it illustrates the therapeutic potential of targeting the m(6)A pathway to restrict coronavirus reproduction. Twit Text FOAVip Targeting the m(6)A RNA modification pathway blocks SARS-CoV-2 and HCoV-OC43 replication ????Genes Dev http://www.kidney.de/pget.php?&tw=1&pmid=34168039 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34168039 #FOAvip English Wikipedia <ref>{{Cite pmid|34168039}}</ref> Targeting the m(6)A RNA modification pathway blocks SARS-CoV-2 and HCoV-OC43 replication #MMPMID34168039 Burgess HM; Depledge DP; Thompson L; Srinivas KP; Grande RC; Vink EI; Abebe JS; Blackaby WP; Hendrick A; Albertella MR; Kouzarides T; Stapleford KA; Wilson AC; Mohr I Genes Dev 2021[Jul]; 35 (13-14): 1005-1019 PMID34168039show ga N(6)-methyladenosine (m(6)A) is an abundant internal RNA modification, influencing transcript fate and function in uninfected and virus-infected cells. Installation of m(6)A by the nuclear RNA methyltransferase METTL3 occurs cotranscriptionally; however, the genomes of some cytoplasmic RNA viruses are also m(6)A-modified. How the cellular m(6)A modification machinery impacts coronavirus replication, which occurs exclusively in the cytoplasm, is unknown. Here we show that replication of SARS-CoV-2, the agent responsible for the COVID-19 pandemic, and a seasonal human beta-coronavirus HCoV-OC43, can be suppressed by depletion of METTL3 or cytoplasmic m(6)A reader proteins YTHDF1 and YTHDF3 and by a highly specific small molecule METTL3 inhibitor. Reduction of infectious titer correlates with decreased synthesis of viral RNAs and the essential nucleocapsid (N) protein. Sites of m(6)A modification on genomic and subgenomic RNAs of both viruses were mapped by methylated RNA immunoprecipitation sequencing (meRIP-seq). Levels of host factors involved in m(6)A installation, removal, and recognition were unchanged by HCoV-OC43 infection; however, nuclear localization of METTL3 and cytoplasmic m(6)A readers YTHDF1 and YTHDF2 increased. This establishes that coronavirus RNAs are m(6)A-modified and host m(6)A pathway components control beta-coronavirus replication. Moreover, it illustrates the therapeutic potential of targeting the m(6)A pathway to restrict coronavirus reproduction. |Adenosine/analogs & derivatives/genetics/metabolism[MESH] |Cell Line[MESH] |Coronavirus Infections/metabolism/virology[MESH] |Coronavirus OC43, Human/*physiology[MESH] |Gene Expression Regulation/drug effects[MESH] |Host-Pathogen Interactions/drug effects[MESH] |Humans[MESH] |Methyltransferases/antagonists & inhibitors/metabolism[MESH] |Nucleocapsid Proteins[MESH] |RNA Processing, Post-Transcriptional/*genetics[MESH] |RNA, Viral/metabolism[MESH] |RNA-Binding Proteins/metabolism[MESH] |SARS-CoV-2/*physiology[MESH]Targeting the m(6)A RNA modification pathway blocks SARS-CoV-2 and HCo(epmc).pdf DeepDyve Pubget Overpricing