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10.1016/j.isci.2021.103144 http://scihub22266oqcxt.onion/10.1016/j.isci.2021.103144 34545347!8443536!34545347     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34545347&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       iScience 2021 ; 24 (10): 103144 Nephropedia Template TP {{tp|p=34545347|t=2021. The circadian clock component BMAL1 regulates SARS-CoV-2 entry and replication in lung epithelial cells |pdf=|usr=}}{{34545347}} gab.com Text The circadian clock component BMAL1 regulates SARS-CoV-2 entry and replication in lung epithelial cells JO: iScience http://www.kidney.de/pget.php?&tw=1&pmid=34545347 #FOAvip The coronavirus disease 2019 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) coronavirus, is a global health issue with unprecedented challenges for public health. SARS-CoV-2 primarily infects cells of the respiratory tract via spike glycoprotein binding to angiotensin-converting enzyme (ACE2). Circadian rhythms coordinate an organism's response to its environment and can regulate host susceptibility to virus infection. We demonstrate that silencing the circadian regulator Bmal1 or treating lung epithelial cells with the REV-ERB agonist SR9009 reduces ACE2 expression and inhibits SARS-CoV-2 entry and replication. Importantly, treating infected cells with SR9009 limits SARS-CoV-2 replication and secretion of infectious particles, showing that post-entry steps in the viral life cycle are influenced by the circadian system. Transcriptome analysis revealed that Bmal1 silencing induced interferon-stimulated gene transcripts in Calu-3 lung epithelial cells, providing a mechanism for the circadian pathway to limit SARS-CoV-2 infection. Our study highlights alternative approaches to understand and improve therapeutic targeting of SARS-CoV-2. Twit Text FOAVip The circadian clock component BMAL1 regulates SARS-CoV-2 entry and replication in lung epithelial cells ????iScience http://www.kidney.de/pget.php?&tw=1&pmid=34545347 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34545347 #FOAvip English Wikipedia <ref>{{Cite pmid|34545347}}</ref> The circadian clock component BMAL1 regulates SARS-CoV-2 entry and replication in lung epithelial cells #MMPMID34545347 Zhuang X; Tsukuda S; Wrensch F; Wing PAC; Schilling M; Harris JM; Borrmann H; Morgan SB; Cane JL; Mailly L; Thakur N; Conceicao C; Sanghani H; Heydmann L; Bach C; Ashton A; Walsh S; Tan TK; Schimanski L; Huang KA; Schuster C; Watashi K; Hinks TSC; Jagannath A; Vausdevan SR; Bailey D; Baumert TF; McKeating JA iScience 2021[Oct]; 24 (10): 103144 PMID34545347show ga The coronavirus disease 2019 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) coronavirus, is a global health issue with unprecedented challenges for public health. SARS-CoV-2 primarily infects cells of the respiratory tract via spike glycoprotein binding to angiotensin-converting enzyme (ACE2). Circadian rhythms coordinate an organism's response to its environment and can regulate host susceptibility to virus infection. We demonstrate that silencing the circadian regulator Bmal1 or treating lung epithelial cells with the REV-ERB agonist SR9009 reduces ACE2 expression and inhibits SARS-CoV-2 entry and replication. Importantly, treating infected cells with SR9009 limits SARS-CoV-2 replication and secretion of infectious particles, showing that post-entry steps in the viral life cycle are influenced by the circadian system. Transcriptome analysis revealed that Bmal1 silencing induced interferon-stimulated gene transcripts in Calu-3 lung epithelial cells, providing a mechanism for the circadian pathway to limit SARS-CoV-2 infection. Our study highlights alternative approaches to understand and improve therapeutic targeting of SARS-CoV-2. ?The circadian clock component BMAL1 regulates SARS-CoV-2 entry and rep(epmc).pdf DeepDyve Pubget Overpricing