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10.1016/j.bbrc.2020.04.010 http://scihub22266oqcxt.onion/10.1016/j.bbrc.2020.04.010 C7144854!7144854!32291076     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32291076&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       Biochem+Biophys+Res+Commun 2020 ; 526 (4): 947-52 Nephropedia Template TP {{tp|p=32291076|t=2020. EZH2-mediated H3K27me3 inhibits ACE2 expression |pdf=|usr=}}{{32291076}} gab.com Text EZH2-mediated H3K27me3 inhibits ACE2 expression JO: Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=32291076 #FOAvip The outbreak of corona virus disease 2019 (COVID-19) caused by SARS-CoV-2 infection is spreading globally and quickly, leading to emerging health issues. SARS-CoV-2 enters into and infects host cells through its spike glycoprotein recognizing the cell receptor Angiotensin-converting enzyme II (ACE2). Here, we noticed that ACE2 was further enhanced by SARS-CoV-2 infection. Human germ cells and early embryos express high level of ACE2. Notably, RNA-seq result showed that reduction of H3K27me3, but not H3K4/9/36me3, led to upregulation of Ace2 expression in mouse germ cell line GC-2. In agreement with this result, we found in human embryonic stem cells that ACE2 expression was significantly increased in absence of EZH2, the major enzyme catalyzing H3K27me3. ChIP-seq analysis further confirmed decrease of H3K27me3 signal and increase of H3K27ac signal at ACE2 promoter upon EZH2 knockout. Therefore, we propose that EZH2-mediated H3K27me3 at ACE2 promoter region inhibits ACE2 expression in mammalian cells. This regulatory pattern may also exist in other human cells and tissues. Our discovery provides clues for pathogenesis and targeted drug therapy towards ACE2 expression for prevention and adjuvant therapy of COVID-19. Twit Text FOAVip EZH2-mediated H3K27me3 inhibits ACE2 expression ????Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=32291076 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32291076 #FOAvip English Wikipedia <ref>{{Cite pmid|32291076}}</ref> EZH2-mediated H3K27me3 inhibits ACE2 expression #MMPMID32291076 Li Y; Li H; Zhou L Biochem Biophys Res Commun 2020[Jun]; 526 (4): 947-52 PMID32291076show ga The outbreak of corona virus disease 2019 (COVID-19) caused by SARS-CoV-2 infection is spreading globally and quickly, leading to emerging health issues. SARS-CoV-2 enters into and infects host cells through its spike glycoprotein recognizing the cell receptor Angiotensin-converting enzyme II (ACE2). Here, we noticed that ACE2 was further enhanced by SARS-CoV-2 infection. Human germ cells and early embryos express high level of ACE2. Notably, RNA-seq result showed that reduction of H3K27me3, but not H3K4/9/36me3, led to upregulation of Ace2 expression in mouse germ cell line GC-2. In agreement with this result, we found in human embryonic stem cells that ACE2 expression was significantly increased in absence of EZH2, the major enzyme catalyzing H3K27me3. ChIP-seq analysis further confirmed decrease of H3K27me3 signal and increase of H3K27ac signal at ACE2 promoter upon EZH2 knockout. Therefore, we propose that EZH2-mediated H3K27me3 at ACE2 promoter region inhibits ACE2 expression in mammalian cells. This regulatory pattern may also exist in other human cells and tissues. Our discovery provides clues for pathogenesis and targeted drug therapy towards ACE2 expression for prevention and adjuvant therapy of COVID-19. äEZH2-mediated H3K27me3 inhibits ACE2 expression (epmc).pdf DeepDyve Pubget Overpricing