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10.1016/j.cellsig.2021.110064 http://scihub22266oqcxt.onion/10.1016/j.cellsig.2021.110064 34146659!8213541!34146659     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Signal 2021 ; 85 (ä): 110064 Nephropedia Template TP {{tp|p=34146659|t=2021. TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2 |pdf=|usr=}}{{34146659}} gab.com Text TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2 JO: Cell Signal http://www.kidney.de/pget.php?&tw=1&pmid=34146659 #FOAvip Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease 2019, it binds to angiotensin-converting enzyme 2 (ACE2) to enter into human cells. The expression level of ACE2 potentially determine the susceptibility and severity of COVID-19, it is thus of importance to understand the regulatory mechanism of ACE2 expression. Tripartite motif containing 28 (TRIM28) is known to be involved in multiple processes including antiviral restriction, endogenous retrovirus latency and immune response, it is recently reported to be co-expressed with SARS-CoV-2 receptor in type II pneumocytes; however, the roles of TRIM28 in ACE2 expression and SARS-CoV-2 cell entry remain unclear. This study showed that knockdown of TRIM28 induces ACE2 expression and increases pseudotyped SARS-CoV-2 cell entry of A549 cells and primary pulmonary alveolar epithelial cells (PAEpiCs). In a co-culture model of NK cells and lung epithelial cells, our results demonstrated that NK cells inhibit TRIM28 and promote ACE2 expression in lung epithelial cells, which was partially reversed by depletion of interleukin-2 and blocking of granzyme B in the co-culture medium. Furthermore, TRIM28 knockdown enhanced interferon-gamma (IFN-gamma)- induced ACE2 expression through a mechanism involving upregulating IFN-gamma receptor 2 (IFNGR2) in both A549 and PAEpiCs. The upregulated ACE2 induced by TRIM28 knockdown and co-culture of NK cells was partially reversed by dexamethasone in A549 cells. Our study identified TRIM28 as a novel regulator of ACE2 expression and SARS-CoV-2 cell entry. Twit Text FOAVip TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2 ????Cell Signal http://www.kidney.de/pget.php?&tw=1&pmid=34146659 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34146659 #FOAvip English Wikipedia <ref>{{Cite pmid|34146659}}</ref> TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2 #MMPMID34146659 Wang Y; Fan Y; Huang Y; Du T; Liu Z; Huang D; Wang Y; Wang N; Zhang P Cell Signal 2021[Sep]; 85 (ä): 110064 PMID34146659show ga Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease 2019, it binds to angiotensin-converting enzyme 2 (ACE2) to enter into human cells. The expression level of ACE2 potentially determine the susceptibility and severity of COVID-19, it is thus of importance to understand the regulatory mechanism of ACE2 expression. Tripartite motif containing 28 (TRIM28) is known to be involved in multiple processes including antiviral restriction, endogenous retrovirus latency and immune response, it is recently reported to be co-expressed with SARS-CoV-2 receptor in type II pneumocytes; however, the roles of TRIM28 in ACE2 expression and SARS-CoV-2 cell entry remain unclear. This study showed that knockdown of TRIM28 induces ACE2 expression and increases pseudotyped SARS-CoV-2 cell entry of A549 cells and primary pulmonary alveolar epithelial cells (PAEpiCs). In a co-culture model of NK cells and lung epithelial cells, our results demonstrated that NK cells inhibit TRIM28 and promote ACE2 expression in lung epithelial cells, which was partially reversed by depletion of interleukin-2 and blocking of granzyme B in the co-culture medium. Furthermore, TRIM28 knockdown enhanced interferon-gamma (IFN-gamma)- induced ACE2 expression through a mechanism involving upregulating IFN-gamma receptor 2 (IFNGR2) in both A549 and PAEpiCs. The upregulated ACE2 induced by TRIM28 knockdown and co-culture of NK cells was partially reversed by dexamethasone in A549 cells. Our study identified TRIM28 as a novel regulator of ACE2 expression and SARS-CoV-2 cell entry. |Alveolar Epithelial Cells/metabolism/virology[MESH] |Angiotensin-Converting Enzyme 2/*drug effects/immunology[MESH] |Antiviral Agents/*pharmacology[MESH] |Epithelial Cells/metabolism/virology[MESH] |Humans[MESH] |Lung/metabolism/virology[MESH] |Peptidyl-Dipeptidase A/metabolism[MESH] |SARS-CoV-2/*pathogenicity[MESH] |Tripartite Motif-Containing Protein 28/drug effects/*immunology[MESH]TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2 (epmc).pdf DeepDyve Pubget Overpricing