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10.1038/s41392-021-00653-w http://scihub22266oqcxt.onion/10.1038/s41392-021-00653-w 34117216!8193598!34117216     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Signal+Transduct+Target+Ther 2021 ; 6 (1): 233 Nephropedia Template TP {{tp|p=34117216|t=2021. Molecular mechanism of interaction between SARS-CoV-2 and host cells and interventional therapy |pdf=|usr=}}{{34117216}} gab.com Text Molecular mechanism of interaction between SARS-CoV-2 and host cells and interventional therapy JO: Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=34117216 #FOAvip The pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has resulted in an unprecedented setback for global economy and health. SARS-CoV-2 has an exceptionally high level of transmissibility and extremely broad tissue tropism. However, the underlying molecular mechanism responsible for sustaining this degree of virulence remains largely unexplored. In this article, we review the current knowledge and crucial information about how SARS-CoV-2 attaches on the surface of host cells through a variety of receptors, such as ACE2, neuropilin-1, AXL, and antibody-FcgammaR complexes. We further explain how its spike (S) protein undergoes conformational transition from prefusion to postfusion with the help of proteases like furin, TMPRSS2, and cathepsins. We then review the ongoing experimental studies and clinical trials of antibodies, peptides, or small-molecule compounds with anti-SARS-CoV-2 activity, and discuss how these antiviral therapies targeting host-pathogen interaction could potentially suppress viral attachment, reduce the exposure of fusion peptide to curtail membrane fusion and block the formation of six-helix bundle (6-HB) fusion core. Finally, the specter of rapidly emerging SARS-CoV-2 variants deserves a serious review of broad-spectrum drugs or vaccines for long-term prevention and control of COVID-19 in the future. Twit Text FOAVip Molecular mechanism of interaction between SARS-CoV-2 and host cells and interventional therapy ????Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=34117216 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34117216 #FOAvip English Wikipedia <ref>{{Cite pmid|34117216}}</ref> Molecular mechanism of interaction between SARS-CoV-2 and host cells and interventional therapy #MMPMID34117216 Zhang Q; Xiang R; Huo S; Zhou Y; Jiang S; Wang Q; Yu F Signal Transduct Target Ther 2021[Jun]; 6 (1): 233 PMID34117216show ga The pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has resulted in an unprecedented setback for global economy and health. SARS-CoV-2 has an exceptionally high level of transmissibility and extremely broad tissue tropism. However, the underlying molecular mechanism responsible for sustaining this degree of virulence remains largely unexplored. In this article, we review the current knowledge and crucial information about how SARS-CoV-2 attaches on the surface of host cells through a variety of receptors, such as ACE2, neuropilin-1, AXL, and antibody-FcgammaR complexes. We further explain how its spike (S) protein undergoes conformational transition from prefusion to postfusion with the help of proteases like furin, TMPRSS2, and cathepsins. We then review the ongoing experimental studies and clinical trials of antibodies, peptides, or small-molecule compounds with anti-SARS-CoV-2 activity, and discuss how these antiviral therapies targeting host-pathogen interaction could potentially suppress viral attachment, reduce the exposure of fusion peptide to curtail membrane fusion and block the formation of six-helix bundle (6-HB) fusion core. Finally, the specter of rapidly emerging SARS-CoV-2 variants deserves a serious review of broad-spectrum drugs or vaccines for long-term prevention and control of COVID-19 in the future. |*Host-Pathogen Interactions[MESH] |*Virus Attachment[MESH] |*Virus Internalization[MESH] |COVID-19/epidemiology/*metabolism/pathology/*therapy[MESH] |Humans[MESH]Molecular mechanism of interaction between SARS-CoV-2 and host cells a(epmc).pdf DeepDyve Pubget Overpricing