Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/s41467-021-21972-0 http://scihub22266oqcxt.onion/10.1038/s41467-021-21972-0 33741941!7979852!33741941     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2021 ; 12 (1): 1726 Nephropedia Template TP {{tp|p=33741941|t=2021. Alpha-1 antitrypsin inhibits TMPRSS2 protease activity and SARS-CoV-2 infection |pdf=|usr=}}{{33741941}} gab.com Text Alpha-1 antitrypsin inhibits TMPRSS2 protease activity and SARS-CoV-2 infection JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=33741941 #FOAvip SARS-CoV-2 is a respiratory pathogen and primarily infects the airway epithelium. As our knowledge about innate immune factors of the respiratory tract against SARS-CoV-2 is limited, we generated and screened a peptide/protein library derived from bronchoalveolar lavage for inhibitors of SARS-CoV-2 spike-driven entry. Analysis of antiviral fractions revealed the presence of alpha(1)-antitrypsin (alpha(1)AT), a highly abundant circulating serine protease inhibitor. Here, we report that alpha(1)AT inhibits SARS-CoV-2 entry at physiological concentrations and suppresses viral replication in cell lines and primary cells including human airway epithelial cultures. We further demonstrate that alpha(1)AT binds and inactivates the serine protease TMPRSS2, which enzymatically primes the SARS-CoV-2 spike protein for membrane fusion. Thus, the acute phase protein alpha(1)AT is an inhibitor of TMPRSS2 and SARS-CoV-2 entry, and may play an important role in the innate immune defense against the novel coronavirus. Our findings suggest that repurposing of alpha(1)AT-containing drugs has prospects for the therapy of COVID-19. Twit Text FOAVip Alpha-1 antitrypsin inhibits TMPRSS2 protease activity and SARS-CoV-2 infection ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=33741941 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33741941 #FOAvip English Wikipedia <ref>{{Cite pmid|33741941}}</ref> Alpha-1 antitrypsin inhibits TMPRSS2 protease activity and SARS-CoV-2 infection #MMPMID33741941 Wettstein L; Weil T; Conzelmann C; Muller JA; Gross R; Hirschenberger M; Seidel A; Klute S; Zech F; Prelli Bozzo C; Preising N; Fois G; Lochbaum R; Knaff PM; Mailander V; Standker L; Thal DR; Schumann C; Stenger S; Kleger A; Lochnit G; Mayer B; Ruiz-Blanco YB; Hoffmann M; Sparrer KMJ; Pohlmann S; Sanchez-Garcia E; Kirchhoff F; Frick M; Munch J Nat Commun 2021[Mar]; 12 (1): 1726 PMID33741941show ga SARS-CoV-2 is a respiratory pathogen and primarily infects the airway epithelium. As our knowledge about innate immune factors of the respiratory tract against SARS-CoV-2 is limited, we generated and screened a peptide/protein library derived from bronchoalveolar lavage for inhibitors of SARS-CoV-2 spike-driven entry. Analysis of antiviral fractions revealed the presence of alpha(1)-antitrypsin (alpha(1)AT), a highly abundant circulating serine protease inhibitor. Here, we report that alpha(1)AT inhibits SARS-CoV-2 entry at physiological concentrations and suppresses viral replication in cell lines and primary cells including human airway epithelial cultures. We further demonstrate that alpha(1)AT binds and inactivates the serine protease TMPRSS2, which enzymatically primes the SARS-CoV-2 spike protein for membrane fusion. Thus, the acute phase protein alpha(1)AT is an inhibitor of TMPRSS2 and SARS-CoV-2 entry, and may play an important role in the innate immune defense against the novel coronavirus. Our findings suggest that repurposing of alpha(1)AT-containing drugs has prospects for the therapy of COVID-19. |*COVID-19 Drug Treatment[MESH] |Antibodies, Viral/blood[MESH] |Antiviral Agents/pharmacology[MESH] |COVID-19/blood[MESH] |Caco-2 Cells[MESH] |Humans[MESH] |Immunoglobulin G/blood[MESH] |Molecular Docking Simulation[MESH] |SARS-CoV-2/*drug effects[MESH] |Serine Endopeptidases/*metabolism[MESH] |Serine Proteinase Inhibitors/*pharmacology[MESH] |Spike Glycoprotein, Coronavirus/metabolism[MESH] |Virus Internalization/drug effects[MESH] |Virus Replication/drug effects[MESH]Alpha-1 antitrypsin inhibits TMPRSS2 protease activity and SARS-CoV-2 (epmc).pdf DeepDyve Pubget Overpricing