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10.1016/j.molcel.2022.04.033 http://scihub22266oqcxt.onion/10.1016/j.molcel.2022.04.033 35594856!9108100!35594856     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cell 2022 ; 82 (13): 2385-2400.e9 Nephropedia Template TP {{tp|p=35594856|t=2022. Human NLRP1 is a sensor of pathogenic coronavirus 3CL proteases in lung epithelial cells |pdf=|usr=}}{{35594856}} gab.com Text Human NLRP1 is a sensor of pathogenic coronavirus 3CL proteases in lung epithelial cells JO: Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=35594856 #FOAvip Inflammation observed in SARS-CoV-2-infected patients suggests that inflammasomes, proinflammatory intracellular complexes, regulate various steps of infection. Lung epithelial cells express inflammasome-forming sensors and constitute the primary entry door of SARS-CoV-2. Here, we describe that the NLRP1 inflammasome detects SARS-CoV-2 infection in human lung epithelial cells. Specifically, human NLRP1 is cleaved at the Q333 site by multiple coronavirus 3CL proteases, which triggers inflammasome assembly and cell death and limits the production of infectious viral particles. Analysis of NLRP1-associated pathways unveils that 3CL proteases also inactivate the pyroptosis executioner Gasdermin D (GSDMD). Subsequently, caspase-3 and GSDME promote alternative cell pyroptosis. Finally, analysis of pyroptosis markers in plasma from COVID-19 patients with characterized severe pneumonia due to autoantibodies against, or inborn errors of, type I interferons (IFNs) highlights GSDME/caspase-3 as potential markers of disease severity. Overall, our findings identify NLRP1 as a sensor of SARS-CoV-2 infection in lung epithelia. Twit Text FOAVip Human NLRP1 is a sensor of pathogenic coronavirus 3CL proteases in lung epithelial cells ????Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=35594856 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35594856 #FOAvip English Wikipedia <ref>{{Cite pmid|35594856}}</ref> Human NLRP1 is a sensor of pathogenic coronavirus 3CL proteases in lung epithelial cells #MMPMID35594856 Planes R; Pinilla M; Santoni K; Hessel A; Passemar C; Lay K; Paillette P; Valadao AC; Robinson KS; Bastard P; Lam N; Fadrique R; Rossi I; Pericat D; Bagayoko S; Leon-Icaza SA; Rombouts Y; Perouzel E; Tiraby M; Zhang Q; Cicuta P; Jouanguy E; Neyrolles O; Bryant CE; Floto AR; Goujon C; Lei FZ; Martin-Blondel G; Silva S; Casanova JL; Cougoule C; Reversade B; Marcoux J; Ravet E; Meunier E Mol Cell 2022[Jul]; 82 (13): 2385-2400.e9 PMID35594856show ga Inflammation observed in SARS-CoV-2-infected patients suggests that inflammasomes, proinflammatory intracellular complexes, regulate various steps of infection. Lung epithelial cells express inflammasome-forming sensors and constitute the primary entry door of SARS-CoV-2. Here, we describe that the NLRP1 inflammasome detects SARS-CoV-2 infection in human lung epithelial cells. Specifically, human NLRP1 is cleaved at the Q333 site by multiple coronavirus 3CL proteases, which triggers inflammasome assembly and cell death and limits the production of infectious viral particles. Analysis of NLRP1-associated pathways unveils that 3CL proteases also inactivate the pyroptosis executioner Gasdermin D (GSDMD). Subsequently, caspase-3 and GSDME promote alternative cell pyroptosis. Finally, analysis of pyroptosis markers in plasma from COVID-19 patients with characterized severe pneumonia due to autoantibodies against, or inborn errors of, type I interferons (IFNs) highlights GSDME/caspase-3 as potential markers of disease severity. Overall, our findings identify NLRP1 as a sensor of SARS-CoV-2 infection in lung epithelia. |*COVID-19/genetics/metabolism/virology[MESH] |*Coronavirus 3C Proteases/genetics/metabolism[MESH] |*Epithelial Cells/metabolism[MESH] |*Inflammasomes/genetics/metabolism[MESH] |*NLR Proteins/genetics/metabolism[MESH] |*SARS-CoV-2/enzymology/genetics/metabolism/pathogenicity[MESH] |Caspase 3/metabolism[MESH] |Humans[MESH] |Lung/metabolism/virology[MESH] |Peptide Hydrolases/genetics/metabolism[MESH] |Phosphate-Binding Proteins/genetics/metabolism[MESH] |Pore Forming Cytotoxic Proteins/genetics/metabolism[MESH]Human NLRP1 is a sensor of pathogenic coronavirus 3CL proteases in lun(epmc).pdf DeepDyve Pubget Overpricing