SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation - Pan, Pan; Shen, Miaomiao; Yu, Zhenyang; Ge, Weiwei; Chen, Keli; Tian, Mingfu; Xiao, Feng; Wang, Zhenwei; Wang, Jun; Jia, Yaling; Wang, Wenbiao; Wan, Pin; et al. (Nature communications, 2021)
Keywords: 13/109; 13/21; 13/51; 13/89; 14/19; 38; 42; 45; 45/111; 631/250/254; 631/250/256/2177; 631/326/596/2553; 82/51; 96/95; Animal models; Animals; Caspase-1; Cells, Cultured; Coronavirus Nucleocapsid Proteins - metabolism; Coronaviruses; COVID-19; COVID-19 - metabolism; COVID-19 - virology; Cytokine storm; Cytokines; Cytokines - metabolism; HEK293 Cells; Humanities and Social Sciences; Humans; IL-1β; Infections; Inflammasomes; Inflammasomes - genetics; Inflammasomes - metabolism; Inflammation; Inflammation - metabolism; Inhibitors; Interleukin 6; Lung Injury - genetics; Lung Injury - metabolism; Lungs; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; multidisciplinary; N protein; NLR Family, Pyrin Domain-Containing 3 Protein - genetics; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism; Phosphoproteins - metabolism; Protein Binding; Proteins; SARS-CoV-2 - metabolism; SARS-CoV-2 - physiology; Science; Science (multidisciplinary); Sepsis; Severe acute respiratory syndrome coronavirus 2; THP-1 Cells; Viral diseases