Parimal Samir

TL;DR: It is suggested that blocking the cytokine-mediated inflammatory cell death signaling pathway identified here may benefit patients with COVID-19 or other infectious and autoinflammatory diseases by limiting tissue damage/inflammation.

TL;DR: The findings suggest that macrophages use the availability of DDX3X to interpret stress signals and choose between pro-survival stress granules and pyroptotic ASC specks, and suggest a rheostat-like mechanistic paradigm for regulating live-or-die cell-fate decisions under stress conditions.

TL;DR: The activation of PANoptosis by bacterial and viral triggers is described and protein interactions that reveal the formation of a PANoptosome complex are reported, which molecules from the pyroptotic, apoptotic, and necroptotic cell death pathways interacted to form a single molecular complex that is termed the PAN optosome.

TL;DR: Putative components of the PANoptosome are reviewed and a phylogenetic analysis of their molecular domains and interaction motifs that support complex assembly are presented to present potential mechanisms governing PANoptosis based on evolutionary analysis.

TL;DR: A model of pathogen-induced priming and inhibition of TAK1 is used to demonstrate RIPK1 kinase activity–independent inflammasome activation and pyroptosis, apoptosis, and necroptosis that drive myeloid proliferation and sepsis in TAK 1-deficient animals.