Inflamasomme inhibition prevents immune activation, HIV-1 pathogenesis and the splenic content of HIV-1 total DNA in humanized mice when administrated early after HIV-1 infection.

Purified Pannexin 1 channels activated by caspase cleavage in proteoliposomes reconstitute a permeation pathway for intercellular signaling molecules important in inflammation and cell clearance.

Amphibians, reptiles, and birds engage pyroptosis using caspase-1 and GSDMA, filling an evolutionary gap in which caspase-1 cleaves GSDME in fish and GSDMD in mammals.

Cleavage of pannexin-1 channel by caspases facilitates the loss of intracellular ATP level and attenuates glycolytic metabolism of apoptotic cells.

The cryo-EM structures of XKR9 define the architecture and caspase-mediated activation of a protein family that is involved in the exposure of phosphatidylserine during apoptosis leading to the engulfment of apoptotic cells by macrophages.

Retention of Caspase-8 confers a selective advantage to glioblastoma and represents a novel therapeutic target.

Caspase-11 catalytic activity and autoprocessing play key roles upstream rather than downstream of its assembly into higher-order inflammasome complexes in response to cytosolic bacterial lipopolysaccharide.

Characterization of the effects of complement- and inflammasome-mediated inflammation on choroidal neovascularization in a mouse model of neovascular age-related macular degeneration suggests synergistic benefits from targeting both forms of inflammation.

A picorna-like virus promotes the accumulation of caspase-cleaved drosophila inhibitor of apoptosis 1 by inducing the degradation of NTAN1, a key N-end rule degradation pathway component, leading to apoptosis inhibition and viral replication enhancement.

Rab11a-mediated endosomal trafficking in macrophages regulates potassium channel localization and activity at the cell surface and the downstream activation of the inflammasome and is a potential therapeutic target in acute or chronic inflammatory states.