Myc expression is shown to cause sublethal activation of Caspase-3 and downstream endonuclease G, which causes DNA double strand breaks and oncogenic transformation in human cells.

Genetic labeling of cells that survive executioner caspase activity in Drosophila reveals distinct patterns in different tissues.

Functional divergence of caspase 3 and 7 in vertebrate is mediated by key residue mutation.

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

A phosphorylation of receptor interacting RIPK3 switches its pro-necroptosis function to apoptosis that promotes luteal regression which induced by Prostaglandin F2alpha.

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.

Zika virus infection induces the gasdermin E-mediated pyroptosis in placental cells through TNF-α-caspase-8-caspase-3 signaling pathway, which contributes to adverse fetal outcomes in pregnant mouse model.

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.

A broadly used gene expression regulatory mechanism inactivates targets by CED-3-caspase-mediated proteolysis and works in parallel to miRNAs for diverse non-apoptotic developmental functions.