Structures of the death domain of the p75 neurotrophin receptor in complex with downstream effectors show how competitive protein-protein interactions orchestrate the hierarchical activation of downstream pathways in non-catalytic receptors.

Prokaryotic TRADD-N and Death-like adaptor domains in diverse predicted apoptosis and immune systems from multicellular prokaryotes and metazoans indicate the common origin of key apoptosis mechanisms required for the stabilization of multicellularity.

Autophagy is critical for the turnover of inflammatory signaling complexes containing RHIM-domain proteins.

The enzyme phosphodiesterase 2A2 localises at the mitochondrial membrane and its inhibition results in a local increase in cAMP concentration, mitochondrial elongation and resistance to apoptosis.

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

Structure-led protein engineering can expand the effector recognition profile of plant intracellular NLR immune receptors, providing a proof-of-principle for the development of novel disease resistance mechanisms in plants.

Loading of CD95 and CD95L-derived sequences into the RNA-induced silencing complex elicits a distinct form of RNAi-mediated cell death of cancer cells that results from the targeting of multiple survival genes.

Cryo-EM shows that the NADase activity of SARM1 is allosterically inhibited by physiological concentrations of NAD+ that stabilizes an auto-inhibited conformation of SARM1, explaining how NAD+ depletion may inflict neurodegeneration.

Mammalian Dscams require different intracellular interactions in different cell types during neural circuit formation to promote self-avoidance.

A cryo-electron microscopy model of the active human apoptosome illuminates how this "wheel of death" binds the protease procaspase-9 to initiate programmed cell death.