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Clearance of engineered Salmonella which trigger regulated cell death is dependent upon the cellular 'bucket list,' which is determined both by cell death signaling pathway and by cell type infected.

HOXA9 is a transcriptional maintenance factor for anti-apoptotic genes that accelerate MYC-driven leukemia.

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.

The phagocytic receptor CED-1 is kept at the appropriate level by E3 ligase trim-21-mediated ubiquitination-proteasomal degradation for apoptotic cell clearance, which is independent of retromer-dependent recycling and lysosomal degradation.

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.

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

Multifaceted properties of the water-soluble derivative of antibiotic heliomycin enable it to offer greater antitumor value than its parent compound by inhibiting the tNOX-NAD⁺-SIRT1 axis to induce apoptosis.

A second anti-apoptotic protein binding site in PUMA confers resistance to BH3 mimetic drugs and binds the protein to membranes.

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.

Telomere shortening with age promotes a switch from p53-dependent apoptosis to senescence prompted by tissue damage that triggers conflicting mTOR/AKT signalling, lower OxPhos defences and ROS, mitochondria dysfunction and senescence.