Anna Senik

TL;DR: A novel sequence of events in which Cat D triggers Bax activation, Bax induces the selective release of mitochondrial AIF, and the latter is responsible for the early apoptotic phenotype is defined.

TL;DR: It appears that all structures involved in the maintenance and pre-apoptotic disruption of the delta psi m, as well as a mitochondrial apoptotic factor(s), are present in rho [symbol: see text] cells and thus are controlled by the nuclear rather than by the mitochondrial genome.

TL;DR: In activated T cells, anti-CD2 and staurosporine induce a caspase-independent cell death pathway that exhibits prominent cytoplasmic features of apoptosis, however, casp enzyme activation is required for the proteolytic degradation of nuclear substrates such as PARP and lamins together with the DNA fragmentation and extreme chromatin condensation that occur in apoptotic cells.

TL;DR: A commitment phase to apoptosis was defined that is entirely caspase independent and that is characterized by cell volume loss, partial chromatin condensation, and release into the cytosol and the nucleus of mitochondrial ‘‘apoptosis-inducing factor ’’ (AIF).

TL;DR: Evidence is now accumulating that a caspase-independent pathway exists, shown by in vitro experiments with broad-range caspases inhibitors, that is triggered first in activated T lymphocytes subjected to apoptotic stimuli that do not rely on receptors with death domains.