The output data from the genome-wide cell death screen were curated by further optimizing the automated counting parameters, and by removing any miscounted replicates and other artifacts identified upon inspection.
Overexpression of the C.elegans p53 homolog, cep- 1, caused wide-spread cell death independently of caspase activation.
Organotypic hippocampal slices were pre-treated with sAPPα (0.03-10 nM) or PBS for 24 h before treatment with NMDA (30 μM, 30 min) to induce partial, hippocampal-wide neuronal cell death.
Cytomegalovirus ensures its own survival in the host cells, producing a wide range of cell death suppressors [ 136], among these is a viral mitochondrion-localized inhibitor of apoptosis (vMIA) with a wide anti-apoptotic activity against both extrinsic and intrinsic apoptosis-inducing stimuli.
A wide range of cell death assays have been developed for cell culture and histopathology, and there is an ongoing community effort to translate these methods to the clinic.
Classical apoptosis is caused by the activation of caspases, a family of intracellular cysteine proteases that lie in a latent state in cells but become activated in response to a wide variety of cell death stimuli [ 2].
Samples were analyzed for genome-wide modulation of cell death pathways, differential activation of p53, and the role of survivin family molecules in drug resistance.
Thus, the vast majority of the literature on caspase-1 has focussed on its role in inflammation, with a wider role in cell death rarely considered, except for the pyroptotic cell death of macrophages associated with infection by intracellular pathogens.
It has been described that LLO is highly lytic for the nucleated cells and it can induce a wide range of different cell death types [ 9– 23].
It was the early electron microscopic investigations of Kerr et al. (1972) and Wyllie et al. (1980) that led to their formulation of the concept of apoptosis as a wide-spread form of cell death in a variety of tissues and physiological situations.
In this regard it is of interest that not only are levels of KLK6 significantly elevated in high-grade glioma (glioblastoma multiforme (GBM), grade IV astrocytoma) and associated with poor patient survival, but in addition KLK6 promotes the resistance of glioma cells to a wide variety of cell death-inducing agents, including staurosporine, cisplatin, radiation and temozolomide [ 5].
