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Boolean models are effectively used to characterize large cell death signaling networks.
The active synthesis of MMPs in vitro speaks against large cell death, however, and the concentrations of anti-inflammatory molecules were chosen to match those reached in tissues in vivo after systemic administration.
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Despite this prolonged and severe fragmentation of DNA however, no large scale cell death was observed in either group.
Some studies [27], [28], [29] have linked OX1R with the apoptotic pathway, where orexin stimulates OX1R to induce large scale cell death in cancer cell lines.
No large scale cell death was apparent, which suggests that at this concentration, the main deleterious effect of mDUX is to interfere with cell and tissue movements, in addition to any effects it may have on myogenesis.
After an initial period of biotrophic infection, the morphogenetic differentiation of thin filamentous necrotrophic secondary hyphae from the thick biotrophic primary hyphae occurs and this transition, referred to as the biotrophy-necrotrophy switch, coincides with large scale cell death and tissue collapse.
However, this did not lead to large-scale cell death and the cultures eventually recovered, indicating that redundant pathways or compensating mechanisms exist to deal with H2O2 induced oxidative stress.
Notably, large-scale cell death occurred in the presence of DSTD combined with chemotherapy.
CY treatment increases the concentration of extracellular DNA levels due to the large amount of cell death, so it seems logical to surmise that DNAse may reduce the local concentration of DNA in the spleen and thus, impair the autoantigen-mediated expansion of high affinity DNA-reactive B cells.
This would explain the large effect on cell death seen in cells depleted of CK2α'.
Tumours exhibited large areas of cell death caused by ultrasound-mediated microbubble exposure.
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