Sentence examples for full cell death from inspiring English sources
The appearance of 100% CPE was observed in HEp-2 at 48 hpi, whereas full cell death was observed at 120 hpi in CHO-K1 cells.
These results altogether indicate that in a p53- and BAX-independent context Sall2 is needed for Noxa induction, a necessary step for full cell death response to doxorubicin in Jurkat cells.
In sharp contrast, TRAIL triggered full-blown cell death induction in HCT116 PIK3CA-mut cells treated with proteasome inhibitors such as bortezomib and MG132.
Indeed, pre-treatment with the proteasome inhibitors bortezomib or MG132 resulted in almost full-blown cell death induction, whereas the proteasome inhibitors alone showed only modest cytotoxic activity.
Clearance of dying cells during salivary gland development in Drosophila melanogaster involves autophagy and in this context it appears that the full-blown cell death response is dependent on caspases and ATGs (Ref. 100).
Furthermore, while caspase-8/-10 actisity is required for the full induction of cell death with treatment, the death receptor pathways are not.
It is therefore likely that the full range of cell death pathways induced by gzmB has evolved due to selective pressure from pathogens like ECTV via its strategy to inhibit selective apoptosis pathways.
Thus one potential explanation for the full suppression of cell death in lesion mimics when both sid2 and eds1 are mutated could be that both nuclear and cytosolic regulators of cell death are removed.
However, when insufficient ROS are produced to induce acute cellular demise, cells will suffer from prolonged oxidative stress whereby the intracellular antioxidative capacity is reduced in the absence of full execution of cell death pathways.
These results may indicate that DDC has the ability to identify early apoptotic cells and that use of TUNEL alone may not reveal the full spectrum of cell death stages.
Results showed that the caspase-3-selective inhibitor provided full protection against cell death induced by this N-BP, thus implicating activation of caspase-3 in its mechanism of action.
