The amyloid oligomers and fibrils may induce cell membrane disruption and lead to cell apoptosis.
Foam may induce cell death, and may limit the performance of down-stream processing steps.
Although IAP antagonists in Drosophila such as Reaper, Hid and Grim may induce cell death without mitochondrial membrane permeabilization, it is surprising that all three localize to mitochondria.
Bem1 may induce cell polarization by mediating a positive feedback loop whereby Cdc24 is preferentially recruited/activated at the site of Cdc42GTP accumulation [19], [20], [21].
Exogenous agents that increase ROS generation or decrease antioxidant capacity will shift the redox balance and result in an overall increase in the level of ROS, which when above a cellular tolerability threshold may induce cell death [11].
In contrast, an excessive autophagy rate may induce cell death.
These data suggest that sigma-2 ligands may induce cell death by impairing cell-cycle progression.
Furthermore, t-BHP-induces a cellular redox imbalance may induce cell apoptosis [ 5].
CHOP may induce cell death by promoting protein synthesis and oxidation in the stressed ER.
DNA damaging agents may induce cell cycle arrest and induce autophagy and mitophagy, by delaying apoptosis.
Hence, niclosamide may induce cell death in myeloma cells in part by inhibiting STAT3 activation.
