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We reported for the first time that artemisinin may induce apoptotic cell lysis depending on cancer cell type.
The low occurrence and significant delay of apoptosis among cortical neurons lacking presenilins suggest that loss of presenilins may induce apoptotic neuronal death through disruption of cellular homeostasis rather than direct activation of apoptosis pathways.
Additionally, they may induce apoptotic death by activating some apoptosis proteins like caspase-3 via an apoptosis pathway [ 28].
This results in generation of DNA strand breaks, which may induce apoptotic signal transduction and thus kill the tumour cells (Pegg, 1990; Karran and Bignami, 1994).
It has been suggested that p53 may induce apoptotic cell death by down-regulating bcl-2 and up-regulating bax expression [ 21, 22].
In addition, some evidence exists that CCl4 may induce apoptotic cell death of hepatocytes [ 44], although this might be a secondary effect and has not been investigated in more detail to date.
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How these two receptors may interact to induce apoptotic cell ingestion needs further investigation.
The figure demonstrates too that the amount of necrotic cells (left top quadrants) were much lower in treated cells than in control ones, indicating that CAERS and CFEZO agents may not only induce apoptotic cell death, but they also suppress necrotic cell death.
Previous studies have shown that hyperoxia may induce non-apoptotic or apoptotic epithelial cell death, depending on the species, cell-type specificities of hyperoxic insult, and culture condition [ 1- 9].
Moreover, when activated in stem/progenitor cells, p53 may induce their apoptotic death by stimulating pro-apoptotic proteins (like Bak proteins) or by the down-regulating anti-apoptotic factors (such as Bcl-2 and Bcl-xL) [ 14].
The increase in TS1 binding may have been due to the irradiation of the cells, which may have induced apoptotic caspase-cleavage of K18 and subsequently an increased exposure of the keratin 8 epitope [42].
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