These findings suggest that at least one of the biochemical steps required for mitosis, activation of cyclin A-dependent protein kinases, is an important event during apoptosis
2006
Key concepts
Scholarcy highlights
- HeLa cells by staurosporine, caffeine, 6-dimethylaminopurine, and okadak acid, agents that activate M-phase-promoting factor and induce premature mitosis in treated hamster cel lines
- In an initial attempt to understand the mechanisms by which bcl-2 suppresses apoptosis, we examined the subcellular distribution of cyclins and cyclin-dependent protein kinase in Bcl-2+ and control cells
- Apoptosis shares a number of morphological features with mitosis, including cell rounding, surface blebbing, lamin disassembly, and chromatin condensation
- We have shown that apoptosis can be induced in HeLa cells by the same chemical agents known to induce premature mitosis in hamster cells and that overexpression of bcl-2 blocks this response
- The induction of apoptosis was accompanied in all cases by activation ofcyclin A-dependent protein kinases
- Staurosporine, and okadaic acid are known to activate cyclin B-Cdc2 in S-phase-arrested hamster cells, to our knowledge, stimulation of cyclin A-dependent kinase activity has not been recognized as a consequence of tumor necrosis factor a binding
- tumor necrosis factor a and chemicals related to staurosporine, okadaic acid, caffeine, or 6-DMAP might, be used in conjunction with an S-phasearresting agent such as HU to selectively kill actively dividing tumor cells
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