Abstract:
:Since cell death by apoptosis is achieved through complex interactions between numerous molecular components, cells may fail to die when stimulated because of molecular abnormalities in the apoptosis pathway or in its control mechanisms. Such inappropriate cell survival is well established when apoptosis is suppressed by elevated expression of bcl-2, at least for some cell types. Many cells undergo apoptosis at moderate levels of DNA damage and suppression of such apoptosis might be expected to increase the rate of mutation because of the persistence of cells with damaged DNA. We and others have now confirmed this prediction in bcl-2 transfected cells. Suppression of the apoptosis pathway can only lead to inappropriate cell survival if it relates to events before the cell becomes committed to die. We have analyzed this question for agents that inhibit the caspases, the site-specific proteases which form the biochemical core of the process of apoptosis. We have shown that inhibition of certain caspases does lead to the survival of Jurkat human T-cells induced to undergo Fas-mediated apoptosis.
journal_name
Toxicol Lettjournal_title
Toxicology lettersauthors
Williams GT,Critchlow MR,Hedge VL,O'Hare KBdoi
10.1016/s0378-4274(98)00343-9keywords:
subject
Has Abstractpub_date
1998-12-28 00:00:00pages
485-9eissn
0378-4274issn
1879-3169pii
S0378-4274(98)00343-9journal_volume
102-103pub_type
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