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PMID:8663032

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Citation

Borner, C (1996) Diminished cell proliferation associated with the death-protective activity of Bcl-2. J. Biol. Chem. 271:12695-8

Abstract

The oncogene product Bcl-2 effectively spares cells from programmed cell death (apoptosis). The molecular mechanism underlying this death-protective activity has, however, remained enigmatic. Here we show that induction of Bcl-2 expression is consistently associated with a retardation of mammalian cell proliferation due to a prolongation of the G1 phase of the cell cycle. Whereas cells lacking Bcl-2 expression die from any point of the cell cycle in response to apoptotic agents, Bcl-2-overexpressing cells accumulate in the G0/G1 phase and are protected from cell death. Co-expression of Bax, a negative regulator of Bcl-2, reverts both the cell death protective and proliferation retarding activities of Bcl-2. Moreover, a Bcl-2 mutant defective in death protection does not affect cell division. These findings indicate that Bcl-2 contributes to cell survival by diminishing the rate of cell proliferation.

Links

PubMed

Keywords

Animals; Apoptosis/physiology; Base Sequence; Cell Division/physiology; Cell Line; DNA Primers; Mice; Molecular Sequence Data; Proto-Oncogene Proteins/physiology; Proto-Oncogene Proteins c-bcl-2; Rats

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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References

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