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PMID:8663032
Citation |
Borner, C (1996) Diminished cell proliferation associated with the death-protective activity of Bcl-2. J. Biol. Chem. 271:12695-8 |
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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. |
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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 |
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Significance
Annotations
Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
References
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