Molecular Human Reproduction, Vol 4, 1099-1109, Copyright © 1998 by Oxford University Press
A Basu and S Haldar
Each cell is under constant surveillance to maintain the integrity of its
genome. Genomic lesions in a cell must be repaired before the onset of DNA
replication and cell division. In the scenario that the genomic lesion is
not repairable, the damaged cells are disposed in an orderly manner known
as programmed cell death or apoptosis. Apoptosis and cell cycle progression
are two intimately linked phenomena. Uncontrollable cell proliferation
perturbs the cellular homeostasis and this can lead to malignancies, as
well as organ dysfunction and developmental abnormalities. The biological
pathway controlling cell fate is sequentially organized at the molecular
level. Recent studies have made important contributions in advancing our
knowledge of the mechanisms of cell cycle control and apoptosis regulation.
A oncogene-derived protein, Bcl2, confers negative control in the pathway
of cellular suicide machinery. A Bcl2-homologous protein, Bax, promotes
cell death by competing with Bcl2. While Bax-Bax homodimers act as
apoptosis inducers, Bcl2-Bax heterodimer formation evokes a survival signal
for the cells. Both Bcl2 and Bax are transcriptional targets for the tumour
suppressor protein, p53, which induces cell cycle arrest or apoptosis in
response to DNA damage. In all, the coordinate performance of these
molecules is crucial for controlling life and death of a cell.
REVIEW, TUTORIAL
The relationship between BcI2, Bax and p53: consequences for cell cycle progression and cell death
Rammelkamp Center for Education & Research, Department of Pharmacology, MetroHealth/Case Western Reserve University, Cleveland, OH 44109-1998, USA.
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