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Following
DNA damage, e.g. by radiation, p53 levels rise, and
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proliferating
cells arrest in G1. This allows time for DNA repair
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prior
to the next round of replication. This arrest is mediated by
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stimulation
of expression of p21CIP1, the cyclin kinase inhibitor.
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Very
high p53 levels, or susceptible cell types, e.g. lymphocytes,
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are
triggered to undergo apoptosis. Bcl-2 acts between p53 and the
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caspase:
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