Abstract
The p16INK4a/pRB/E2F and p19ARF/p53 tumor suppressor pathways are disrupted in most human cancers. Both p19ARF and p53 are required for the induction of senescence in primary mouse embryonic fibroblasts (MEFs), but little is known about their downstream targets. Disruption of E2F-mediated transcriptional repression in MEFs caused a general increase in
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