Regulation of a Senescence Checkpoint Response by the E2F1 Transcription Factor and p14 ^ARF Tumor Suppressor

Abstract excerpt

Normal cells do not divide indefinitely due to a process known as replicative senescence. Human cells arrest growth with a senescent phenotype when they acquire one or more critically short telomeres as a consequence of cell division. Recent evidence suggests that certain types of DNA damage, chromatin remodeling, and oncogenic forms of Ras or Raf can also elicit a senescence response. We show here that E2F1, a...

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