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Vol. 12, No. 15, pp. 2434-2442, August 1, 1998
1 Cold Spring Harbor Laboratory, Cold Spring Harbor, New
York 11724 USA;
2 Department of Tumor Cell Biology and
4 Howard Hughes Medical Institute, St. Jude Children's
Research Hospital, Memphis, Tennessee 38105 USA;
3 Department
of Biological Sciences, Columbia University, New York,
New York 10027 USA
The adenovirus E1A oncogene activates p53 through a
signaling pathway involving the retinoblastoma protein and the tumor
suppressor p19ARF. The ability of E1A to induce p53 and its
transcriptional targets is severely compromised in ARF-null
cells, which remain resistant to apoptosis following serum depletion or
adriamycin treatment. Reintroduction of p19ARF restores p53
accumulation and resensitizes ARF-null cells to apoptotic
signals. Therefore, p19ARF functions as part of a
p53-dependent failsafe mechanism to counter uncontrolled proliferation.
Synergistic effects between the p19ARF and DNA damage
pathways in inducing p53 may contribute to E1A's ability to enhance
radio- and chemosensitivity.
[Key Words: E1A signaling; p53; p19ARF tumor suppressor]
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