J Biol Chem. 2003 Feb 14;278(7):4981-9. Epub 2002 Nov 21.

Association of p14ARF with the p120E4F transcriptional repressor enhances cell cycle inhibition.

Rizos H, Diefenbach E, Badhwar P, Woodruff S, Becker TM, Rooney RJ, Kefford RF.

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Westmead Institute for Cancer Research, University of Sydney, Westmead Hospital, Westmead, New South Wales 2145, Australia. helen_rizos@wmi.usyd.edu.au

Abstract

The p14(ARF) tumor suppressor is a key regulator of cellular proliferation and is frequently inactivated in human cancer. This tumor suppressor functions in the p53 and pRb cell cycle regulatory pathways and can effectively activate both pathways to induce growth arrest or cell death. We now report that p14(ARF) forms a complex with the E1A-regulated transcriptional repressor, p120(E4F). p120(E4F) contacts p14(ARF) and p53 to form a ternary complex in vivo and enhances p14(ARF)-induced G(2) cell cycle arrest in a p53-dependent manner. We suggest that the interaction of p14(ARF) and p120(E4F) forms an important link between the p14(ARF) and p53 tumor suppressor proteins, both of which exhibit enhanced cell cycle inhibitory activity in the presence of this transcriptional repressor.

PMID:: 12446718; [PubMed - indexed for MEDLINE]

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Association of p14ARF with the p120E4F transcriptional repressor enhances cell cycle inhibition.
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