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Molecular and Cellular Biology, September 2001, p. 5913-5924, Vol. 21, No. 17
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.17.5913-5924.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

AMF1 (GPS2) Modulates p53 Transactivation

Yu-Cai Peng, Felix Kuo, David E. Breiding, Yu-Fang Wang, Claire P. Mansur, and Elliot J. Androphy*

Department of Dermatology, New England Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02111

Received 3 January 2001/Returned for modification 8 February 2001/Accepted 1 June 2001

We have reported that the papillomavirus E2 protein binds the nuclear factor AMF1 (also called G-protein pathway suppressor 2 or GPS2) and that their interaction is necessary for transcriptional activation by E2. It has also been shown that AMF1 can influence the activity of cellular transcription factors. These observations led us to test whether AMF1 regulates the functions of p53, a critical transcriptional activator that integrates stress signals and regulates cell cycle and programmed cell death. We report that AMF1 associates with p53 in vivo and in vitro and facilitates the p53 response by augmenting p53-dependent transcription. Overexpression of AMF1 in U2OS cells increases basal level p21WAF1/CIP1 expression and causes a G1 arrest. U2OS cells stably overexpressing AMF1 show increased apoptosis upon exposure to UV irradiation. These data demonstrate that AMF1 modulates p53 activities.

* Corresponding author. Mailing address: Department of Dermatology, New England Medical Center, Box 166, 750 Washington St., Boston, MA 02111. Phone: (617) 636-1493. Fax: (617) 636-6190. E-mail: eandrophy{at}lifespan.org.

Molecular and Cellular Biology, September 2001, p. 5913-5924, Vol. 21, No. 17
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.17.5913-5924.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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