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Molecular and Cellular Biology, September 2001, p. 5913-5924, Vol. 21, No. 17
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.
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
*
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.
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