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Molecular and Cellular Biology, April 2001, p. 2956-2966, Vol. 21, No. 8
Institut de Génétique
Moléculaire de Montpellier, CNRS UMR 5535, IFR 24, 34293 Montpellier Cedex 5, France,1 and Jordan
Laboratory, Department of Haematology, University Hospital, 3584 CX
Utrecht, The Netherlands2
Received 31 July 2000/Returned for modification 22 September
2000/Accepted 3 January 2001
E4F is a ubiquitously expressed GLI-Krüppel-related
transcription factor which has been identified for its capacity to
regulate transcription of the adenovirus E4 gene in response to E1A.
However, cellular genes regulated by E4F are still unknown. Some of
these genes are likely to be involved in cell cycle progression since ectopic p120E4F expression induces cell cycle
arrest in G1. Although p21WAF1
stabilization was proposed to mediate E4F-dependent cell cycle arrest,
we found that p120E4F can induce a
G1 block in p21
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.8.2956-2966.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Cyclin A Is a Mediator of
p120E4F-Dependent Cell Cycle Arrest in
G1

/
cells, suggesting that
other proteins are essential for the
p120E4F-dependent block in G1. We
show here that cyclin A promoter activity can be repressed by
p120E4F and that this repression correlates
with p120E4F binding to the cyclic
AMP-responsive element site of the cyclin A promoter. In addition,
enforced expression of cyclin A releases p120E4F-arrested cells from the G1
block. These data identify the cyclin A gene as a cellular target for
p120E4F and suggest a mechanism for
p120E4F-dependent cell cycle regulation.
*
Corresponding author. Mailing address: Institut de
Génétique Moléculaire de Montpellier, CNRS UMR 5535, IFR 24, 1919 Route de Mende, 34293 Montpellier Cedex 5, France. Phone:
(33) 4 67 61 36 50. Fax: (33) 4 67 04 02 31. E-mail:
vignais{at}jones.igm.cnrs-mop.fr.
Present address: IGBMC, Parc d'innovation, 67404 Illkirch, France.
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