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Molecular and Cellular Biology, November 1998, p. 6316-6324, Vol. 18, No. 11
Dana-Farber Cancer Institute and Harvard
Medical School1 and
Howard Hughes
Medical Institute,3 Boston, Massachusetts
02115, and
Sanofi Recherche, Labege,
France2
Received 30 April 1998/Returned for modification 11 June
1998/Accepted 27 July 1998
p73 is a recently identified member of the p53 family. Previously
it was shown that p73 can, when overproduced in p53-defective tumor
cells, activate p53-responsive promoters and induce apoptosis. In this
report we describe the generation of anti-p73 monoclonal antibodies and
confirm that two previously described p73 isoforms are produced in
mammalian cells. Furthermore, we show that these two isoforms can bind
to canonical p53 DNA-binding sites in electrophoretic mobility shift
assays. Despite the high degree of similarity between p53 and p73, we
found that adenovirus E1B 55K, simian virus 40 T, and human
papillomavirus E6 do not physically interact with p73. The observation
that viral oncoproteins discriminate between p53 and p73 suggests that
the functions of these two proteins may differ under physiological
conditions. Furthermore, they suggest that inactivation of p73 may not
be required for transformation.
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Viral Oncoproteins Discriminate between p53 and
the p53 Homolog p73
*
Corresponding author. Mailing address: Dana-Farber
Cancer Institute, 44 Binney St., Boston, MA 02115. Phone: (617)
632-3975. Fax: (617) 632-4760. E-mail:
william_kaelin{at}dfci.harvard.edu.
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