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J. Biol. Chem., Vol. 278, Issue 4, 2249-2255, January 24, 2003
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From the Although extensive homology exists between
related genes p53 and p73, recent data suggest
that the family members have divergent roles. We demonstrate that the
differential regulatory roles of p53 family member p73 are highly
cell-context and promoter-specific. Full-length p73 expressed in the
transformed leukemia cell line Jurkat behaves as a specific dominant
negative transcriptional repressor of the cell cycle inhibitor gene
p21 and blocks p53-mediated apoptosis. These findings
provide evidence for a new mechanism in oncogenesis through which the
functional properties of p73 can be altered in an inheritable and
cell-specific fashion independent of transcriptional coding.
Novel Cell-specific and Dominant Negative Anti-apoptotic Roles of
p73 in Transformed Leukemia Cells*,
,,§,, and¶
Laboratory of Receptor Biology and Gene
Expression and Laboratory of Pathology, NCI, National Institutes of
Health, Bethesda, Maryland 20892 and the § Department of
Microbiology, Howard University, Washington, D. C. 20001
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
The on-line version of this article (available at
http://www.jbc.org) contains supplemental Fig. 1.
¶
To whom correspondence should be addressed: Laboratory of
Receptor Biology and Gene Expression and Laboratory of Pathology, DHHS/NCI/CCR, National Institutes of Health, Advanced Technology Center, Rm. 134C, 8717 Grovemont Circle, Bethesda, MD 20892. Tel.: 301-496-1055; Fax: 301-435-7558; E-mail: gardnerk@mail.nih.gov.
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