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J. Biol. Chem., Vol. 276, Issue 19, 16310-16317, May 11, 2001
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From the Department of Pathology, Harvard Medical School and
§ Department of Radiation Biology, Harvard School of Public
Health, Boston, Massachusetts 02115
p300 and CREB-binding protein (CBP) are related
transcriptional coactivators that possess histone acetyltransferase
activity. Inactivation of p300/CBP is part of the mechanism by which
adenovirus E1A induces oncogenic transformation of cells. Recently, the
importance of p300/CBP has been demonstrated directly in several
organisms including mouse, Drosophila, and
Caenorhabditis elegans where p300/CBP play an indispensable
role in differentiation, in patterning, and in cell fate determination
and proliferation during development. CBP/p300s are modified by
phosphorylation during F9 cell differentiation as well as adenovirus
infection, suggesting that phosphorylation may play a role in the
regulation of p300/CBP activity. Here we show that the
mitogen-activated/extracellular response kinase kinase 1 (MEKK1)
enhances p300-mediated transcription. We identify several domains
within p300 that can respond to MEKK1-induced transcriptional
activation. Interestingly, activation of p300-mediated transcription by
MEKK1 does not appear to require the downstream kinase JNK and may
involve either a direct phosphorylation of p300 by MEKK1 or by other
non-JNK MEKK1-directed downstream kinases. Finally, we present evidence
that p300 is important for MEKK1 to induce apoptosis. Taken together,
these results identify MEKK1 as a kinase that is likely to be involved
in the regulation of the transactivation potential of p300 and support
a role of p300 in MEKK1-induced apoptosis.
Stimulation of p300-mediated Transcription by
the Kinase MEKK1*
,
*
This work was supported in part by National Institutes of
Health Grant GM58012 (to Y. S.).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.
Supported by a Spanish Government fellowship and by a Taplin
Postdoctoral fellowship.
¶
To whom correspondence should be addressed: Dept. of
Pathology, Harvard Medical School, Warren Alpert Bldg., Rm. 120, 200 Longwood Ave., Boston, MA 02115. Tel.: 617-432-4318; Fax: 617-432-1313; E-mail: yang_shi@hms.harvard.edu.
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