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J Biol Chem, Vol. 274, Issue 4, 1879-1882, January 22, 1999
B and p53 Signaling
From the Vascular Research Division, Department of Pathology,
Brigham and Women's Hospital and Harvard Medical School,
Boston, Massachusetts 02115
Transcriptional coactivators may function as
nuclear integrators by coordinating diverse signaling events. Here we
show that the p65 (RelA) component of nuclear factor-
B (NF-B) and
p53 mutually repress each other's ability to activate transcription. Additionally, tumor necrosis factor-activated NF-B is inhibited by
UV light-induced p53. Both p65 and p53 depend upon the coactivator CREB-binding protein (CBP) for maximal activity. Increased levels of
the coactivator relieve p53-mediated repression of NF-B activity and
p65-mediated repression of p53-dependent gene expression. Nuclear competition for limiting amounts of CBP provides a novel mechanism for altering the balance between the expression of
NF-B-dependent proliferation or survival genes and
p53-dependent genes involved in cell cycle arrest and apoptosis.
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