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J. Biol. Chem., Vol. 266, Issue 13, 8248-8254, 05, 1991
XK Zhang, JM Dong and JF Chiu
We show here that the alpha-fetoprotein gene (AFP) promoter can be
regulated by AP-1 activity using transient transfection assays. AFP
promoter activity induced by c-jun/c-fos can be repressed by cotransfected
glucocorticoid receptor. The DNA sequence conferring AP-1 activity was
located in the proximal promoter region. Gel retardation assays using the
AFP proximal promoter identified an AP-1-like sequence which can bind to
bacterially expressed c-jun protein. This AP-1-like element, when cloned
into the tk promoter, responds to the AP-1 activity of c-jun/c-fos products
in both CV-1 and F-9 cells. The element overlaps with a consensus
glucocorticoid-responsive element which was shown to confer negative
modulation of AFP promoter activity. A 23-base pair DNA element containing
the overlapping glucocorticoid- responsive element and AP-1 sites can be
positively regulated by glucocorticoid receptor in the absence of
c-jun/c-fos products. When plasmids expressing glucocorticoid receptor,
c-jun and c-fos are cotransfected together, they repress each other. Thus,
these data demonstrate that negative regulation of the AFP gene by
glucocorticoid may be due to the interference of AP-1 activity by
glucocorticoid receptor either by direct competition for DNA binding or via
protein- protein interaction. They provide another example of
transcriptional regulation of developing-associated genes between two major
signal transduction pathways in response to extracellular stimuli. This
supports the model that expression of alpha-fetoprotein is regulated during
development by the effect on transcription of antagonism between
glucocorticoid receptor and fos/jun.
Regulation of alpha-fetoprotein gene expression by antagonism between AP-1 and the glucocorticoid receptor at their overlapping binding site
Department of Biochemistry, University of Vermont, College of Medicine, Burlington 05405.
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