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J Biol Chem, Vol. 274, Issue 9, 5279-5284, February 26, 1999
From the Metal response element-binding transcription
factor-1 (MTF-1) binds specifically to metal response elements (MREs)
and transactivates metallothionein (MT) gene expression in response to
zinc and cadmium. This investigation contrasts the mechanism of mouse
MT gene (mMT-I) promoter activation by cadmium and zinc in IMR-32 human
neuroblastoma cells to determine whether MTF-1 binding to the MRE is
necessary for activation by these metals. Cadmium activated a mMT-1
promoter (
Cadmium-mediated Activation of the Metal Response Element in
Human Neuroblastoma Cells Lacking Functional Metal Response
Element-binding Transcription Factor-1
,,
Departments of Pharmacology,
150 base pairs) luciferase reporter 20-25-fold through a
MRE-dependent mechanism. In contrast, zinc had little
effect on the mMT-1 luciferase reporter. IMR-32 cells lacked MRE
binding activity, and treatment with zinc in vitro or
in vivo did not generate a MTF-1·MRE complex, suggesting
that IMR-32 cells lack functional MTF-1. Overexpression of mMTF-1
regenerated a zinc-mediated induction of the MRE without affecting
cadmium activation. Because no other transition metals tested activated
the MRE, this effect appeared to be cadmium-specific. These data
demonstrate that in IMR-32 human neuroblastoma cells, zinc and cadmium
can use independent mechanisms for activation of the mMT-I promoter and
cadmium-mediated MRE activation is independent of MTF-1 and zinc.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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