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Papers In Press, published online ahead of print March 21, 2002
Hematology/Oncology, Children's Hospital of Pittsburgh, Pittsburgh, PA 15213
Corresponding Author: edward_prochownik{at}poplar.chp.edu
Using cDNA microarrays, we recently identified a large number of transcripts that are differentially regulated by the c-Myc oncoprotein in myeloid cells. Here, we characterize here one of these, termed MT-MC1 (Myc Target in Myeloid Cells-1). MT-MC1 is a widely expressed nuclear protein whose over-expression, unlike that of previously reported c-Myc targets, recapitulates multiple c-Myc phenotypes. These include promotion of apoptosis, alteration of morphology, enhancement of anchorage-independent growth, tumorigenic conversion, promotion of genomic instability, and inhibition of hematopoietic differentiation. The MT-MC1 promoter is a direct c-Myc target; it contains two consensus E-box elements, both of which bind c-Myc-Max heterodimers. Mutation of either site abrogates DNA binding by c-Myc-Max and renders the promoter c-Myc unresponsive. Finally, MT-MC1 regulates the expression of several other c-Myc target genes. MT-MC1 represents a proximal and direct c-Myc target that recapitulates many of the properties typically associated with Myc oncoprotein over-expression.
J. Biol. Chem, 10.1074/jbc.M200860200
Submitted on January 28, 2002
Revised on March 19, 2002
Accepted on March 20, 2002
MT-MC1, a novel c-Myc target, recapitulates multiple c-Myc phenotypes
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