Abstract
Recent findings indicate that we should rethink how Myc oncoproteins transactivate their target genes. It appears that Mnt, a transcription factor that mediates transrepression at Myc's E-boxes, plays a crucial role in keeping the cell cycle in check. By removing Mnt, either via conventional knockout techniques or via RNA interference, cells become hyper-proliferative, susceptible to apoptosis and can be transformed by Ras--all hallmarks of Myc overexpression. These findings indicate that Myc's ability to function as an oncogene may rely, at least in part, on its ability to effectively antagonize Mnt's transrepression and tumor suppressor functions.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
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Basic-Leucine Zipper Transcription Factors
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism*
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Fibroblasts / cytology
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Fibroblasts / metabolism
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Gene Expression Regulation*
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Mice
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Mice, Knockout
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Proto-Oncogene Proteins c-myc / metabolism*
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RNA Interference
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Repressor Proteins / genetics
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Repressor Proteins / metabolism*
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Transcription Factors / genetics
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Transcription Factors / metabolism*
Substances
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Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
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Basic-Leucine Zipper Transcription Factors
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DNA-Binding Proteins
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Mnt protein, mouse
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Myc associated factor X
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Proto-Oncogene Proteins c-myc
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Repressor Proteins
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Transcription Factors
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Max protein, mouse