Abstract
Myc proteins play a central role in promoting cell proliferation and contribute to a diverse array of cancers. My function appears completely dependent on heterodimerization with Max through related bHLHZip regions. Max interaction with Myc is required for DNA binding at so-called E-box sequences and Myc-dependent transcriptional activation. The repressor with similar DNA binding specificity raised the possibility that Mnt may serve a general role as a Myc antagonist.
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.
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Review
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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Cell Division / physiology
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Cell Transformation, Neoplastic / metabolism
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DNA-Binding Proteins / metabolism*
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Gene Deletion
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Gene Expression Regulation, Neoplastic / physiology
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Genes, Suppressor
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Mammary Neoplasms, Experimental / metabolism*
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Mice
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Nuclear Proteins / antagonists & inhibitors
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Nuclear Proteins / genetics*
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Proto-Oncogene Proteins c-myc / antagonists & inhibitors
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Proto-Oncogene Proteins c-myc / genetics*
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Repressor Proteins*
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Transcription Factors*
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Transcription, Genetic / genetics
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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Nuclear Proteins
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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