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Open AccessJournal ArticleDOI

The ornithine decarboxylase gene is a transcriptional target of c-Myc.

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TLDR
It is demonstrated that c-Myc is a potent transactivator of ODC promoter-reporter gene constructs in fibroblasts that requires the CACGTG repeat, suggesting that ODC is regulated by Myc at the level of transcription initiation.
Abstract
Constitutive c-myc expression suppresses cell cycle arrest, promotes entry into S phase, and results in the growth factor-independent expression of ornithine decarboxylase (ODC; EC 4.1.1.17). The ODC gene contains a conserved repeat of the Myc binding site, CACGTG, in intron 1. In this report, we demonstrate that c-Myc is a potent transactivator of ODC promoter-reporter gene constructs in fibroblasts that requires the CACGTG repeat. These sites conferred Myc responsiveness on heterologous promoter constructs, suggesting that ODC is regulated by Myc at the level of transcription initiation. Analysis of deletion and point mutants of c-myc revealed that domains required for transactivation of the ODC promoter did not include the leucine zipper of the Myc protein. This suggests that Myc may interact with transcription factors other than Max to transactivate the ODC gene.

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The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation

TL;DR: Metabolic tracer analysis revealed a Myc-dependent metabolic pathway linking glutaminolysis to the biosynthesis of polyamines, which may represent a general mechanism for metabolic reprogramming under patho-physiological conditions.
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c-Myc target genes involved in cell growth, apoptosis, and metabolism

TL;DR: The c-myc gene was discovered as the cellular homolog of the retroviral v- myc oncogene 20 years ago and found to be activated in various animal and human tumors, suggesting that it is critical for development.
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Reflecting on 25 years with MYC

TL;DR: Just over 25 years ago, MYC, the human homologue of a retroviral oncogene, was identified and each incremental insight into MYC regulation and function has had an impact on numerous biological disciplines, including the understanding of molecular oncogenesis in general.
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The Myc/Max/Mad Network and the Transcriptional Control of Cell Behavior

TL;DR: The Myc/Max/Mad network comprises a group of transcription factors whose distinct interactions result in gene-specific transcriptional activation or repression and can be viewed as a functional module which acts to convert environmental signals into specific gene-regulatory programs.
Journal ArticleDOI

MYC oncogenes and human neoplastic disease

TL;DR: Data is indicated that these oncoproteins actually serve quite different roles in vivo, indicating that the deregulated expression of each MYC gene is reproducibly associated with only certain naturally occurring malignancies in humans and that these genes are not interchangeable with respect to their aberrant functional consequences.
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