ArticleCommunications biology2020
FUBP1 and FUBP2 enforce distinct epigenetic setpoints for MYC expression in primary single murine cells.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Dynamic Supercoiling Sponsors Transcription Amplification by MYC.bioRxiv : the preprint server for biology · 2026Article
- A tumorigenesis threshold for endogenous Myc revealed by dosage-compensation for Myc-haploinsufficiency in the absence of p53.bioRxiv : the preprint server for biology · 2025Article
- Ribosome Profiling Reveals Translational Reprogramming via mTOR Activation in Omacetaxine-Resistant Multiple Myeloma.Molecular cancer research : MCR · 2025Article
- FUBP1 in human cancer: Characteristics, functions, and potential applications.Translational oncology · 2024Review
- Proximity labeling defines the phagosome lumen proteome of murine and primary human macrophages.bioRxiv : the preprint server for biology · 2024Article
- Article
- MYC: a complex problem.Trends in cell biology · 2023Review
- Psi promotes Drosophila wing growth via direct transcriptional activation of cell cycle targets and repression of growth inhibitors.Development (Cambridge, England) · 2023Article
- Classification of adult-type diffuse gliomas: Impact of the World Health Organization 2021 update.Brain pathology (Zurich, Switzerland) · 2022Review
- Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).Frontiers in molecular biosciences · 2022Article
- The Simple Biology of Flipons and Condensates Enhances the Evolution of Complexity.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Physiologically, MYC levels must be precisely set to faithfully amplify the transcriptome, but in cancer MYC is quantitatively misregulated. Here, we study the variation of MYC amongst single primary cells (B-cells and murine embryonic fibroblasts, MEFs) for the repercussions of variable cellular MYC-levels and setpoints. Because FUBPs have been proposed to be molecular "cruise controls" that constrain MYC expression, their role in determining basal or activated MYC-levels was also examined. Growing cells remember low and high-MYC setpoints through multiple cell divisions and are limited by the same expression ceiling even after modest MYC-activation. High MYC MEFs are enriched for mRNAs regulating inflammation and immunity. After strong stimulation, many cells break through the ceiling and intensify MYC expression. Lacking FUBPs, unstimulated MEFs express levels otherwise attained only with stimulation and sponsor MYC chromatin changes, revealed by chromatin marks. Thus, the FUBPs enforce epigenetic setpoints that restrict MYC expression.
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Registered trials
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