ArticleNature cell biology2011
E-box-independent regulation of transcription and differentiation by MYC.
Article in Nature cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Targeting c-Myc-p300-CARM1 complex induces ferroptosis and reduces CD8International journal of biological sciences · 2026Article
- Integrative pan-cancer genomic analysis highlights mitochondrial protein p32 as a potential therapeutic target in Myc-driven tumorigenesis.Medical oncology (Northwood, London, England) · 2025Article
- Super-enhancer-driven MLX mediates redox balance maintenance via SLC7A11 in osteosarcoma.Cell death & disease · 2023Article
- The Four Homeostasis Knights: In Balance upon Post-Translational Modifications.International journal of molecular sciences · 2022Review
- Review
- MYC: a multipurpose oncogene with prognostic and therapeutic implications in blood malignancies.Journal of hematology & oncology · 2021Review
- Strategies to generate functionally normal neutrophils to reduce infection and infection-related mortality in cancer chemotherapy.Pharmacology & therapeutics · 2019Review
- Apelin inhibition prevents resistance and metastasis associated with anti-angiogenic therapy.EMBO molecular medicine · 2019Article
- Tracing MYC Expression for Small Molecule Discovery.Cell chemical biology · 2019Article
- 3D Mammary Epithelial Cell Models: A Goldmine of DCIS Biomarkers and Morphogenetic Mechanisms.Cancers · 2019Article
- Myc phosphorylation in its basic helix-loop-helix region destabilizes transient α-helical structures, disrupting Max and DNA binding.The Journal of biological chemistry · 2018Article
- The Bromodomain Inhibitor JQ1 Enhances the Responses to All-International journal of stem cells · 2018Article
- Article
- C-Myc regulation by costimulatory signals modulates the generation of CD8+ memory T cells during viral infection.Open biology · 2016Article
- p53 activity contributes to defective interfollicular epidermal differentiation in hyperproliferative murine skin.The British journal of dermatology · 2016Article
- MYC-driven aggressive B-cell lymphomas: biology, entity, differential diagnosis and clinical management.Oncotarget · 2015Review
- Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles.Nature cell biology · 2015Article
- Knockdown of SALL4 Protein Enhances All-trans Retinoic Acid-induced Cellular Differentiation in Acute Myeloid Leukemia Cells.The Journal of biological chemistry · 2015Article
- Not Just a Sum? Identifying Different Types of Interplay between Constituents in Combined Interventions.PloS one · 2015Article
- A Cbx8-containing polycomb complex facilitates the transition to gene activation during ES cell differentiation.PLoS genetics · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MYC proto-oncogene is a key player in cell homeostasis that is commonly deregulated in human carcinogenesis(1). MYC can either activate or repress target genes by forming a complex with MAX (ref. 2). MYC also exerts MAX-independent functions that are not yet fully characterized(3). Cells possess an intrinsic pathway that can abrogate MYC-MAX dimerization and E-box interaction, by inducing phosphorylation of MYC in a PAK2-dependent manner at three residues located in its helix-loop-helix domain(4). Here we show that these carboxy-terminal phosphorylation events switch MYC from an oncogenic to a tumour-suppressive function. In undifferentiated cells, MYC-MAX is targeted to the promoters of retinoic-acid-responsive genes by its direct interaction with the retinoic acid receptor-α (RARα). MYC-MAX cooperates with RARα to repress genes required for differentiation, in an E-box-independent manner. Conversely, on C-terminal phosphorylation of MYC during differentiation, the complex switches from a repressive to an activating function, by releasing MAX and recruiting transcriptional co-activators. Phospho-MYC synergizes with retinoic acid to eliminate circulating leukaemic cells and to decrease the level of tumour invasion. Our results identify an E-box-independent mechanism for transcriptional regulation by MYC that unveils previously unknown functions for MYC in differentiation. These may be exploited to develop alternative targeted therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.