ArticleGenome biology2014
Sequence specificity incompletely defines the genome-wide occupancy of Myc.
Article in Genome biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 82 citations in OpenAlex.
- MYC serine 62 phosphorylation promotes its association with DNA double-strand breaks to facilitate repair and cell survival under genotoxic stress.Genes & development · 2026Article
- Article
- Chromatin-dependent motif syntax defines differentiation trajectories.Molecular cell · 2025Article
- Review
- Mutations to transcription factor MAX allosterically increase DNA selectivity by altering folding and binding pathways.Nature communications · 2025Article
- Transcriptional regulation by MYC: an emerging new model.Oncogene · 2025Review
- BET-directed PROTACs in triple negative breast cancer cell lines MDA-MB-231 and MDA-MB-436.Breast cancer research and treatment · 2024Article
- DFF-ChIP: a method to detect and quantify complex interactions between RNA polymerase II, transcription factors, and chromatin.Nucleic acids research · 2024Article
- Bromodomain Protein-directed Agents and MYC in Small Cell Lung Cancer.Current cancer drug targets · 2024Review
- Measuring the impact of chromatin context on transcription factor binding affinities.Nature biotechnology · 2023Article
- Review
- Targeting MYC with modular synthetic transcriptional repressors derived from bHLH DNA-binding domains.Nature biotechnology · 2023Article
- A New Insight into MYC Action: Control of RNA Polymerase II Methylation and Transcription Termination.Biomedicines · 2023Article
- E-box binding transcription factors in cancer.Frontiers in oncology · 2023Review
- MYC function and regulation in physiological perspective.Frontiers in cell and developmental biology · 2023Review
- EZH2 noncanonically binds cMyc and p300 through a cryptic transactivation domain to mediate gene activation and promote oncogenesis.Nature cell biology · 2022Article
- MYC assembles and stimulates topoisomerases 1 and 2 in a "topoisome".Molecular cell · 2022Article
- Deep learning for MYC binding site recognition.Frontiers in bioinformatics · 2022Article
- Article
- MYC protein interactors in gene transcription and cancer.Nature reviews. Cancer · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe Myc-Max heterodimer is a transcription factor that regulates expression of a large number of genes. Genome occupancy of Myc-Max is thought to be driven by Enhancer box (E-box) DNA elements, CACGTG or variants, to which the heterodimer binds in vitro.
resultsBy analyzing ChIP-Seq datasets, we demonstrate that the positions occupied by Myc-Max across the human genome correlate with the RNA polymerase II, Pol II, transcription machinery significantly better than with E-boxes. Metagene analyses show that in promoter regions, Myc is uniformly positioned about 100 bp upstream of essentially all promoter proximal paused polymerases with Max about 15 bp upstream of Myc. We re-evaluate the DNA binding properties of full length Myc-Max proteins. Electrophoretic mobility shift assay results demonstrate Myc-Max heterodimers display significant sequence preference, but have high affinity for any DNA. Quantification of the relative affinities of Myc-Max for all possible 8-mers using universal protein-binding microarray assays shows that sequences surrounding core 6-mers significantly affect binding. Compared to the in vitro sequence preferences,Myc-Max genomic occupancy measured by ChIP-Seq is largely, although not completely, independent of sequence specificity.
conclusionsWe quantified the affinity of Myc-Max to all possible 8-mers and compared this with the sites of Myc binding across the human genome. Our results indicate that the genomic occupancy of Myc cannot be explained by its intrinsic DNA specificity and suggest that the transcription machinery and associated promoter accessibility play a predominant role in Myc recruitment.
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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.