ArticlePloS one2008
Analysis of Myc-induced histone modifications on target chromatin.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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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Who cites it
84 citing papers in PubMed, 129 citations in OpenAlex.
- circACTN4 promotes breast cancer cell cycle progression and oncogenesis via c-MYC induced histone H4 acetylation.Oncology research · 2025Article
- Topoisomerase 1 Inhibition in MYC-Driven Cancer Promotes Aberrant R-Loop Accumulation to Induce Synthetic Lethality.Cancer research · 2023Article
- BRD4 and MYC: power couple in transcription and disease.The FEBS journal · 2023Review
- Tumor-suppressive disruption of cancer subtype-associated super enhancer circuits by small molecule treatment.NAR cancer · 2023Article
- Lessons in aging from Myc knockout mouse models.Frontiers in cell and developmental biology · 2023Review
- Article
- Polyploidy and Myc Proto-Oncogenes Promote Stress Adaptation via Epigenetic Plasticity and Gene Regulatory Network Rewiring.International journal of molecular sciences · 2022Review
- DOT1L Is a Novel Cancer Stem Cell Target for Triple-Negative Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- A MYC inhibitor selectively alters the MYC and MAX cistromes and modulates the epigenomic landscape to regulate target gene expression.Science advances · 2022Article
- MYC protein interactors in gene transcription and cancer.Nature reviews. Cancer · 2021Review
- Inhibition of polo-like kinase 1 (PLK1) facilitates reactivation of gamma-herpesviruses and their elimination.PLoS pathogens · 2021Article
- The regulatory function of tandem repeat VNTR2-1 in hTERT gene involves basic Helix-loop-helix family transcription factors.Environmental and molecular mutagenesis · 2021Article
- Differentiating cancer cells reveal early large-scale genome regulation by pericentric domains.Biophysical journal · 2021Article
- Oligodendroglial Epigenetics, from Lineage Specification to Activity-Dependent Myelination.Life (Basel, Switzerland) · 2021Review
- c-Myc promotes lymphatic metastasis of pancreatic neuroendocrine tumor through VEGFC upregulation.Cancer science · 2021Article
- Genome-Wide Analysis of c-MYC-Regulated mRNAs and miRNAs and c-MYC DNA-Binding by Next-Generation Sequencing.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Identifying and Validating MYC:Protein Interactors in Pursuit of Novel Anti-MYC Therapies.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Long non-coding RNAs and MYC association in hematological malignancies.Annals of hematology · 2020Review
- Myc-mediated SDHA acetylation triggers epigenetic regulation of gene expression and tumorigenesis.Nature metabolism · 2020Article
- Silencing or inhibition of H3K79 methyltransferase DOT1L induces cell cycle arrest by epigenetically modulating c-Myc expression in colorectal cancer.Clinical epigenetics · 2019Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-myc proto-oncogene is induced by mitogens and is a central regulator of cell growth and differentiation. The c-myc product, Myc, is a transcription factor that binds a multitude of genomic sites, estimated to be over 10-15% of all promoter regions. Target promoters generally pre-exist in an active or poised chromatin state that is further modified by Myc, contributing to fine transcriptional regulation (activation or repression) of the afferent gene. Among other mechanisms, Myc recruits histone acetyl-transferases to target chromatin and locally promotes hyper-acetylation of multiple lysines on histones H3 and H4, although the identity and combination of the modified lysines is unknown. Whether Myc dynamically regulates other histone modifications (or marks) at its binding sites also remains to be addressed. Here, we used quantitative chromatin immunoprecipitation (qChIP) to profile a total of 24 lysine-acetylation and -methylation marks modulated by Myc at target promoters in a human B-cell line with a regulatable c-myc transgene. Myc binding promoted acetylation of multiple lysines, primarily of H3K9, H3K14, H3K18, H4K5 and H4K12, but significantly also of H4K8, H4K91 and H2AK5. Dimethylation of H3K79 was also selectively induced at target promoters. A majority of target promoters showed co-induction of multiple marks - in various combinations - correlating with recruitment of the two HATs tested (Tip60 and HBO1), incorporation of the histone variant H2A.Z and transcriptional activation. Based on this and previous findings, we surmise that Myc recruits the Tip60/p400 complex to achieve a coordinated histone acetylation/exchange reaction at activated promoters. Our data are also consistent with the additive and redundant role of multiple acetylation events in transcriptional activation.
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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.