ArticleJournal of molecular biology2008
Histone H3K4me3 binding is required for the DNA repair and apoptotic activities of ING1 tumor suppressor.
Article in Journal of molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 122 citations in OpenAlex.
- ING Proteins and Neural Development in Newborns from Alcohol- and/or Drug-Abusing Pregnant Women.International journal of molecular sciences · 2026Review
- Predicting the Impact of Deleterious Single-Nucleotide Polymorphisms in the p47ING1a Isoform of Human ING1 Gene.Genetics research · 2026Article
- Exploring KAT6 as a therapeutic target in breast cancer: epigenetic approaches for precision medicine.NPJ breast cancer · 2025Review
- A pair of readers of histone H3K4 methylation recruit Polycomb repressive complex 2 to regulate photoperiodic flowering.Nature communications · 2025Article
- ING5: multifaceted roles beyond tumor suppression in cellular physiology and disease.Epigenetics & chromatin · 2025Review
- Inhibitor of Growth Proteins: Epigenetic Regulators Shaping Neurobiology.Biomolecules · 2025Review
- Deep learning with a small dataset predicts chromatin remodelling contribution to winter dormancy of apple axillary buds.Tree physiology · 2024Article
- Readout of histone methylation by Trim24 locally restricts chromatin opening by p53.Nature structural & molecular biology · 2023Article
- Structure of a SIN3-HDAC complex from budding yeast.Nature structural & molecular biology · 2023Article
- Two assembly modes for SIN3 histone deacetylase complexes.Cell discovery · 2023Article
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- The chromatin reader protein ING5 is required for normal hematopoietic cell numbers in the fetal liver.Frontiers in immunology · 2023Article
- Review
- CG7379 and ING1 suppress cancer cell invasion by maintaining cell-cell junction integrity.Open biology · 2021Article
- Histone H3 N-terminal mimicry drives a novel network of methyl-effector interactions.The Biochemical journal · 2021Article
- ING Proteins: Tumour Suppressors or Oncoproteins.Cancers · 2021Review
- Use of signals of positive and negative selection to distinguish cancer genes and passenger genes.eLife · 2021Article
- H3K4me2 regulates the recovery of protein biosynthesis and homeostasis following DNA damage.Nature structural & molecular biology · 2020Article
- Understanding the interplay between CpG island-associated gene promoters and H3K4 methylation.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020Review
- Coordinated regulation of cellular identity-associated H3K4me3 breadth by the COMPASS family.Science advances · 2020Article
18 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
13 authors at 7 institutions in 2 countries.
Funding
Abstract
Inhibitor of growth 1 (ING1) is implicated in oncogenesis, DNA damage repair, and apoptosis. Mutations within the ING1 gene and altered expression levels of ING1 are found in multiple human cancers. Here, we show that both DNA repair and apoptotic activities of ING1 require the interaction of the C-terminal plant homeodomain (PHD) finger with histone H3 trimethylated at Lys4 (H3K4me3). The ING1 PHD finger recognizes methylated H3K4 but not other histone modifications as revealed by the peptide microarrays. The molecular mechanism of the histone recognition is elucidated based on a 2.1 A-resolution crystal structure of the PHD-H3K4me3 complex. The K4me3 occupies a deep hydrophobic pocket formed by the conserved Y212 and W235 residues that make cation-pi contacts with the trimethylammonium group. Both aromatic residues are essential in the H3K4me3 recognition, as substitution of these residues with Ala disrupts the interaction. Unlike the wild-type ING1, the W235A mutant, overexpressed in the stable clones of melanoma cells or in HT1080 cells, was unable to stimulate DNA repair after UV irradiation or promote DNA-damage-induced apoptosis, indicating that H3K4me3 binding is necessary for these biological functions of ING1. Furthermore, N216S, V218I, and G221V mutations, found in human malignancies, impair the ability of ING1 to associate with H3K4me3 or to induce nucleotide repair and cell death, linking the tumorigenic activity of ING1 with epigenetic regulation. Together, our findings reveal the critical role of the H3K4me3 interaction in mediating cellular responses to genotoxic stresses and offer new insight into the molecular mechanism underlying the tumor suppressive activity of ING1.
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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.