ArticleNature communications2022
DAXX-ATRX regulation of p53 chromatin binding and DNA damage response.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The trial behind it
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
30 citing papers in PubMed, 48 citations in OpenAlex.
- Epigenetic regulation of transgenes.Journal of biotechnology · 2026Review
- Expanded GEP-NET organoid culture for personalized therapy evaluation.Science advances · 2026Article
- Endothelial cell-specific DNA methylation alterations in breast cancer.Communications biology · 2026Article
- DAXX promotes SUMOylation of chromatin-trapped DNMT1.Journal of biochemistry · 2026Article
- Review
- CDKN2A homozygous deletions and TSC2 somatic mutations in metastatic pancreatic neuroendocrine tumors.NPJ precision oncology · 2025Article
- Genomic and Demographic Characteristics of Angiosarcoma as Described in the AACR Project GENIE Registry.Cancers · 2025Article
- Review
- Structure and Function of PML Nuclear Bodies: A Brief Overview of Key Cellular Roles.Biomolecules · 2025Review
- DNA-Templated Spatially Controlled Proteolysis Targeting Chimera for Cyclin D1-CDK4/6 Complex Protein Degradation.Journal of the American Chemical Society · 2025Article
- DAXX-dependent H3.3 deposition maintains myoblast cell identity independently of other histone chaperone complexes.iScience · 2025Article
- p53 reveals principles of chromatin remodeling and enhancer activation.Nucleic acids research · 2025Article
- Effect of deubiquitinases in head and neck squamous cell carcinoma (Review).Oncology letters · 2025Review
- Loss of DAXX/ATRX Protein Expression Results in Ischemia Resistance and Radiation Sensitivity in Pancreatic Neuroendocrine Tumor Cells and Is Associated with Improved Response to Trans-Arterial Radioembolization.Neuroendocrinology · 2025Article
- Aristolochic acids-hijacked p53 promotes liver cancer cell growth by inhibiting ferroptosis.Acta pharmacologica Sinica · 2025Article
- Beginning at the ends: telomere and telomere-based cancer therapeutics.Molecular genetics and genomics : MGG · 2024Review
- Article
- Determinants of p53 DNA binding, gene regulation, and cell fate decisions.Cell death and differentiation · 2024Review
- Loss of miR-101-3p in melanoma stabilizes genomic integrity, leading to cell death prevention.Cellular & molecular biology letters · 2024Article
- Connecting the mechanisms of tumor sex differences with cancer therapy.Molecular and cellular biochemistry · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
DAXX and ATRX are tumor suppressor proteins that form a histone H3.3 chaperone complex and are frequently mutated in cancers with the alternative lengthening of telomeres (ALT). Here, we show that DAXX and ATRX knock-out (KO) U87-T cells that have acquired ALT-like features have defects in p53 chromatin binding and DNA damage response. RNA-seq analysis revealed that p53 pathway is among the most perturbed. ChIP-seq and ATAC-seq revealed a genome-wide reduction in p53 DNA-binding and corresponding loss of chromatin accessibility at many p53 response elements across the genome. Both DAXX and ATRX null cells showed a depletion of histone H3.3 and accumulation of γH2AX at many p53 sites, including subtelomeres. These findings indicate that loss of DAXX or ATRX can compromise p53 chromatin binding and p53 DNA damage response in ALT-like cells, providing a link between histone composition, chromatin accessibility and tumor suppressor function of p53.
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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.