ArticlePloS one2012
Loss of Atrx sensitizes cells to DNA damaging agents through p53-mediated death pathways.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- ATRX loss couples genome instability at a G-rich repeat to dysregulation of human alpha-globin expression.Nature communications · 2026Article
- IDH inhibition in gliomas: from preclinical models to clinical trials.Nature reviews. Neurology · 2024Review
- Knockdown of ATRX enhances radiosensitivity in glioblastoma.Chinese neurosurgical journal · 2024Article
- Preclinical Models of Low-Grade Gliomas.Cancers · 2023Review
- Classification of adult-type diffuse gliomas: Impact of the World Health Organization 2021 update.Brain pathology (Zurich, Switzerland) · 2022Review
- Article
- The Personalisation of Glioblastoma Treatment Using Whole Exome Sequencing: A Pilot Study.Genes · 2020Article
- Alternative lengthening of telomeres: from molecular mechanisms to therapeutic outlooks.Cell & bioscience · 2020Review
- Observational
- Glial ensheathment of the somatodendritic compartment regulates sensory neuron structure and activity.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Inferences of individual drug responses across diverse cancer types using a novel competing endogenous RNA network.Molecular oncology · 2018Article
- Mutant ATRX: uncovering a new therapeutic target for glioma.Expert opinion on therapeutic targets · 2018Review
- Atrx inactivation drives disease-defining phenotypes in glioma cells of origin through global epigenomic remodeling.Nature communications · 2018Article
- Prospective Feasibility Trial for Genomics-Informed Treatment in Recurrent and Progressive Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- ATRX and DAXX: Mechanisms and Mutations.Cold Spring Harbor perspectives in medicine · 2017Review
- The Role of ATRX in Glioma Biology.Frontiers in oncology · 2017Review
- Histone variant H3.3 provides the heterochromatic H3 lysine 9 tri-methylation mark at telomeres.Nucleic acids research · 2015Article
- Unbiased phosphoproteomic method identifies the initial effects of a methacrylic acid copolymer on macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Toward precision medicine in glioblastoma: the promise and the challenges.Neuro-oncology · 2015Review
- Loss of ATRX and DAXX expression identifies poor prognosis for smooth muscle tumours of uncertain malignant potential and early stage uterine leiomyosarcoma.The journal of pathology. Clinical research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Prevalent cell death in forebrain- and Sertoli cell-specific Atrx knockout mice suggest that Atrx is important for cell survival. However, conditional ablation in other tissues is not associated with increased death indicating that diverse cell types respond differently to the loss of this chromatin remodeling protein. Here, primary macrophages isolated from Atrx(f/f) mice were infected with adenovirus expressing Cre recombinase or β-galactosidase, and assayed for cell survival under different experimental conditions. Macrophages survive without Atrx but undergo rapid apoptosis upon lipopolysaccharide (LPS) activation suggesting that chromatin reorganization in response to external stimuli is compromised. Using this system we next tested the effect of different apoptotic stimuli on cell survival. We observed that survival of Atrx-null cells were similar to wild type cells in response to serum withdrawal, anti-Fas antibody, C2 ceramide or dexamethasone treatment but were more sensitive to 5-fluorouracil (5-FU). Cell survival could be rescued by re-introducing Atrx or by removal of p53 demonstrating the cell autonomous nature of the effect and its p53-dependence. Finally, we demonstrate that multiple primary cell types (myoblasts, embryonic fibroblasts and neurospheres) were sensitive to 5-FU, cisplatin, and UV light treatment. Together, our results suggest that cells lacking Atrx are more sensitive to DNA damaging agents and that this may result in enhanced death during development when cells are at their proliferative peak. Moreover, it identifies potential treatment options for cancers associated with ATRX mutations, including glioblastoma and pancreatic neuroendocrine tumors.
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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.