ArticleCell cycle (Georgetown, Tex.)2015
ATM regulates cell fate choice upon p53 activation by modulating mitochondrial turnover and ROS levels.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Potential Mechanisms of MAP Kinase JNK's Involvement in Modulating Cancer Cell Fate in a Cisplatin Concentration-Dependent Manner.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Radiotherapy in Li-Fraumeni Syndrome: From Biological Concern to Personalized Clinical Decision-Making.Cureus · 2026Review
- ATM knock out alters calcium signalling and augments contraction in skeletal muscle cells differentiated from human urine-derived stem cells.Cell death discovery · 2025Article
- FAM193A is a positive regulator of p53 activity.Cell reports · 2023Article
- Article
- The suppression of ATR/Chk1 pathway by Elimusertib ATR inhibitor in triple negative breast cancer cells.American journal of translational research · 2023Article
- PPM1D suppresses p53-dependent transactivation and cell death by inhibiting the Integrated Stress Response.Nature communications · 2022Article
- MDM2 inhibitors-mediated disruption of mitochondrial metabolism: A novel therapeutic strategy for retinoblastoma.Frontiers in oncology · 2022Review
- Resistance mechanisms to inhibitors of p53-MDM2 interactions in cancer therapy: can we overcome them?Cellular & molecular biology letters · 2021Review
- Role of Amino Acid Arginine and Nitric Oxide in Mechanisms of Cytoprotective Effect of Non-Opiate Leu-Enkephalin Analogue In Vitro.Bulletin of experimental biology and medicine · 2021Article
- Ataxia Telangiectasia Mutated Protein Kinase: A Potential Master Puppeteer of Oxidative Stress-Induced Metabolic Recycling.Oxidative medicine and cellular longevity · 2021Review
- Oxidized ATM promotes breast cancer stem cell enrichment through energy metabolism reprogram-mediated acetyl-CoA accumulation.Cell death & disease · 2020Article
- Mitochondria: A Galaxy in the Hematopoietic and Leukemic Stem Cell Universe.International journal of molecular sciences · 2020Review
- Kinome screen of ferroptosis reveals a novel role of ATM in regulating iron metabolism.Cell death and differentiation · 2020Article
- Inhibition of p53 inhibitors: progress, challenges and perspectives.Journal of molecular cell biology · 2019Review
- ROS and the DNA damage response in cancer.Redox biology · 2019Review
- Article
- Inhibition of ATM kinase upregulates levels of cell death induced by cannabidiol and γ-irradiation in human glioblastoma cells.Oncotarget · 2019Article
- Autophagy Inhibition Mediates Apoptosis Sensitization in Cancer Therapy by Relieving FOXO3a Turnover.Developmental cell · 2018Article
- Actionable perturbations of damage responses by TCL1/ATM and epigenetic lesions form the basis of T-PLL.Nature communications · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Despite extensive study, the mechanisms of cell fate choice upon p53 activation remain poorly understood. Using genome-wide shRNA screening, we recently identified the ATM kinase as synthetic lethal with Nutlin-3, an MDM2 inhibitor that leads to non-genotoxic p53 activation. Here, we demonstrate that while this synthetic lethal interaction relies upon components of both the intrinsic and extrinsic apoptotic pathways (e.g., BAX and BID), it is not due to significant ATM effects on the expression of p53 target genes. Instead, loss of ATM activity results in increased mitochondria and reactive oxygen species that drive apoptosis. Finally, we provide evidence that pharmacologic inhibition of ATM blocks autophagy in direct opposition to p53, which activates this process, and that inhibition of autophagy is sufficient to elicit an apoptotic response when combined with Nutlin-3.
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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.