ArticleCell cycle (Georgetown, Tex.)2010
ATM activation in the presence of oxidative stress.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 180 citations in OpenAlex.
- ATM-kinase deficiency triggers early multi-compartment remodeling of the cerebellar microenvironment.Acta neuropathologica communications · 2026Article
- Article
- Nuclear compression-mediated DNA damage drives ATR-dependent Lamin expression and mouse ESC differentiation.Nucleic acids research · 2025Article
- Quantification of liver fat fraction using T1-weighted mDixon MRI in young patients with ataxia telangiectasia undergoing whole-body MRI: an exploratory study.Orphanet journal of rare diseases · 2025Article
- OGG1 and MUTYH repair activities promote telomeric 8-oxoguanine induced senescence in human fibroblasts.Nature communications · 2025Article
- Role of Oxidative Stress in the Occurrence, Development, and Treatment of Breast Cancer.Antioxidants (Basel, Switzerland) · 2025Review
- Making PI3K superfamily enzymes run faster.Advances in biological regulation · 2025Review
- Temporal coordination of the transcription factor response to HNature communications · 2024Article
- Disproportionate Expression of ATM in Cerebellar Cortex During Human Neurodevelopment.Cerebellum (London, England) · 2024Article
- ATM inhibition blocks glucose metabolism and amplifies the sensitivity of resistant lung cancer cell lines to oncogene driver inhibitors.Cancer & metabolism · 2023Article
- Hepatic fibrosis: a manifestation of the liver disease evolution in patients with Ataxia-telangiectasia.Orphanet journal of rare diseases · 2023Article
- Analysis of Copy Number Variation in the Whole Genome of Normal-Haired and Long-Haired Tianzhu White Yaks.Genes · 2022Article
- ATM Regulates Differentiation of Myofibroblastic Cancer-Associated Fibroblasts and Can Be Targeted to Overcome Immunotherapy Resistance.Cancer research · 2022Article
- Cell Fate following Irradiation of MDA-MB-231 and MCF-7 Breast Cancer Cells Pre-Exposed to the Tetrahydroisoquinoline Sulfamate Microtubule Disruptor STX3451.Molecules (Basel, Switzerland) · 2022Article
- Tracing brain genotoxic stress in Parkinson's disease with a novel single-cell genetic sensor.Science advances · 2022Article
- The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease.International journal of molecular sciences · 2022Review
- PPARγ regulates the expression of genes involved in the DNA damage response in an inflamed endometrium.Scientific reports · 2022Article
- DNA repair protein DNA-PK protects PC12 cells from oxidative stress-induced apoptosis involving AKT phosphorylation.Molecular biology reports · 2022Article
- The interplay of autophagy and oxidative stress in the pathogenesis and therapy of retinal degenerative diseases.Cell & bioscience · 2022Review
- ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.Frontiers in cell and developmental biology · 2022Article
46 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
3 authors at 1 institution in 1 country.
Funding
Abstract
The Ataxia-Telangiectasia mutated (ATM) kinase is regarded as the major regulator of the cellular response to DNA double strand breaks (DSBs). In response to DSBs, ATM dimers dissociate into active monomers in a process promoted by the Mre11-Rad50-Nbs1 (MRN) complex. ATM can also be activated by oxidative stress directly in the form of exposure to H2O2. The active ATM in this case is a disulfide-crosslinked dimer containing 2 or more disulfide bonds. Mutation of a critical cysteine residue in the FATC domain involved in disulfide bond formation specifically blocks ATM activation by oxidative stress. Here we show that ATM activation by DSBs is inhibited in the presence of H2O2 because oxidation blocks the ability of MRN to bind to DNA. However, ATM activation via direct oxidation by H2O2 complements the loss of MRN/DSB-dependent activation and contributes significantly to the overall level of ATM activity in the presence of both DSBs and oxidative stress.
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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.