ReviewOncogene1999
ATM: a mediator of multiple responses to genotoxic stress.
Review in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
87 citing papers in PubMed, 270 citations in OpenAlex.
- Routes of Albumin Overload Toxicity in Renal Tubular Epithelial Cells.International journal of molecular sciences · 2023Article
- Nanoparticle-based radiosensitization strategies for improving radiation therapy.Frontiers in pharmacology · 2023Review
- Dapagliflozin Prevents High-Glucose-Induced Cellular Senescence in Renal Tubular Epithelial Cells.International journal of molecular sciences · 2022Article
- Genome Integrity and Neurological Disease.International journal of molecular sciences · 2022Review
- Crosstalk between Plk1, p53, cell cycle, and G2/M DNA damage checkpoint regulation in cancer: computational modeling and analysis.NPJ systems biology and applications · 2021Article
- The Role of Indoleamine 2,3-Dioxygenase in Renal Tubular Epithelial Cells Senescence under Anoxia or Reoxygenation.Biomolecules · 2021Article
- cGAS regulates the DNA damage response to maintain proliferative signaling in gastric cancer cells.Oncology research · 2021Article
- ATM Paradoxically Promotes Oncogenic Transformation via Transcriptional Reprogramming.Cancer research · 2020Article
- Deubiquitinase USP47-stabilized splicing factor IK regulates the splicing ofCell death discovery · 2020Article
- ATM Expression Is Elevated in Established Radiation-Resistant Breast Cancer Cells and Improves DNA Repair Efficiency.International journal of biological sciences · 2020Article
- MRE11-RAD50-NBS1 complex alterations and DNA damage response: implications for cancer treatment.Molecular cancer · 2019Review
- Article
- Sensitization strategies in lung cancer.Oncology letters · 2016Article
- The impact of glutamine supplementation on the symptoms of ataxia-telangiectasia: a preclinical assessment.Molecular neurodegeneration · 2016Article
- A central role of TRAX in the ATM-mediated DNA repair.Oncogene · 2016Article
- Cell-free Xenopus egg extracts for studying DNA damage response pathways.The International journal of developmental biology · 2016Review
- ATM gene mutations in sporadic breast cancer patients from Brazil.SpringerPlus · 2015Article
- Article
- Functional overlaps between XLF and the ATM-dependent DNA double strand break response.DNA repair · 2014Review
- Phosphoproteomic analysis of protein phosphorylation networks in Tetrahymena thermophila, a model single-celled organism.Molecular & cellular proteomics : MCP · 2014Article
27 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ATM protein kinase is the product of the gene responsible for the pleiotropic recessive disorder ataxia-telangiectasia. ATM-deficient cells show enhanced sensitivity and greatly reduced responses to genotoxic agents that generate DNA double strand breaks (DSBs), such as ionizing radiation and radiomimetic chemicals, but exhibit normal responses to DNA adducts and base modifications induced by other agents. Therefore, DSBs are most likely the predominant signal for the activation of ATM-mediated pathways. Identification of the ATM gene triggered extensive research aimed at elucidating the numerous functions of its large multifaceted protein product. While ATM has both nuclear and cytoplasmic functions, this review will focus on its roles in the nucleus where it plays a central role in the very early stages of damage detection and serves as a master controller of cellular responses to DSBs. By activating key regulators of multiple signal transduction pathways, ATM mediates the efficient induction of a signaling network responsible for repair of the damage, and for cellular recovery and survival.
Indexed as
Identifiers
What OpenQuestion holds
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.