ArticleMolecular cell2017
Regulation of the DNA Damage Response by DNA-PKcs Inhibitory Phosphorylation of ATM.
Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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
81 citing papers in PubMed, 126 citations in OpenAlex.
- DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026Review
- CNOT7 facilitates radiation resistance in colorectal cancer through TRIM21/XRCC6-mediated non-homologous end joining repair.Cell death & disease · 2025Article
- Unlocking the Therapeutic Potential of DNA-PKcs in Cancer: Comprehensive Insights into Mechanisms and Clinical Applications.Cancers · 2025Review
- Article
- Photodynamic Therapy and Dietary Antioxidants: A Dual Strategy for Genome Stability and DNA Damage Repair.Cancer medicine · 2025Review
- Re-epithelialization of cancer cells increases autophagy and DNA damage: Implications for breast cancer dormancy and relapse.Science signaling · 2025Article
- Phosphorylated BLM peptide acts as an agonist for DNA damage response.Nucleic acids research · 2025Article
- RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.PLoS genetics · 2024Article
- Alpha-synuclein modulates the repair of genomic DNA double-strand breaks in a DNA-PKNeurobiology of disease · 2024Article
- Cell Proliferation and Apoptosis-Key Players in the Lung Aging Process.International journal of molecular sciences · 2024Review
- DNA-PK controls Apollo's access to leading-end telomeres.Nucleic acids research · 2024Article
- A-T neurodegeneration and DNA damage-induced transcriptional stress.DNA repair · 2024Review
- Article
- Structure and function of the apical PIKKs in double-strand break repair.Current opinion in structural biology · 2023Review
- ATM phosphorylates the FATC domain of DNA-PKcs at threonine 4102 to promote non-homologous end joining.Nucleic acids research · 2023Article
- Drug Discovery Targeting Post-Translational Modifications in Response to DNA Damages Induced by Space Radiation.International journal of molecular sciences · 2023Review
- Live-cell tracking of γ-H2AX kinetics reveals the distinct modes of ATM and DNA-PK in the immediate response to DNA damage.Journal of cell science · 2023Article
- Ku-DNA binding inhibitors modulate the DNA damage response in response to DNA double-strand breaks.NAR cancer · 2023Article
- Multi-OMICs landscape of SARS-CoV-2-induced host responses in human lung epithelial cells.iScience · 2023Article
- CRISPR-based gene editing of non-homologous end joining factors biases DNA repair pathway choice toward single-strand annealing inCurrent research in biotechnology · 2023Article
21 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
6 authors at 2 institutions in 1 country.
Funding
Abstract
Ataxia-telangiectasia mutated (ATM) regulates the DNA damage response as well as DNA double-strand break repair through homologous recombination. Here we show that ATM is hyperactive when the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) is chemically inhibited or when the DNA-PKcs gene is deleted in human cells. Pre-incubation of ATM protein with active DNA-PKcs also significantly reduces ATM activity in vitro. We characterize several phosphorylation sites in ATM that are targets of DNA-PKcs and show that phospho-mimetic mutations at these residues significantly inhibit ATM activity and impair ATM signaling upon DNA damage. In contrast, phospho-blocking mutations at one cluster of sites increase the frequency of apoptosis during normal cell growth. DNA-PKcs, which is integral to the non-homologous end joining pathway, thus negatively regulates ATM activity through phosphorylation of ATM. These observations illuminate an important regulatory mechanism for ATM that also controls DNA repair pathway choice.
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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.