ArticleBMC biology2021
Sustained CHK2 activity, but not ATM activity, is critical to maintain a G1 arrest after DNA damage in untransformed cells.
Article in BMC biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Ro 08-2750 increases radiation-induced cytotoxicity in DLBCL by dysregulating the DNA damage response.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026Article
- Article
- DNA damage checkpoints balance a tradeoff between diploid- and polyploid-derived arrest failures.Cell reports · 2025Article
- The histone acetyltransferase CBP participates in regulating the DNA damage response through ATM after double-strand breaks.Genome biology · 2025Article
- DNA damage checkpoints balance a tradeoff between diploid- and polyploid-derived arrest failures.bioRxiv : the preprint server for biology · 2025Article
- Melatonin ameliorates zearalenone-induced ovarian damage in mice through antioxidative effects.Frontiers in veterinary science · 2025Article
- Daunorubicin induces GLI1‑dependent apoptosis in colorectal cancer cell lines.International journal of oncology · 2024Article
- Advances in the mechanism of CDK4/6 inhibitor resistance in HR+/HER2- breast cancer.Therapeutic advances in medical oncology · 2024Review
- Molecular portraits of cell cycle checkpoint kinases in cancer evolution, progression, and treatment responsiveness.Science advances · 2023Article
- The Landscape and Therapeutic Targeting ofCurrent issues in molecular biology · 2023Review
- Diallyl Disulfide Induces Chemosensitization to Sorafenib, Autophagy, and Cell Cycle Arrest and Inhibits Invasion in Hepatocellular Carcinoma.Pharmaceutics · 2022Article
- Targeting the DNA Damage Response and DNA Repair Pathways to Enhance Radiosensitivity in Colorectal Cancer.Cancers · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe G1 checkpoint is a critical regulator of genomic stability in untransformed cells, preventing cell cycle progression after DNA damage. DNA double-strand breaks (DSBs) recruit and activate ATM, a kinase which in turn activates the CHK2 kinase to establish G1 arrest. While the onset of G1 arrest is well understood, the specific role that ATM and CHK2 play in regulating G1 checkpoint maintenance remains poorly characterized.
resultsHere we examine the impact of ATM and CHK2 activities on G1 checkpoint maintenance in untransformed cells after DNA damage caused by DSBs. We show that ATM becomes dispensable for G1 checkpoint maintenance as early as 1 h after DSB induction. In contrast, CHK2 kinase activity is necessary to maintain the G1 arrest, independently of ATM, ATR, and DNA-PKcs, implying that the G1 arrest is maintained in a lesion-independent manner. Sustained CHK2 activity is achieved through auto-activation and its acute inhibition enables cells to abrogate the G1-checkpoint and enter into S-phase. Accordingly, we show that CHK2 activity is lost in cells that recover from the G1 arrest, pointing to the involvement of a phosphatase with fast turnover.
conclusionOur data indicate that G1 checkpoint maintenance relies on CHK2 and that its negative regulation is crucial for G1 checkpoint recovery after DSB induction.
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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.