ReviewCurrent opinion in cell biology2009
Kinases that control the cell cycle in response to DNA damage: Chk1, Chk2, and MK2.
Review in Current opinion in cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 266 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
266 citing papers in PubMed, 500 citations in OpenAlex.
- An Ancestral Mechanism of Calmodulin Binding to Cds1 Kinase Inhibits Catalytic Activity.IUBMB life · 2026Article
- Interaction of flavonoids with DNA: implications in cancer treatment.Molecular biology reports · 2026Review
- In Vitro and In Vivo Efficacy of Romidepsin Alone and in Addition to Standard of Care for Treatment of Ewing Sarcoma.Cancers · 2025Article
- Unconventional binding of calmodulin to CHK2 kinase inhibits catalytic activity.The Biochemical journal · 2025Article
- Molecular Mechanisms and Clinical Divergences in HPV-Positive Cervical vs. Oropharyngeal Cancers: A Critical Narrative Review.BMC medicine · 2025Review
- Depletion of BRD9-mediated R-loop accumulation inhibits leukemia cell growth via transcription-replication conflict.Nucleic acids research · 2025Article
- Dual Disruption of DNA Repair by a Novel CHK2 Inhibitor, ART-446, and Olaparib is a Promising Strategy for Triple-Negative Breast Cancer Therapy.Biomolecules & therapeutics · 2025Article
- Unraveling systemic responses to NQO1-activated IB-DNQ and Rucaparib single and dual agent therapy in triple-negative breast cancers.bioRxiv : the preprint server for biology · 2025Article
- Krüppel-like Factor 4-Deficient Cells Are Sensitive to Etoposide-Induced DNA Damage.Current issues in molecular biology · 2025Article
- Tumorigenesis Caused by Aberrant Expression of GANP, a Central Component in the Mammalian TREX-2 Complex-Lessons from Transcription-Coupled DNA Damages.International journal of molecular sciences · 2024Review
- REXO5 promotes genomic integrity through regulating R-loop using its exonuclease activity.Leukemia · 2024Article
- From Crypts to Cancer: A Holistic Perspective on Colorectal Carcinogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Cryo-EM structure of the CDK2-cyclin A-CDC25A complex.Nature communications · 2024Article
- Deciphering the molecular landscape of ionising radiation-induced eye damage with the help of genomic data mining.Arhiv za higijenu rada i toksikologiju · 2024Article
- The DNA Damage Response (DDR) landscape of endometrial cancer defines discrete disease subtypes and reveals therapeutic opportunities.NAR cancer · 2024Article
- Eugenol as a potential adjuvant therapy for gingival squamous cell carcinoma.Scientific reports · 2024Article
- Musashi-2 (MSI2) regulation of DNA damage response in lung cancer.Research square · 2024Article
- Advances in synthetic lethality modalities for glioblastoma multiforme.Open medicine (Warsaw, Poland) · 2024Review
- SF3B1 hotspot mutations confer sensitivity to PARP inhibition by eliciting a defective replication stress response.Nature genetics · 2023Article
- Biphasic JNK-Erk signaling separates the induction and maintenance of cell senescence after DNA damage induced by topoisomerase II inhibition.Cell systems · 2023Article
206 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
Abstract
In response to DNA damage eukaryotic cells activate cell cycle checkpoints -- complex kinase signaling networks that prevent further progression through the cell cycle. Parallel to implementing a cell cycle arrest, checkpoint signaling also mediates the recruitment of DNA repair pathways. If the extent of damage exceeds repair capacity, additional signaling cascades are activated to ensure elimination of these damaged cells. The DNA damage response has traditionally been divided into two major kinase branches. The ATM/Chk2 module is activated after DNA double strand breaks and the ATR/Chk1 pathway responds primarily to DNA single strand breaks or bulky lesions. Both pathways converge on Cdc25, a positive regulator of cell cycle progression, which is inhibited by Chk1-mediated or Chk2-mediated phosphorylation. Recently a third effector kinase complex consisting of p38MAPK and MK2 has emerged. This pathway is activated downstream of ATM and ATR in response to DNA damage. MK2 has been shown to share substrate homology with both Chk1 and Chk2. Here we will discuss recent advances in our understanding of the eukaryotic DNA damage response with emphasis on the Chk1, Chk2, and the newly emerged effector kinases p38MAPK and MK2.
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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.