ArticleFrontiers in oncology2013
Response to DNA damage: why do we need to focus on protein phosphatases?
Article in Frontiers in oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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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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.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Study of post-translational modifications of p53 in multiple myeloma.Blood cancer journal · 2026Article
- An ATM-PPM1D Circuit Controls the Processing and Restart of DNA Replication Forks.bioRxiv : the preprint server for biology · 2025Article
- Fatty acid oxidation facilitates DNA double-strand break repair by promoting PARP1 acetylation.Cell death & disease · 2023Article
- Maintaining Genome Integrity: Protein Kinases and Phosphatases Orchestrate the Balancing Act of DNA Double-Strand Breaks Repair in Cancer.International journal of molecular sciences · 2023Review
- Chronic arsenic exposure suppresses ATM pathway activation in human keratinocytes.Toxicology and applied pharmacology · 2022Article
- PP1 regulatory subunit NIPP1 regulates transcription of E2F1 target genes following DNA damage.Cancer science · 2021Article
- Oncogenic WIP1 phosphatase attenuates the DNA damage response and sensitizes p53 mutant Jurkat cells to apoptosis.Oncology letters · 2021Article
- MHC Phosphopeptides: Promising Targets for Immunotherapy of Cancer and Other Chronic Diseases.Molecular & cellular proteomics : MCP · 2021Review
- Cell Cycle and DNA Repair Regulation in the Damage Response: Protein Phosphatases Take Over the Reins.International journal of molecular sciences · 2020Review
- Slowly Repaired Bulky DNA Damages Modulate Cellular Redox Environment Leading to Premature Senescence.Oxidative medicine and cellular longevity · 2020Article
- Protein phosphatase 2A controls ongoing DNA replication by binding to and regulating cell division cycle 45 (CDC45).The Journal of biological chemistry · 2019Article
- Identification of intracellular cavin target proteins reveals cavin-PP1alpha interactions regulate apoptosis.Nature communications · 2019Article
- Review
- Protein phosphatases in chromatin structure and function.Biochimica et biophysica acta. Molecular cell research · 2019Review
- Article
- A novel mathematical model of ATM/p53/NF- κB pathways points to the importance of the DDR switch-off mechanisms.BMC systems biology · 2016Article
- Wip1 phosphatase in breast cancer.Oncogene · 2015Review
- Modulation of LSD1 phosphorylation by CK2/WIP1 regulates RNF168-dependent 53BP1 recruitment in response to DNA damage.Nucleic acids research · 2015Article
- Wild-type p53-induced phosphatase 1 (Wip1) forestalls cellular premature senescence at physiological oxygen levels by regulating DNA damage response signaling during DNA replication.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
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
Eukaryotic cells are continuously threatened by unavoidable errors during normal DNA replication or various sources of genotoxic stresses that cause DNA damage or stalled replication. To maintain genomic integrity, cells have developed a coordinated signaling network, known as the DNA damage response (DDR). Following DNA damage, sensor molecules detect the presence of DNA damage and transmit signals to downstream transducer molecules. This in turn conveys the signals to numerous effectors, which initiate a large number of specific biological responses, including transient cell cycle arrest mediated by checkpoints, DNA repair, and apoptosis. It is recently becoming clear that dephosphorylation events are involved in keeping DDR factors inactive during normal cell growth. Moreover, dephosphorylation is required to shut off checkpoint arrest following DNA damage and has been implicated in the activation of the DDR. Spatial and temporal regulation of phosphorylation events is essential for the DDR, and fine-tuning of phosphorylation is partly mediated by protein phosphatases. While the role of kinases in the DDR has been well documented, the complex roles of protein dephosphorylation have only recently begun to be investigated. Therefore, it is important to focus on the role of phosphatases and to determine how their activity is regulated upon DNA damage. In this work, we summarize current knowledge on the involvement of serine/threonine phosphatases, especially the protein phosphatase 1, protein phosphatase 2A, and protein phosphatase Mg(2+)/Mn(2+)-dependent families, in the DDR.
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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.