CHK2 kinase in the DNA damage response and beyond
Open accessAbstract
The serine/threonine kinase CHK2 is a key component of the DNA damage response. In human cells, following genotoxic stress, CHK2 is activated and phosphorylates >20 proteins to induce the appropriate cellular response, which, depending on the extent of damage, the cell type, and other factors, could be cell cycle checkpoint activation, induction of apoptosis or senescence, DNA repair, or tolerance of the damage. Recently, CHK2 has also been found to have cellular functions independent of the presence of nuclear DNA lesions. In particular, CHK2 participates in several molecular processes involved in DNA structure modification and cell cycle progression. In this review, we discuss the activity of CHK2 in response to DNA damage and in the maintenance of the biological functions in unstressed cells. These activities are also considered in relation to a possible role of CHK2 in tumorigenesis and, as a consequence, as a target of cancer therapy.
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Another important target of CHEK2 phosphorylation is p53, a critical transcriptional regulator of cellular senescence.
“Another important target of CHEK2 phosphorylation is p53 [169], a critical transcriptional regulator of cellular senescence [130].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [169]
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Self-citationRegulation of the female mouse germ cell cycle during entry into meiosis
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Cooperative functions of Chk1 and Chk2 reduce tumour susceptibility in vivo
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The E3 ligase PIRH2 polyubiquitylates CHK2 and regulates its turnover
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Determination of substrate specificity and putative substrates of Chk2 kinase
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Senescence: an antiviral defense that is tumor suppressive?
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Promyelocytic Leukemia Activates Chk2 by Mediating Chk2 Autophosphorylation
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Per3, a circadian gene, is required for Chk2 activation in human cells
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The cell cycle checkpoint kinase CHK2 mediates DNA damage-induced stabilization of TTK/hMps1
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The Shelterin Protein TRF2 Inhibits Chk2 Activity at Telomeres in the Absence of DNA Damage
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DNA Damage-Induced Cell Cycle Regulation and Function of Novel Chk2 Phosphoresidues
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Self-citationRegulation of Chk2 Ubiquitination and Signaling through Autophosphorylation of Serine 379
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Checkpoint Mediators: Relaying Signals from DNA Strand Breaks
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Mice with the CHEK2 *1100delC SNP are predisposed to cancer with a strong gender bias
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The Viral Oncoprotein Tax Sequesters DNA Damage Response Factors by Tethering MDC1 to Chromatin
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A novel Chk1/2–Lats2–14-3-3 signaling pathway regulates P-body formation in response to UV damage
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Self-citationREGγ/PA28γ proteasome activator interacts with PML and Chk2 and affects PML nuclear bodies number
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Stability of Checkpoint Kinase 2 Is Regulated via Phosphorylation at Serine 456
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Loss of the tumour-suppressor genes CHK2 and BRCA1 results in chromosomal instability
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Phosphorylation of von Hippel-Lindau protein by checkpoint kinase 2 regulates p53 transactivation
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Caenorhabditis elegans Chk2‐like gene is essential for meiosis but dispensable for DNA repair
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Interdependent Phosphorylation within the Kinase Domain T-loop Regulates CHK2 Activity*
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ATM and Chk2 kinase target the p53 cofactor Strap
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Fleury, H., Malaquin, N., Tu, V., Gilbert, S., Martinez, A., Olivier, M.-A., Sauriol, S. A., Communal, L., Leclerc-Desaulniers, K., Carmona, E., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-10460-1 · Cited by 228 · see citing works
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Sensitization of cancer cells to paclitaxel-induced apoptosis by canagliflozin
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- Authors
- Zannini, L., Delia, D., & Buscemi, G.
- Affiliations
- Fondazione IRCCS Istituto Nazionale dei Tumori (IT)
- University of Milan (IT)
- Corresponding author
- Delia, D.
- Buscemi, G.
- Venue
- Journal of Molecular Cell Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-11-17
- Volume
- 6
- Issue
- 6
- Pages
- 442-457
- ISSN
- 1674-2788 (ISSN-L)
- PMC
- PMC4296918
- OpenAlex
- W1484740038
- Cited by
- 455
- References
- 155
- Citations by year
- 2026: 27 · 2025: 44 · 2024: 55 · 2023: 50 · 2022: 44 · 2021: 40 · 2020: 56 · 2019: 39 · 2018: 38 · 2017: 35 · 2016: 21 · 2015: 6
- FWCI
- 1.95
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Journal of Molecular Cell Biology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Ministero della Salute (GR-2010)
- Associazione Italiana per la Ricerca sul Cancro
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- Chk2, DNA damage response, cell cycle checkpoints, apoptosis, cellular senescence, DNA repair, genotoxic stress, cell cycle progression, carcinogenesis, cancer therapy targets
- MeSH terms
- Animals, Cell Transformation, Neoplastic, DNA Damage, Humans, Phosphorylation, Cell Cycle Checkpoints, Checkpoint Kinase 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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