Regulation of DNA repair throughout the cell cycle
Abstract
The repair of DNA lesions that occur endogenously or in response to diverse genotoxic stresses is indispensable for genome integrity. DNA lesions activate checkpoint pathways that regulate specific DNA-repair mechanisms in the different phases of the cell cycle. Checkpoint-arrested cells resume cell-cycle progression once damage has been repaired, whereas cells with unrepairable DNA lesions undergo permanent cell-cycle arrest or apoptosis. Recent studies have provided insights into the mechanisms that contribute to DNA repair in specific cell-cycle phases and have highlighted the mechanisms that ensure cell-cycle progression or arrest in normal and cancerous cells.
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The NER pathway is the primary mechanism in cells for removal of helix-distorting, replication-blocking bulky DNA adducts induced by exogenous agents such as UV radiation and genotoxic chemicals.
“The NER pathway is the primary mechanism in cells for removal of helix-distorting, replication-blocking bulky DNA adducts that are induced by exogenous agents such as UV radiation and a variety of genotoxic chemicals [1], [2].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [2]
ATR is predominantly responsible for the DNA damage response upon UVR exposure.
“Previous studies support that ATR is predominantly responsible for DDR upon UVR exposure”
From ATR- and ATM-Mediated DNA Damage Response Is Dependent on Excision Repair Assembly during G1 but Not in S Phase of Cell Cycle (2016) · cites this paper as [26]
H2AX is phosphorylated both in G1 and S phases by ATR in response to UV irradiation.
“H2AX is phosphorylated both in G1 and S phases by ATR in response to UV irradiation [26;32–38].”
From ATR- and ATM-Mediated DNA Damage Response Is Dependent on Excision Repair Assembly during G1 but Not in S Phase of Cell Cycle (2016) · cites this paper as [26]
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- Authors
- Branzei, D., & Foiani, M.
- Affiliations
- IFOM (IT)
- University of Milan (IT)
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2008-02-20
- Volume
- 9
- Issue
- 4
- Pages
- 297-308
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- OpenAlex
- W2093814864
- Cited by
- 1,228
- References
- 159
- Citations by year
- 2026: 18 · 2025: 51 · 2024: 54 · 2023: 48 · 2022: 50 · 2021: 72 · 2020: 71 · 2019: 91 · 2018: 119 · 2017: 107 · 2016: 57 · 2015: 66 · 2014: 61 · 2013: 77 · 2012: 67
- FWCI
- 5.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Universitätsbibliographie, Universität Duisburg-Essen (submittedVersion)
- Funders
- 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 › Fungal and yeast genetics research
- Keywords
- DNA repair, cell cycle, DNA damage checkpoint, cell cycle arrest, cell cycle progression, genome stability, genotoxic stress, apoptosis, DNA lesions, cancer cells
- MeSH terms
- Animals, Cell Cycle, DNA Damage, DNA Repair, Humans, Protein Kinases, Small Ubiquitin-Related Modifier Proteins, Ubiquitination
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