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Maintaining genome stability at the replication fork
Open accessAbstract
Aberrant DNA replication is a major source of the mutations and chromosome rearrangements that are associated with pathological disorders. When replication is compromised, DNA becomes more prone to breakage. Secondary structures, highly transcribed DNA sequences and damaged DNA stall replication forks, which then require checkpoint factors and specialized enzymatic activities for their stabilization and subsequent advance. These mechanisms ensure that the local DNA damage response, which enables replication fork progression and DNA repair in S phase, is coupled with cell cycle transitions. The mechanisms that operate in eukaryotic cells to promote replication fork integrity and coordinate replication with other aspects of chromosome maintenance are becoming clear.
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“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 [35]
In the citing paper
“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 [35]
In the citing paper
“To maintain genome stability, the DDR pathways are conserved surveillance mechanisms coordinating DNA repair, cell cycle progression, transcription, apoptosis, and senescence [19, 39–41].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [41]
In the citing paper
“5′-primed ssDNA coated with RPA (RPA-ssDNA) is the determinant DNA structure for ATR activation in response to stalled DNA replication forks or DNA damage [41, 94–96].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [41]
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Metadata
- Authors
- Branzei, D., & Foiani, M.
- Affiliations
- IFOM (IT)
- University of Milan (IT)
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2010-03
- Volume
- 11
- Issue
- 3
- Pages
- 208-219
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- OpenAlex
- W2063979868
- Cited by
- 786
- References
- 155
- Citations by year
- 2026: 16 · 2025: 15 · 2024: 27 · 2023: 22 · 2022: 30 · 2021: 36 · 2020: 51 · 2019: 48 · 2018: 38 · 2017: 56 · 2016: 70 · 2015: 67 · 2014: 73 · 2013: 82 · 2012: 73
- FWCI
- 6.60
- Type
- journal article
- Language
- en
- Open access
- green
- zenodo.org
- Licence
- other-oa
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Universitätsbibliographie, Universität Duisburg-Essen (submittedVersion)
- Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, other-oa)
- Funders
- Associazione Italiana per la Ricerca sul Cancro
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Keywords
- genome stability, DNA replication, replication fork, replication fork stalling, DNA secondary structure, DNA damage response, DNA repair, S phase, chromosome maintenance, genetic mutations, chromosomal rearrangements
- MeSH terms
- Animals, DNA, DNA Damage, DNA Repair, DNA Replication, Humans, Models, Biological, Nucleic Acid Conformation, Replication Origin, Genomic Instability
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