ATR signalling: more than meeting at the fork
Open accessAbstract
Preservation of genome integrity via the DNA-damage response is critical to prevent disease. ATR (ataxia telangiectasia mutated- and Rad3-related) is essential for life and functions as a master regulator of the DNA-damage response, especially during DNA replication. ATR controls and co-ordinates DNA replication origin firing, replication fork stability, cell cycle checkpoints and DNA repair. Since its identification 15 years ago, a model of ATR activation and signalling has emerged that involves localization to sites of DNA damage and activation through protein–protein interactions. Recent research has added an increasingly detailed understanding of the canonical ATR pathway, and an appreciation that the canonical model does not fully capture the complexity of ATR regulation. In the present article, we review the ATR signalling process, focusing on mechanistic findings garnered from the identification of new ATR-interacting proteins and substrates. We discuss how to incorporate these new insights into a model of ATR regulation and point out the significant gaps in our understanding of this essential genome-maintenance pathway.
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RPA-coated 5'-primed single-stranded DNA is the determinant DNA structure for ATR activation in response to stalled replication forks or DNA damage.
“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 [94]
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References 130 · Cited by 316
- Authors
- Nam, E. A., & Cortez, D.
- Affiliations
- Vanderbilt University (US)
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2011-05-27
- Volume
- 436
- Issue
- 3
- Pages
- 527-536
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC3678388
- OpenAlex
- W2155650828
- Cited by
- 316
- References
- 130
- Citations by year
- 2026: 10 · 2025: 9 · 2024: 18 · 2023: 12 · 2022: 10 · 2021: 8 · 2020: 11 · 2019: 14 · 2018: 21 · 2017: 32 · 2016: 34 · 2015: 38 · 2014: 32 · 2013: 39 · 2012: 21
- FWCI
- 2.87
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biochemical Journal (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA102729, CA102729)
- 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 › DNA and Nucleic Acid Chemistry
- Keywords
- DNA damage response, DNA replication, replication fork stability, cell cycle checkpoints, DNA repair, genome stability, protein-protein interaction
- MeSH terms
- MutL Protein Homolog 1, Animals, Ataxia Telangiectasia, Carrier Proteins, DNA Damage, DNA Repair, DNA Helicases, DNA-Binding Proteins, Humans, Nuclear Proteins, Protein Processing, Post-Translational, Signal Transduction, Protein Serine-Threonine Kinases, Protein Structure, Tertiary, Cell Cycle Proteins, Adaptor Proteins, Signal Transducing, Proto-Oncogene Proteins c-ets, BH3 Interacting Domain Death Agonist Protein, MutS DNA Mismatch-Binding Protein, Fanconi Anemia Complementation Group Proteins, Ataxia Telangiectasia Mutated Proteins
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