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DNA Damage Induced by Temozolomide Signals to both ATM and ATR: Role of the Mismatch Repair System
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“Alternatively, in response to the DNA methylating agent temozolomide, the ATR-Chk1 checkpoint is activated to arrest cell cycle at G2/M transition. This is followed by ATM-Chk2 checkpoint activation, suggesting ATR functions earlier than ATM [143].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [143]
Citations
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ATM and ATR as therapeutic targets in cancer
Weber, A. M., & Ryan, A. J. (2014) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2014.12.001 · Cited by 676
Chemoradiotherapy in Malignant Glioma: Standard of Care and Future Directions
Stupp, R., Hegi, M. E., Gilbert, M. R., & Chakravarti, A. (2007) · Journal of Clinical Oncology · doi:10.1200/jco.2007.11.8554 · Cited by 531
Metadata
- Authors
- Caporali, S., Falcinelli, S., Starace, G., Russo, M. T., Bonmassar, E., Jiricny, J., & D’Atri, S.
- Affiliations
- University of Zurich (CH)
- Corresponding author
- D’Atri, Stefania
- Venue
- Molecular Pharmacology
- Publisher
- Elsevier BV
- Published
- 2004-09
- Volume
- 66
- Issue
- 3
- Pages
- 478-491
- ISSN
- 0026-895X (ISSN-L)
- OpenAlex
- W4405993409
- Cited by
- 131
- References
- 41
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 6 · 2022: 4 · 2021: 10 · 2020: 1 · 2019: 5 · 2018: 7 · 2017: 8 · 2016: 5 · 2015: 4 · 2014: 10 · 2013: 8 · 2012: 7
- FWCI
- 1.89
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Pharmacology (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Glioma Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- temozolomide, DNA mismatch repair, ATM kinase, ATR kinase, G2/M checkpoint, DNA damage signaling, Chk1 phosphorylation, Chk2 phosphorylation, p53 Ser15 phosphorylation, apoptosis, methylating agents, DNA repair
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