DNA damage repair and transcription: Double-strand breaks: signaling pathways and repair mechanisms
Open accessAbstract
Double-strand breaks arise frequently in the course of endogenous - normal and pathological - cellular DNA metabolism or can result from exogenous agents such as ionizing radiation. It is generally accepted that these lesions represent one of the most severe types of DNA damage with respect to preservation of genomic integrity. Therefore, cells have evolved complex mechanisms that include cell-cycle arrest, activation of various genes, including those associated with DNA repair, and in certain cases induction of the apoptotic pathway to respond to double-strand breaks. In this review we discuss recent progress in our understanding of cellular responses to DNA double-strand breaks. In addition to an analysis of the current paradigms of detection, signaling and repair, insights into the significance of chromatin remodeling in the double-strand break-response pathways are provided.
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Unrepaired double-strand breaks can cause chromosomal aberrations and loss of function of proteins needed for cell survival or viability.
“If not repaired, DSBs can lead to chromosomal aberrations and the dysfunction of key proteins for cell survival or viability [45–47].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [45]
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γH2AX: a sensitive molecular marker of DNA damage and repair
Mah, L.-J., El-Osta, A., & Karagiannis, T. C. (2010) · Leukemia · doi:10.1038/leu.2010.6 · Cited by 1,557 · see citing works
Self-citationYan, S., Sorrell, M., & Berman, Z. (2014) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-014-1666-4 · Cited by 247 · see citing works
- Authors
- Karagiannis, T. C., & El-Osta, A.
- Affiliations
- Peter MacCallum Cancer Centre (AU)
- ORCID
- Karagiannis, T.C.
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2004-08
- Volume
- 61
- Issue
- 17
- Pages
- 2137-47
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11138614
- OpenAlex
- W2412757439
- Cited by
- 78
- References
- 0
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 3 · 2020: 4 · 2019: 2 · 2017: 3 · 2016: 5 · 2015: 1 · 2014: 2 · 2013: 6 · 2012: 4
- FWCI
- 1.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- DNA double-strand breaks, DNA repair, transcription, cell cycle arrest, DNA repair signaling, apoptosis, chromatin remodeling, genome stability, ionizing radiation, endogenous DNA damage
- MeSH terms
- Animals, Chromatin, DNA Damage, DNA Repair, Humans, Recombination, Genetic, Signal Transduction
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