ReviewFrontiers in cell and developmental biology2021
To Join or Not to Join: Decision Points Along the Pathway to Double-Strand Break Repair vs. Chromosome End Protection.
Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Unveiling the cut-and-repair cycle of designer nucleases in human stem and T cells via CLEAR-time dPCR.Nature communications · 2025Article
- Weaponizing CRISPR/Cas9 for selective elimination of cells with an aberrant genome.DNA repair · 2025Article
- An mRNA vaccine induces antimycobacterial immunity by activating DNA damage repair and autophagy.Molecular therapy. Nucleic acids · 2025Article
- Deciphering repair pathways of clustered DNA damage in human TK6 cells: insights from atomic force microscopy direct visualization.Nucleic acids research · 2025Article
- Utilizing insights of DNA repair machinery to discover MMEJ deletions and novel mechanisms.Nucleic acids research · 2024Article
- DNA-PK and ATM drive phosphorylation signatures that antagonistically regulate cytokine responses to herpesvirus infection or DNA damage.Cell systems · 2024Article
- Structure and mechanism in non-homologous end joining.DNA repair · 2023Article
- Dose-Dependent Shift in Relative Contribution of Homologous Recombination to DNA Repair after Low-LET Ionizing Radiation Exposure: Empirical Evidence and Numerical Simulation.Current issues in molecular biology · 2023Article
- Hornerin mediates phosphorylation of the polo-box domain in Plk1 by Chk1 to induce death in mitosis.Cell death and differentiation · 2023Article
- Cisplatin-induced cell death increases the degradation of the MRE11-RAD50-NBS1 complex through the autophagy/lysosomal pathway.Cell death and differentiation · 2023Article
- TRIM24 is critical for the cellular response to DNA double-strand breaks through regulating the recruitment of MRN complex.Oncogene · 2023Article
- Kinome-wide screening uncovers a role for Bromodomain Protein 3 in DNA double-stranded break repair.DNA repair · 2023Article
- Article
- High-throughput screen to identify compounds that prevent or target telomere loss in human cancer cells.NAR cancer · 2022Article
- Gastric Cancer Risk and Pathogenesis inCancers · 2022Review
- Comparison of the Medical Uses and Cellular Effects of High and Low Linear Energy Transfer Radiation.Toxics · 2022Review
- Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation of DNA double-strand breaks (DSBs) and telomeres are diametrically opposed in the cell. DSBs are considered one of the most deleterious forms of DNA damage and must be quickly recognized and repaired. Telomeres, on the other hand, are specialized, stable DNA ends that must be protected from recognition as DSBs to inhibit unwanted chromosome fusions. Decisions to join DNA ends, or not, are therefore critical to genome stability. Yet, the processing of telomeres and DSBs share many commonalities. Accordingly, key decision points are used to shift DNA ends toward DSB repair vs. end protection. Additionally, DSBs can be repaired by two major pathways, namely homologous recombination (HR) and non-homologous end joining (NHEJ). The choice of which repair pathway is employed is also dictated by a series of decision points that shift the break toward HR or NHEJ. In this review, we will focus on these decision points and the mechanisms that dictate end protection vs. DSB repair and DSB repair choice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.