# Double Stranded Break Repair: Mechanisms and Methods

## Introduction to Double Stranded Break Repair

A double stranded break (DSB) is a form of DNA damage in which both phosphodiester backbones of the [DNA double helix](/blog/guides/dna-double-helix) are severed at sites that are either directly opposite one another or separated by only a few nucleotide pairs. Unlike single stranded lesions, which leave the complementary strand intact as a template for repair, a DSB physically disrupts the continuity of the chromosome. If left unrepaired, a single DSB is sufficient to trigger cell cycle arrest and, in many contexts, programmed cell death. If misrepaired, DSBs generate chromosomal rearrangements—deletions, duplications, inversions, and translocations—that are hallmarks of cancer cells.

The cellular response to DSBs is organized around two mechanistically distinct pathways: non-homologous end joining (NHEJ) and [homologous recombination](/knowledge/molecular-biology/homologous-recombination) (HR). NHEJ directly ligates the two broken ends after limited processing, requiring no template and operating throughout the cell cycle. HR, by contrast, uses a homologous DNA sequence—typically the sister chromatid—as a template to restore the original sequence with high fidelity, but it is restricted to the S and G2 phases of the cell cycle when a sister chromatid is available. The choice between these pathways is governed by cell cycle position, the nature of the DNA ends, and a network of regulatory proteins that includes 53BP1 and BRCA1. Understanding the molecular logic of DSB repair is essential not only for basic cell biology but also for clinical oncology, where defects in these pathways are exploited therapeutically. For a broader overview of how cells manage genomic lesions, see [DNA Repair](/knowledge/molecular-biology/dna-repair).

## Sources of Double Stranded Breaks

DSBs arise from both endogenous metabolic processes and exogenous environmental agents. The sources differ in their frequency, the chemical nature of the ends they produce, and the repair pathway they preferentially engage.

**Ionizing radiation** (IR), including X-rays and gamma rays, deposits energy in tissue and causes DSBs both directly, by breaking the sugar-phosphate backbone, and indirectly, through the radiolysis of water to generate reactive oxygen species (ROS) that attack DNA. A typical dose of 1 Gy of gamma radiation induces approximately 20–40 DSBs per cell. The ends produced by IR are frequently "dirty"—they carry damaged sugar moieties, abasic sites, or 3′-phosphate and 3′-phosphoglycolate termini that cannot be ligated directly and require processing before rejoining.

**Reactive oxygen species** generated during normal aerobic metabolism—superoxide, hydrogen peroxide, and hydroxyl radical—also produce DSBs, though less frequently than IR. Hydroxyl radical, in particular, abstracts hydrogen atoms from deoxyribose, leading to strand scission. When two such lesions occur in close proximity on opposite strands, a DSB results.

**[Replication fork collapse](/knowledge/molecular-biology/replication-fork-collapse)** is a major endogenous source of DSBs. During S phase, the replication machinery encounters obstacles such as unrepaired single strand lesions, DNA secondary structures, or tightly bound protein–DNA complexes. When a replicative helicase encounters a nick in the template strand, the fork can collapse, generating a one-ended DSB. These replication-associated DSBs are repaired exclusively by HR, because the broken end lacks a second end to ligate.

**Programmed DSBs** are generated deliberately in specific biological contexts. In developing lymphocytes, the RAG1/RAG2 recombinase introduces DSBs at recombination signal sequences during V(D)J recombination to generate antibody and T cell receptor diversity. In meiosis, the Spo11 protein introduces programmed DSBs that initiate [homologous recombination](/knowledge/molecular-biology/homologous-recombination) between maternal and paternal chromosomes, a process required for proper chromosome segregation. In both cases, the repair of these breaks is channeled into specific pathways—NHEJ for V(D)J recombination and HR for meiosis.

**Chemotherapeutic agents** such as bleomycin and the topoisomerase II poisons (etoposide, doxorubicin) also generate DSBs. Topoisomerase II poisons trap the enzyme in a covalent complex with DNA, converting transient enzyme-mediated breaks into persistent DSBs.

## Non-Homologous End Joining (NHEJ)

NHEJ is the dominant DSB repair pathway in mammalian cells, operating in all phases of the cell cycle but with particular importance in G1, when no sister chromatid is available for HR. The pathway is intrinsically error-prone: it ligates two DNA ends directly, and any nucleotide loss or addition at the junction becomes a permanent mutation. Despite this, NHEJ is essential for genome stability because it provides a rapid, template-independent mechanism for restoring chromosome continuity.

### Key Proteins in NHEJ

The NHEJ pathway proceeds through four ordered steps: recognition, end processing, alignment, and ligation.

1. **Recognition by the Ku heterodimer.** The Ku70/Ku80 heterodimer (70 kDa and 80 kDa subunits) binds to DNA ends with high affinity and in a sequence-independent manner. Ku forms a ring-shaped structure that threads onto the [DNA double helix](/blog/guides/dna-double-helix), protecting the ends from nucleolytic degradation and serving as a platform for recruitment of downstream factors. Ku binding occurs within seconds of DSB formation and is the initiating event for NHEJ.

2. **Recruitment of the DNA-PK catalytic subunit.** The DNA-dependent protein kinase catalytic subunit (DNA-PKcs, ~470 kDa) is recruited to the Ku–DNA complex, forming the active DNA-PK holoenzyme. DNA-PKcs undergoes autophosphorylation at multiple sites, including the ABCDE cluster (Ser2612, Ser2624, Thr2638, Thr2647) and the PQR cluster (Ser2023–Ser2056). Autophosphorylation induces a conformational change that allows end processing enzymes access to the DNA termini.

3. **End processing.** Many DSB ends are not directly ligatable. Artemis, a nuclease with 5′→3′ exonuclease and endonuclease activities, is activated by phosphorylation by DNA-PKcs. Artemis trims 5′ and 3′ overhangs and opens hairpin structures. Additional processing enzymes include polynucleotide kinase 3′-phosphatase (PNKP), which removes 3′-phosphates and phosphorylates 5′-hydroxyls, and the DNA polymerases μ and λ, which add nucleotides in a template-independent or template-dependent manner to create short regions of microhomology (2–4 bp) that stabilize the junction.

4. **Ligation by XRCC4–Ligase IV.** The final ligation step is catalyzed by DNA ligase IV in complex with XRCC4. XRCC4 stabilizes ligase IV and recruits it to the DNA ends. The XRCC4-like factor XLF (also called Cernunnos) stimulates ligation by bridging the two Ku-bound DNA ends. In the absence of ligase IV, DSB repair is severely impaired, and ligase IV knockout mice are embryonic lethal.

The error-prone nature of NHEJ is a direct consequence of end processing. If the two ends have compatible overhangs, ligation can be precise. More commonly, however, nucleotides are lost or added, producing small insertions or deletions (indels) at the junction. The repair of programmed DSBs during V(D)J recombination relies on this imprecision to generate junctional diversity in antigen receptors. For a dedicated treatment of this pathway, see [Non Homologous End Joining Repair](/knowledge/molecular-biology/non-homologous-end-joining-repair).

### NHEJ in G1 Phase

In G1 phase, NHEJ is the only available DSB repair pathway. The absence of a sister chromatid precludes HR, and the cell must rejoin broken ends regardless of sequence loss. This is a calculated trade-off: a small deletion at the break site is preferable to a chromosomal fragmentation event that would be lethal. The G1 checkpoint, mediated by p53 and p21, provides time for NHEJ to complete before the cell commits to DNA replication. If NHEJ fails and unrepaired DSBs persist into S phase, the cell may undergo apoptosis or enter senescence.

## Homologous Recombination (HR)

Homologous recombination repairs DSBs using a homologous DNA sequence as a template. In somatic cells, the template is the sister chromatid, which is present after DNA replication. Because the sister chromatid is identical in sequence, HR is essentially error-free. The pathway is complex, requiring the coordinated action of more than a dozen proteins, and is restricted to the S and G2 phases of the cell cycle.

### BRCA1 and BRCA2 in HR

The breast cancer susceptibility proteins BRCA1 and BRCA2 are central to HR. BRCA1 (220 kDa) functions as a scaffold that coordinates the early steps of resection and recruits downstream factors. It forms complexes with BARD1, and together they possess E3 ubiquitin ligase activity. BRCA1 also interacts with PALB2, which in turn recruits BRCA2.

BRCA2 (384 kDa) is the loading factor for RAD51, the recombinase that catalyzes strand invasion. BRCA2 binds to RAD51 monomers and promotes the assembly of RAD51 nucleoprotein filaments on single stranded DNA (ssDNA). BRCA2 also stabilizes RAD51–ssDNA filaments by displacing RPA (replication protein A), which coats ssDNA and must be removed before RAD51 can bind. Cells lacking BRCA2 show a dramatic reduction in RAD51 foci formation and are profoundly defective in HR.

### HR in S/G2 Phases

HR proceeds through several ordered steps:

1. **Resection.** The 5′ ends of the DSB are resected to generate 3′ single stranded DNA overhangs. Resection is initiated by the MRN complex (MRE11–RAD50–NBS1) together with CtIP, which trims the ends to produce short 3′ overhangs. Long-range resection is then carried out by EXO1 (5′→3′ exonuclease) or the BLM helicase in complex with DNA2 nuclease. The resulting ssDNA is immediately coated by RPA, which protects it from nucleases and prevents secondary structure formation.

2. **RAD51 filament formation.** BRCA2 mediates the exchange of RPA for RAD51 on the ssDNA, forming a right-handed helical nucleoprotein filament. RAD51 filaments are the catalytic engine of HR: they search for homologous sequences and catalyze strand invasion.

3. **Strand invasion and D-loop formation.** The RAD51–ssDNA filament invades the homologous duplex DNA of the sister chromatid, base-pairing with the complementary strand and displacing the non-complementary strand to form a displacement loop (D-loop). The 3′ end of the invading strand is then extended by DNA polymerase δ or ε, copying sequence information from the intact template.

4. **Resolution.** The Holliday junctions formed during HR are resolved by structure-specific endonucleases. The MUS81–EME1 complex cleaves one class of junctions, while GEN1 resolves others. Alternatively, the invading strand can be displaced and annealed to the other end of the break in a process called synthesis-dependent strand annealing (SDSA), which produces only non-crossover products. The choice between crossover and non-crossover outcomes is regulated by the BLM–TOP3A–RMI1 complex, which promotes SDSA and suppresses crossing over.

The requirement for a sister chromatid means that HR can only occur after DNA replication. In S phase, HR repairs replication-associated DSBs; in G2, it repairs breaks that arise from residual damage or from IR exposure. The restriction of HR to S/G2 is enforced by cell cycle-dependent phosphorylation of CtIP and by the activity of [cyclin-dependent kinases](/knowledge/molecular-biology/cyclin-dependent-kinase) (CDKs), which phosphorylate multiple HR factors.

## Choice Between NHEJ and HR

The decision to repair a DSB by NHEJ or HR is governed by a competition between two opposing protein complexes at the break site. The key determinant is whether the DNA ends undergo resection.

**53BP1 promotes NHEJ.** The protein 53BP1 (p53-binding protein 1) is recruited to DSB-flanking chromatin, where it binds to dimethylated lysine 20 of histone H4 (H4K20me2) and to ubiquitinated histone H2A. 53BP1 recruits downstream effectors, including RIF1 and the shieldin complex, which block resection. By protecting the DNA ends from nucleolytic attack, 53BP1 channels repair toward NHEJ. In G1, 53BP1 activity is high, and resection is suppressed.

**BRCA1 promotes HR.** In S/G2, BRCA1 counteracts 53BP1. BRCA1 is recruited to DSBs through its interaction with the MRN complex and with ubiquitinated histones. BRCA1 promotes resection by recruiting CtIP and by displacing 53BP1 from the break site. The antagonism between 53BP1 and BRCA1 is a central regulatory node: in BRCA1-deficient cells, 53BP1-dependent NHEJ proceeds even in S phase, leading to aberrant repair and genomic instability.

Additional factors influence pathway choice. The nature of the DNA ends matters: ends with blocked or damaged termini are more likely to undergo resection and enter HR, because they cannot be ligated directly. The cell cycle phase is paramount: CDK activity in S/G2 phosphorylates CtIP and other resection factors, promoting HR. The local chromatin environment also plays a role, with heterochromatic breaks showing a greater dependence on HR.

## Methods to Study Double Stranded Break Repair

Studying DSB repair requires methods to detect breaks, quantify repair efficiency, and distinguish between NHEJ and HR. Several complementary approaches are commonly used.

### γH2AX Foci as a Marker

One of the most widely used methods to detect DSBs is immunofluorescence staining for γH2AX, the phosphorylated form of histone H2AX. Within minutes of DSB formation, the kinase ATM (ataxia-telangiectasia mutated) phosphorylates H2AX at serine 139 in the chromatin flanking the break. This phosphorylation spreads over megabase-scale domains, and the resulting γH2AX signal appears as discrete nuclear foci when visualized by [fluorescence microscopy](/knowledge/diagnostics/imaging/fluorescence-microscopy-principles-applications-and-image-acquisition). Each focus is generally assumed to represent one DSB, although this correlation is approximate.

γH2AX foci are used to quantify DSB induction and repair kinetics. After exposure to IR, the number of foci peaks at 30–60 minutes and declines as repair proceeds, with a half-life of 1–4 hours depending on the cell type and repair pathway. The assay requires fixation of cells, incubation with a primary antibody against γH2AX, and a fluorophore-conjugated secondary antibody. Images are captured by fluorescence or confocal microscopy, and foci are counted either manually or by automated image analysis. A typical experiment might expose cells to 2 Gy of IR, fix at various time points (0, 0.5, 1, 2, 4, 8, 24 hours), and quantify foci to generate a repair curve.

### Reporter Assays for DSB Repair

Reporter-based assays provide a quantitative readout of NHEJ or HR efficiency. These assays use a stably integrated reporter cassette containing a restriction enzyme site that, when cleaved, creates a DSB. Repair of the break restores a functional gene, typically green fluorescent protein (GFP) or luciferase, allowing repair events to be scored by flow cytometry or luminescence.

The DR-GFP assay is the standard for measuring HR. The reporter contains two copies of the GFP gene: one is a full-length but inactive copy (SecGFP) with an I-SceI recognition site, and the other is a truncated fragment (iGFP) that serves as the homologous template. Expression of the I-SceI endonuclease creates a DSB in SecGFP. If the break is repaired by HR using iGFP as a template, a functional GFP gene is restored, and cells become GFP-positive. The frequency of GFP-positive cells, measured by flow cytometry, reflects HR efficiency.

For NHEJ, the EJ5-GFP reporter is commonly used. This reporter contains a GFP gene interrupted by a puromycin resistance cassette flanked by I-SceI sites. Cleavage by I-SceI releases the puromycin cassette, and NHEJ rejoins the ends to restore GFP expression. The frequency of GFP-positive cells reflects NHEJ efficiency.

These assays are typically performed by transfecting cells with an I-SceI expression plasmid, harvesting cells 48–72 hours later, and analyzing GFP expression by flow cytometry. HR frequencies in wild-type cells are typically 0.1–1% of transfected cells, while NHEJ frequencies are 10–50-fold higher, reflecting the dominance of NHEJ in most cell types.

**Comet assay.** The single-cell gel electrophoresis (comet) assay detects DNA strand breaks, including DSBs, in individual cells. Cells are embedded in agarose on a microscope slide, lysed, and subjected to electrophoresis under alkaline or neutral conditions. Broken DNA migrates toward the anode, forming a "comet tail" whose length and intensity are proportional to the amount of DNA damage. The neutral comet assay is more specific for DSBs, while the alkaline version detects both single and double strand breaks. The comet assay is simple, requires few cells, and is useful for comparing DSB levels between cell populations, but it does not distinguish between repair pathways.

**Chromosomal analysis.** Cytogenetic methods, such as Giemsa staining of metaphase chromosomes, can detect chromosomal aberrations resulting from misrepaired DSBs. Dicentric chromosomes, translocations, and radial chromosomes are scored to assess the fidelity of DSB repair. These methods are labor-intensive but provide direct evidence of repair outcomes.

## Clinical Relevance of DSB Repair Defects

Mutations in DSB repair genes are strongly associated with cancer predisposition, immunodeficiency, and neurodegeneration. The most clinically significant examples are the hereditary breast and ovarian cancer syndromes caused by mutations in BRCA1 or BRCA2. Women carrying a deleterious BRCA1 mutation have a 60–80% lifetime risk of breast cancer and a 40–60% risk of ovarian cancer; the corresponding risks for BRCA2 mutation carriers are 45–60% and 15–25%. The tumors that arise in these patients typically show loss of heterozygosity at the BRCA locus, meaning the wild-type allele is lost and the cell is completely deficient in HR.

The therapeutic exploitation of HR deficiency is the basis of PARP inhibitor therapy. Poly(ADP-ribose) polymerase 1 (PARP1) is a DNA damage sensor that binds to single strand breaks and synthesizes poly(ADP-ribose) chains on itself and on histones, recruiting repair factors. When PARP is inhibited, single strand breaks persist and are converted to DSBs during DNA replication. In normal cells, these DSBs are repaired by HR. In BRCA-deficient cells, HR is non-functional, and the DSBs are instead repaired by error-prone NHEJ, leading to genomic catastrophe and cell death. This concept, termed synthetic lethality, underlies the clinical use of PARP inhibitors such as olaparib and niraparib in BRCA-mutant cancers. The selectivity of PARP inhibitors for HR-deficient tumors is a paradigm for targeted cancer therapy.

Defects in NHEJ also cause disease. Mutations in Artemis cause a severe combined immunodeficiency (SCID) characterized by absence of B and T cells, because V(D)J recombination is blocked. Mutations in DNA ligase IV cause a syndrome of immunodeficiency, developmental delay, and bone marrow failure. Mutations in ATM cause ataxia-telangiectasia, a disorder characterized by cerebellar degeneration, immunodeficiency, and a 100-fold increased risk of lymphoid malignancies. ATM is a master regulator of the DSB response, phosphorylating dozens of substrates including H2AX, p53, and BRCA1.

## Common Pitfalls and Misconceptions

Students frequently encounter several conceptual difficulties when learning about DSB repair.

**Confusing NHEJ and HR.** The most common error is to conflate the two pathways. Remember: NHEJ ligates ends directly, requires Ku and ligase IV, is error-prone, and operates in all cell cycle phases. HR uses a homologous template, requires RAD51 and BRCA2, is error-free, and operates only in S/G2. A useful mnemonic: NHEJ is "quick and dirty," HR is "slow and accurate."

**Misunderstanding the role of the sister chromatid.** HR uses the sister chromatid as a template, not the homologous chromosome. The sister chromatid is identical in sequence, whereas the homologous chromosome carries different alleles. Using the homologous chromosome would risk loss of heterozygosity. In meiosis, however, HR between homologous chromosomes is deliberate and required for genetic exchange.

**Overlooking cell cycle regulation.** HR cannot occur in G1 because there is no sister chromatid. Students sometimes propose HR as a repair mechanism for breaks in G1 cells. The cell cycle restriction is absolute: resection is blocked in G1 by 53BP1, and CDK-dependent phosphorylation of resection factors does not occur.

**Assuming NHEJ is always mutagenic.** While NHEJ is error-prone, it is not always mutagenic. If the DNA ends are compatible and no processing is required, ligation can be precise. The error rate depends on the nature of the ends and the extent of processing. In some contexts, such as the repair of RAG-induced breaks during V(D)J recombination, the imprecision of NHEJ is functionally important.

**Confusing γH2AX with a repair protein.** γH2AX is a marker of DSBs, not a repair enzyme. It functions to concentrate repair factors at the break site and to signal damage, but it does not directly catalyze repair. The appearance of γH2AX foci indicates the presence of DSBs, not the activity of a specific repair pathway.

**Neglecting the role of resection in pathway choice.** The decision between NHEJ and HR hinges on resection. If resection occurs, HR proceeds; if resection is blocked, NHEJ proceeds. Understanding the regulation of resection by 53BP1 and BRCA1 is key to understanding pathway choice.

## Frequently Asked Questions

### What is the difference between NHEJ and homologous recombination?

NHEJ ligates the two broken DNA ends directly after minimal processing. It requires the Ku heterodimer, DNA-PKcs, Artemis, and ligase IV–XRCC4. NHEJ is error-prone, frequently introducing small insertions or deletions at the junction, and operates in all cell cycle phases. HR uses a homologous DNA sequence—the sister chromatid—as a template to restore the original sequence. It requires resection to generate 3′ overhangs, RAD51 filament formation, and strand invasion. HR is error-free and restricted to S/G2 phases when a sister chromatid is available.

### When does homologous recombination occur?

HR occurs during the S and G2 phases of the cell cycle, when the sister chromatid is present. It is the primary pathway for repairing replication-associated DSBs and for repairing IR-induced breaks in S/G2. In G1, HR is blocked because resection is inhibited by 53BP1 and because CDK activity is low.

### What is the role of Ku in NHEJ?

Ku is a heterodimer of Ku70 and Ku80 that binds with high affinity to DNA ends. It protects the ends from degradation, recruits DNA-PKcs to form the active DNA-PK complex, and serves as a platform for recruiting downstream NHEJ factors including Artemis, polymerases μ and λ, and ligase IV–XRCC4. Ku binding is the initiating event in NHEJ.

### How is double stranded break repair studied?

DSB repair is studied using γH2AX immunofluorescence to detect and quantify breaks, reporter assays (DR-GFP for HR, EJ5-GFP for NHEJ) to measure repair efficiency, the comet assay to detect strand breaks, and cytogenetic analysis to assess repair fidelity. Each method has strengths and limitations, and they are often used in combination.

### Why are BRCA1 and BRCA2 important in DNA repair?

BRCA1 and BRCA2 are essential for HR. BRCA1 promotes resection of DNA ends and coordinates the recruitment of downstream factors. BRCA2 loads RAD51 onto single stranded DNA, displacing RPA and enabling filament formation and strand invasion. Cells lacking functional BRCA1 or BRCA2 are profoundly defective in HR and rely on error-prone NHEJ, leading to genomic instability and cancer predisposition.

### What happens if double stranded breaks are not repaired?

Unrepaired DSBs trigger cell cycle arrest and, if persistent, apoptosis or senescence. A single unrepaired DSB can be lethal. In cells that survive with unrepaired or misrepaired breaks, chromosomal rearrangements accumulate, driving tumorigenesis. The p53 pathway is central to the cellular response to persistent DSBs.

### What is the role of 53BP1 in DSB repair?

53BP1 promotes NHEJ by protecting DNA ends from resection. It is recruited to DSB-flanking chromatin, where it binds H4K20me2 and ubiquitinated H2A, and recruits downstream effectors including RIF1 and shieldin that block nucleolytic processing. In S/G2, BRCA1 counteracts 53BP1 to promote resection and HR. The balance between 53BP1 and BRCA1 determines pathway choice.

## Key Takeaways

- Double stranded breaks are the most dangerous form of DNA damage; a single unrepaired DSB can cause cell death, and misrepair generates chromosomal rearrangements that drive cancer.
- Two principal repair pathways exist: NHEJ, which ligates ends directly and is error-prone, and HR, which uses the sister chromatid as a template and is error-free.
- NHEJ operates in all cell cycle phases and is mediated by Ku, DNA-PKcs, Artemis, and ligase IV–XRCC4.
- HR is restricted to S/G2 phases and requires resection, RAD51 filament formation, and strand invasion, with BRCA1 and BRCA2 playing essential roles.
- Pathway choice is determined by cell cycle phase and by the antagonism between 53BP1 (promoting NHEJ) and BRCA1 (promoting HR), with resection as the key regulatory step.
- DSB repair is studied using γH2AX foci, reporter assays, the comet assay, and cytogenetic analysis.
- Mutations in DSB repair genes, particularly BRCA1 and BRCA2, predispose to cancer and are the basis for PARP inhibitor therapy, which exploits synthetic lethality in HR-deficient tumors.

## Further Reading

- Ali A et al. *Double-Stranded Break Repair in Mammalian Cells and Precise Genome Editing*. Genes. 2022. [PubMed 35627122](https://doi.org/10.3390/genes13050737)
- Zhang YX, Pan WY, Chen J. *p53 and its isoforms in DNA double-stranded break repair*. Journal of Zhejiang University. Science. B. 2019. [PubMed 31090271](https://doi.org/10.1631/jzus.B1900167)
- van Gent DC, Hoeijmakers JH, Kanaar R. *Chromosomal stability and the DNA double-stranded break connection*. Nature reviews. Genetics. 2001. [PubMed 11256071](https://doi.org/10.1038/35056049)
- Wang D et al. *Experimental reconstruction of double-stranded break repair-mediated plastid DNA insertion into the tobacco nucleus*. The Plant journal : for [cell and molecular biology](/blog/news/cell-and-molecular-biology). 2018. [PubMed 29155472](https://doi.org/10.1111/tpj.13769)
- Wang C, Chan DW, Hendrickson EA. *Kinome-wide screening uncovers a role for Bromodomain Protein 3 in DNA double-stranded break repair*. DNA repair. 2023. [PubMed 36608404](https://doi.org/10.1016/j.dnarep.2022.103445)
- Wang T et al. *WASH interacts with Ku to regulate DNA double-stranded break repair*. iScience. 2022. [PubMed 35036867](https://doi.org/10.1016/j.isci.2021.103676)

## Related Topics

- [Double Strand Break Repair](/knowledge/molecular-biology/double-strand-break-repair)
- [Single Strand Break Repair](/knowledge/molecular-biology/single-strand-break-repair)
- [Double Strand Breaks in DNA](/knowledge/molecular-biology/double-strand-breaks-in-dna)
- [Mismatch Repair](/knowledge/molecular-biology/mismatch-repair)

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* [MAPK Pathway: Mechanism, Function, and Clinical Relevance](/knowledge/molecular-biology/mapk-pathway)
* [Mammalian Cell Culture Bioreactors: A Practical Guide](/knowledge/molecular-biology/mammalian-cell-culture-bioreactor)
* [Nucleotide Formation: Biosynthesis and Assembly of DNA/RNA Building Blocks](/knowledge/molecular-biology/nucleotide-formation)