Log in

Relevant bibliographies by topics / Homology-directed repair (HDR) / Journal articles

To see the other types of publications on this topic, follow the link: Homology-directed repair (HDR).

Journal articles on the topic 'Homology-directed repair (HDR)'

Author: Grafiati

Published: 5 June 2025

Last updated: 2 August 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Homology-directed repair (HDR).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Ye, Zu, Shengfeng Xu, Yin Shi, et al. "GRB2 enforces homology-directed repair initiation by MRE11." Science Advances 7, no. 32 (2021): eabe9254. http://dx.doi.org/10.1126/sciadv.abe9254.

Full text

Abstract:

DNA double-strand break (DSB) repair is initiated by MRE11 nuclease for both homology-directed repair (HDR) and alternative end joining (Alt-EJ). Here, we found that GRB2, crucial to timely proliferative RAS/MAPK pathway activation, unexpectedly forms a biophysically validated GRB2-MRE11 (GM) complex for efficient HDR initiation. GRB2-SH2 domain targets the GM complex to phosphorylated H2AX at DSBs. GRB2 K109 ubiquitination by E3 ubiquitin ligase RBBP6 releases MRE11 promoting HDR. RBBP6 depletion results in prolonged GM complex and HDR defects. GRB2 knockout increased MRE11-XRCC1 complex and

APA, Harvard, Vancouver, ISO, and other styles

2

Davis, Luther, and Nancy Maizels. "Homology-directed repair of DNA nicks via pathways distinct from canonical double-strand break repair." Proceedings of the National Academy of Sciences 111, no. 10 (2014): E924—E932. http://dx.doi.org/10.1073/pnas.1400236111.

Full text

Abstract:

DNA nicks are the most common form of DNA damage, and if unrepaired can give rise to genomic instability. In human cells, nicks are efficiently repaired via the single-strand break repair pathway, but relatively little is known about the fate of nicks not processed by that pathway. Here we show that homology-directed repair (HDR) at nicks occurs via a mechanism distinct from HDR at double-strand breaks (DSBs). HDR at nicks, but not DSBs, is associated with transcription and is eightfold more efficient at a nick on the transcribed strand than at a nick on the nontranscribed strand. HDR at nicks

APA, Harvard, Vancouver, ISO, and other styles

3

Yang, Han, Shuling Ren, Siyuan Yu, et al. "Methods Favoring Homology-Directed Repair Choice in Response to CRISPR/Cas9 Induced-Double Strand Breaks." International Journal of Molecular Sciences 21, no. 18 (2020): 6461. http://dx.doi.org/10.3390/ijms21186461.

Full text

Abstract:

Precise gene editing is—or will soon be—in clinical use for several diseases, and more applications are under development. The programmable nuclease Cas9, directed by a single-guide RNA (sgRNA), can introduce double-strand breaks (DSBs) in target sites of genomic DNA, which constitutes the initial step of gene editing using this novel technology. In mammals, two pathways dominate the repair of the DSBs—nonhomologous end joining (NHEJ) and homology-directed repair (HDR)—and the outcome of gene editing mainly depends on the choice between these two repair pathways. Although HDR is attractive for

APA, Harvard, Vancouver, ISO, and other styles

4

Sakamoto, Yuki, Tetsuya Kokuta, Ai Teshigahara, et al. "Mitotic cells can repair DNA double-strand breaks via a homology-directed pathway." Journal of Radiation Research 62, no. 1 (2020): 25–33. http://dx.doi.org/10.1093/jrr/rraa095.

Full text

Abstract:

Abstract The choice of repair pathways of DNA double-strand breaks (DSBs) is dependent upon the cell cycle phases. While homologous recombination repair (HRR) is active between the S and G2 phases, its involvement in mitotic DSB repair has not been examined in detail. In the present study, we developed a new reporter assay system to detect homology-directed repair (HDR), a major pathway used for HRR, in combination with an inducible DSB-generation system. As expected, the maximal HDR activity was observed in the late S phase, along with minimal activity in the G1 phase and at the G1/S boundary

APA, Harvard, Vancouver, ISO, and other styles

5

Chen, Jilin, Shaoya Li, Yubing He, Jingying Li, and Lanqin Xia. "An update on precision genome editing by homology-directed repair in plants." Plant Physiology 188, no. 4 (2022): 1780–94. http://dx.doi.org/10.1093/plphys/kiac037.

Full text

Abstract:

Abstract Beneficial alleles derived from local landraces or related species, or even orthologs from other plant species, are often caused by differences of one or several single-nucleotide polymorphisms or indels in either the promoter region or the encoding region of a gene and often account for major differences in agriculturally important traits. Clustered regularly interspaced short palindromic repeats-associated endonuclease Cas9 system (CRISPR/Cas9)-mediated precision genome editing enables targeted allele replacement or insertion of flag or foreign genes at specific loci via homology-di

APA, Harvard, Vancouver, ISO, and other styles

6

DiNapoli, Sara E., Raul Martinez-McFaline, Caitlin K. Gribbin, et al. "Synthetic CRISPR/Cas9 reagents facilitate genome editing and homology directed repair." Nucleic Acids Research 48, no. 7 (2020): e38-e38. http://dx.doi.org/10.1093/nar/gkaa085.

Full text

Abstract:

Abstract CRISPR/Cas9 has become a powerful tool for genome editing in zebrafish that permits the rapid generation of loss of function mutations and the knock-in of specific alleles using DNA templates and homology directed repair (HDR). We examined the efficiency of synthetic, chemically modified gRNAs and demonstrate induction of indels and large genomic deletions in combination with recombinant Cas9 protein. We developed an in vivo genetic assay to measure HDR efficiency and we utilized this assay to test the effect of altering template design on HDR. Utilizing synthetic gRNAs and linear dsD

APA, Harvard, Vancouver, ISO, and other styles

7

Buonomo, Sara B. C., Yipin Wu, David Ferguson, and Titia de Lange. "Mammalian Rif1 contributes to replication stress survival and homology-directed repair." Journal of Cell Biology 187, no. 3 (2009): 385–98. http://dx.doi.org/10.1083/jcb.200902039.

Full text

Abstract:

Rif1, originally recognized for its role at telomeres in budding yeast, has been implicated in a wide variety of cellular processes in mammals, including pluripotency of stem cells, response to double-strand breaks, and breast cancer development. As the molecular function of Rif1 is not known, we examined the consequences of Rif1 deficiency in mouse cells. Rif1 deficiency leads to failure in embryonic development, and conditional deletion of Rif1 from mouse embryo fibroblasts affects S-phase progression, rendering cells hypersensitive to replication poisons. Rif1 deficiency does not alter the

APA, Harvard, Vancouver, ISO, and other styles

8

Sun, Ruichen, Robyn Raban, and Omar S. Akbari. "GeneratingAedes aegyptiMutant Strains with Transgenic Cas9." Cold Spring Harbor Protocols 2023, no. 9 (2023): pdb.prot108085. http://dx.doi.org/10.1101/pdb.prot108085.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Sahel, Deepak Kumar, Gangadari Giriprasad, Reena Jatyan, et al. "Next-generation CRISPR/Cas-based ultrasensitive diagnostic tools: current progress and prospects." RSC Advances 14, no. 44 (2024): 32411–35. http://dx.doi.org/10.1039/d4ra04838e.

Full text

Abstract:

CRISPR/Cas has been explored as a powerful molecular scissor that uses a double-strand break mediated non-homologous end joining (NHEJ) or homology-directed repair (HDR) to achieve precise gene editing.

APA, Harvard, Vancouver, ISO, and other styles

10

Haider, Sibtain, and Claudio Mussolino. "Fine-Tuning Homology-Directed Repair (HDR) for Precision Genome Editing: Current Strategies and Future Directions." International Journal of Molecular Sciences 26, no. 9 (2025): 4067. https://doi.org/10.3390/ijms26094067.

Full text

Abstract:

CRISPR–Cas9 is a powerful genome-editing technology that can precisely target and cleave DNA to induce double-strand breaks (DSBs) at almost any genomic locus. While this versatility holds tremendous therapeutic potential, the predominant cellular pathway for DSB repair—non-homologous end-joining (NHEJ)—often introduces small insertions or deletions that disrupt the target site. In contrast, homology-directed repair (HDR) utilizes exogenous donor templates to enable precise gene modifications, including targeted insertions, deletions, and substitutions. However, HDR remains relatively ineffici

APA, Harvard, Vancouver, ISO, and other styles

11

Kaplan, Alanna R., Susan E. Gueble, Yanfeng Liu, et al. "Cediranib suppresses homology-directed DNA repair through down-regulation of BRCA1/2 and RAD51." Science Translational Medicine 11, no. 492 (2019): eaav4508. http://dx.doi.org/10.1126/scitranslmed.aav4508.

Full text

Abstract:

Combining the anti-angiogenic agent cediranib with the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib improves progression-free survival compared to olaparib alone in ovarian cancer patients through an unknown mechanism. PARP inhibitors are used primarily in the treatment of patients with DNA repair–associated (BRCA1/2) mutated cancers because these mutations cause a deficit in homology-directed DNA repair (HDR) that confers sensitivity to these agents. However, the combination of cediranib and olaparib was effective in patients without BRCA1/2 mutations. We report here that cediranib c

APA, Harvard, Vancouver, ISO, and other styles

12

Anguela, Xavier M., Rajiv Sharma, Yannick Doyon, et al. "In Vivo Genome Editing in Neonatal Mouse Liver Preferentially Utilizes Homology Directed Repair." Blood 126, no. 23 (2015): 4422. http://dx.doi.org/10.1182/blood.v126.23.4422.4422.

Full text

Abstract:

Abstract Genome editing has the potential to provide long-term therapeutic gene expression in vivo. We have previously demonstrated efficient editing in a mouse model of hemophilia B through liver-directed adeno-associated viral vector (AAV) delivery of a zinc finger nuclease (ZFN) pair and a corrective donor. We determined that homology is not necessary to achieve efficient levels of genome editing in adult mice, consistent with the fact that quiescent cells, including adult hepatocytes, are not thought to be amenable to homology directed repair (HDR). As a consequence of the donor containing

APA, Harvard, Vancouver, ISO, and other styles

13

Chien, Jasper Che-Yung, Elie Tabet, Kelsey Pinkham, et al. "A multiplexed bioluminescent reporter for sensitive and non-invasive tracking of DNA double strand break repair dynamics in vitro and in vivo." Nucleic Acids Research 48, no. 17 (2020): e100-e100. http://dx.doi.org/10.1093/nar/gkaa669.

Full text

Abstract:

Abstract Tracking DNA double strand break (DSB) repair is paramount for the understanding and therapeutic development of various diseases including cancers. Herein, we describe a multiplexed bioluminescent repair reporter (BLRR) for non-invasive monitoring of DSB repair pathways in living cells and animals. The BLRR approach employs secreted Gaussia and Vargula luciferases to simultaneously detect homology-directed repair (HDR) and non-homologous end joining (NHEJ), respectively. BLRR data are consistent with next-generation sequencing results for reporting HDR (R2 = 0.9722) and NHEJ (R2 = 0.9

APA, Harvard, Vancouver, ISO, and other styles

14

Reuven, Nina, Julia Adler, Nadav Myers, and Yosef Shaul. "CRISPR Co-Editing Strategy for Scarless Homology-Directed Genome Editing." International Journal of Molecular Sciences 22, no. 7 (2021): 3741. http://dx.doi.org/10.3390/ijms22073741.

Full text

Abstract:

The clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 has revolutionized genome editing by providing a simple and robust means to cleave specific genomic sequences. However, introducing templated changes at the targeted site usually requires homology-directed repair (HDR), active in only a small subset of cells in culture. To enrich for HDR-dependent edited cells, we employed a co-editing strategy, editing a gene of interest (GOI) concomitantly with rescuing an endogenous pre-made temperature-sensitive (ts) mutation. By using the repair of the ts mutation as a selectable m

APA, Harvard, Vancouver, ISO, and other styles

15

Chen, Chun-Chin, Elizabeth M. Kass, Wei-Feng Yen, et al. "ATM loss leads to synthetic lethality in BRCA1 BRCT mutant mice associated with exacerbated defects in homology-directed repair." Proceedings of the National Academy of Sciences 114, no. 29 (2017): 7665–70. http://dx.doi.org/10.1073/pnas.1706392114.

Full text

Abstract:

BRCA1 is essential for homology-directed repair (HDR) of DNA double-strand breaks in part through antagonism of the nonhomologous end-joining factor 53BP1. The ATM kinase is involved in various aspects of DNA damage signaling and repair, but how ATM participates in HDR and genetically interacts with BRCA1 in this process is unclear. To investigate this question, we used the Brca1S1598F mouse model carrying a mutation in the BRCA1 C-terminal domain of BRCA1. Whereas ATM loss leads to a mild HDR defect in adult somatic cells, we find that ATM inhibition leads to severely reduced HDR in Brca1S159

APA, Harvard, Vancouver, ISO, and other styles

16

Anuchina, Arina A., Milyausha I. Zaynitdinova, Anna G. Demchenko, Nadezhda A. Evtushenko, Alexander V. Lavrov, and Svetlana A. Smirnikhina. "Bridging Gaps in HDR Improvement: The Role of MAD2L2, SCAI, and SCR7." International Journal of Molecular Sciences 24, no. 7 (2023): 6704. http://dx.doi.org/10.3390/ijms24076704.

Full text

Abstract:

This study aimed to enhance homology-directed repair (HDR) efficiency in CRISPR/Cas-mediated genome editing by targeting three key factors regulating the balance between HDR and non-homologous end joining (NHEJ): MAD2L2, SCAI, and Ligase IV. In order to achieve this, a cellular model using mutated eGFP was designed to monitor HDR events. Results showed that MAD2L2 knockdown and SCR7 treatment significantly improved HDR efficiency during Cas9-mediated HDR repair of the mutated eGFP gene in the HEK293T cell line. Fusion protein Cas9-SCAI did not improve HDR. This study is the first to demonstrat

APA, Harvard, Vancouver, ISO, and other styles

17

Paix, Alexandre, Andrew Folkmann, Daniel H. Goldman, et al. "Precision genome editing using synthesis-dependent repair of Cas9-induced DNA breaks." Proceedings of the National Academy of Sciences 114, no. 50 (2017): E10745—E10754. http://dx.doi.org/10.1073/pnas.1711979114.

Full text

Abstract:

The RNA-guided DNA endonuclease Cas9 has emerged as a powerful tool for genome engineering. Cas9 creates targeted double-stranded breaks (DSBs) in the genome. Knockin of specific mutations (precision genome editing) requires homology-directed repair (HDR) of the DSB by synthetic donor DNAs containing the desired edits, but HDR has been reported to be variably efficient. Here, we report that linear DNAs (single and double stranded) engage in a high-efficiency HDR mechanism that requires only ∼35 nucleotides of homology with the targeted locus to introduce edits ranging from 1 to 1,000 nucleotid

APA, Harvard, Vancouver, ISO, and other styles

18

Reczek, Colleen R., Matthias Szabolcs, Jeremy M. Stark, Thomas Ludwig, and Richard Baer. "The interaction between CtIP and BRCA1 is not essential for resection-mediated DNA repair or tumor suppression." Journal of Cell Biology 201, no. 5 (2013): 693–707. http://dx.doi.org/10.1083/jcb.201302145.

Full text

Abstract:

The CtIP protein facilitates homology-directed repair (HDR) of double-strand DNA breaks (DSBs) by initiating DNA resection, a process in which DSB ends are converted into 3′-ssDNA overhangs. The BRCA1 tumor suppressor, which interacts with CtIP in a phospho-dependent manner, has also been implicated in DSB repair through the HDR pathway. It was recently reported that the BRCA1–CtIP interaction is essential for HDR in chicken DT40 cells. To examine the role of this interaction in mammalian cells, we generated cells and mice that express Ctip polypeptides (Ctip-S326A) that fail to bind BRCA1. Su

APA, Harvard, Vancouver, ISO, and other styles

19

Zhao, Zhihua, Hanshuo Zhang, Tuanlin Xiong, et al. "Suppression of SHROOM1 Improves In Vitro and In Vivo Gene Integration by Promoting Homology-Directed Repair." International Journal of Molecular Sciences 21, no. 16 (2020): 5821. http://dx.doi.org/10.3390/ijms21165821.

Full text

Abstract:

Homologous recombination (HR) is often used to achieve targeted gene integration because of its higher precision and operability compared with microhomology-mediated end-joining (MMEJ) or non-homologous end-joining (NHEJ). It appears to be inefficient for gene integration in animal cells and embryos due to occurring only during cell division. Here we developed genome-wide high-throughput screening and a subsequently paired crRNA library screening to search for genes suppressing homology-directed repair (HDR). We found that, in the reporter system, HDR cells with knockdown of SHROOM1 were enric

APA, Harvard, Vancouver, ISO, and other styles

20

Lim, Pei Xin, and Maria Jasin. "Abstract IA014: BRCA2 promotes genomic integrity and therapy resistance primarily through its role in homology-directed repair." Cancer Research 84, no. 1_Supplement (2024): IA014. http://dx.doi.org/10.1158/1538-7445.dnarepair24-ia014.

Full text

Abstract:

Abstract Tumor suppressor BRCA2 functions in multiple pathways. The role of BRCA2 in homologous recombination, also termed homology-directed repair (HDR), is particularly well known. We also showed that it has a key role in the protection of stalled replication forks from the MRE11 nuclease. Moreover, BRCA2 also suppresses the formation of single-stranded gaps during replication. We have attempted to delineate the relative contributions of these three pathways to the maintenance of genome integrity and chemotherapy response using separation of function alleles. First, we report that mouse and

APA, Harvard, Vancouver, ISO, and other styles

21

Tan, Jiantao, Yaxi Wang, Shuifu Chen, et al. "An Efficient Marker Gene Excision Strategy Based on CRISPR/Cas9-Mediated Homology-Directed Repair in Rice." International Journal of Molecular Sciences 23, no. 3 (2022): 1588. http://dx.doi.org/10.3390/ijms23031588.

Full text

Abstract:

In order to separate transformed cells from non-transformed cells, antibiotic selectable marker genes are usually utilized in genetic transformation. After obtaining transgenic plants, it is often necessary to remove the marker gene from the plant genome in order to avoid regulatory issues. However, many marker-free systems are time-consuming and labor-intensive. Homology-directed repair (HDR) is a process of homologous recombination using homologous arms for efficient and precise repair of DNA double-strand breaks (DSBs). The clustered regularly interspaced short palindromic repeats (CRISPR)/

APA, Harvard, Vancouver, ISO, and other styles

22

Park, Soo Yeun, Zehua Feng, Xiujuan Zhang, et al. "A Versatile Reporter Platform for Evaluating HDR- and NHEJ-Based Genome Editing in Airway Epithelial Cell Cultures Using an rAAV Vector." Viruses 17, no. 6 (2025): 821. https://doi.org/10.3390/v17060821.

Full text

Abstract:

Therapeutic gene editing strategies utilize endogenous DNA repair pathways—nonhomologous end joining (NHEJ) or homology-directed repair (HDR)—to introduce targeted genomic modifications. Because HDR is restricted to dividing cells, whereas NHEJ functions in both dividing and non-dividing cells, NHEJ-based approaches are better suited for in vivo gene editing in the largely post-mitotic airway epithelium. Homology-independent targeted insertion (HITI), an NHEJ-based method, offers a promising strategy for cystic fibrosis (CF) gene therapy. Here, we applied HITI to drive the expression of a prom

APA, Harvard, Vancouver, ISO, and other styles

23

Stark, Jeremy M., Andrew J. Pierce, Jin Oh, Albert Pastink, and Maria Jasin. "Genetic Steps of Mammalian Homologous Repair with Distinct Mutagenic Consequences." Molecular and Cellular Biology 24, no. 21 (2004): 9305–16. http://dx.doi.org/10.1128/mcb.24.21.9305-9316.2004.

Full text

Abstract:

ABSTRACT Repair of chromosomal breaks is essential for cellular viability, but misrepair generates mutations and gross chromosomal rearrangements. We investigated the interrelationship between two homologous-repair pathways, i.e., mutagenic single-strand annealing (SSA) and precise homology-directed repair (HDR). For this, we analyzed the efficiency of repair in mammalian cells in which double-strand break (DSB) repair components were disrupted. We observed an inverse relationship between HDR and SSA when RAD51 or BRCA2 was impaired, i.e., HDR was reduced but SSA was increased. In particular,

APA, Harvard, Vancouver, ISO, and other styles

24

Yun, Ying, Min Wang, Shimeng Guo, and Xin Xie. "Topoisomerase Inhibitors and PIM1 Kinase Inhibitors Improve Gene Editing Efficiency Mediated by CRISPR-Cas9 and Homology-Directed Repair." Molecules 29, no. 12 (2024): 2890. http://dx.doi.org/10.3390/molecules29122890.

Full text

Abstract:

The CRISPR-Cas9 system has emerged as the most prevalent gene editing technology due to its simplicity, high efficiency, and low cost. However, the homology-directed repair (HDR)-mediated gene knock-in in this system suffers from low efficiency, which limits its application in animal model preparation, gene therapy, and agricultural genetic improvement. Here, we report the design and optimization of a simple and efficient reporter-based assay to visualize and quantify HDR efficiency. Through random screening of a small molecule compound library, two groups of compounds, including the topoisome

APA, Harvard, Vancouver, ISO, and other styles

25

Cai, Yuan, Tianlin Cheng, Yichuan Yao, et al. "In vivo genome editing rescues photoreceptor degeneration via a Cas9/RecA-mediated homology-directed repair pathway." Science Advances 5, no. 4 (2019): eaav3335. http://dx.doi.org/10.1126/sciadv.aav3335.

Full text

Abstract:

Although Cas9-mediated genome editing has been widely used to engineer alleles in animal models of human inherited diseases, very few homology-directed repair (HDR)–based genetic editing systems have been established in postnatal mouse models for effective and lasting phenotypic rescue. Here, we developed an HDR-based Cas9/RecA system to precisely correct Pde6b mutation with increased HDR efficiency in postnatal rodless (rd1) mice, a retinitis pigmentosa (RP) mutant model characterized by photoreceptor degeneration and loss of vision. The Cas9/RecA system incorporated Cas9 endonuclease enzyme

APA, Harvard, Vancouver, ISO, and other styles

26

Cha, Sang-Wook. "Generating Nonmosaic Mutants in Xenopus Using CRISPR–Cas in Oocytes." Cold Spring Harbor Protocols 2022, no. 6 (2021): pdb.prot106989. http://dx.doi.org/10.1101/pdb.prot106989.

Full text

Abstract:

In CRISPR–Cas9 genome editing, double-strand DNA breaks (DSBs) primarily undergo repair through nonhomologous end joining (NHEJ), which produces insertion or deletion of random nucleotides within the targeted region (indels). As a result, frameshift mutation-mediated loss-of-function mutants are frequently produced. An alternative repair mechanism, homology-directed repair (HDR), can be used to fix DSBs at relatively low frequency. By injecting a DNA-homology repair construct with the CRISPR–Cas components, specific nucleotide sequences can be introduced within the target region by HDR. We hav

APA, Harvard, Vancouver, ISO, and other styles

27

Karachaliou, N., M. Lefterova, J. F. Draper, et al. "Homology-directed repair (HDR)-defective lung adenocarcinomas (LUACs) in circulating tumor DNA (ctDNA)." Annals of Oncology 29 (October 2018): viii671. http://dx.doi.org/10.1093/annonc/mdy304.003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Murugan, K., B. C. Thommandru, S. Glenn, J. Woodley, and G. Rettig. "STANDARDIZED METHODS IN IPSC FOR CRISPR-BASED EDITING AND HOMOLOGY-DIRECTED REPAIR (HDR)." Cytotherapy 26, no. 6 (2024): S230. http://dx.doi.org/10.1016/j.jcyt.2024.03.470.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Attwood, Kathleen M., Jayme Salsman, Dudley Chung, Sabateeshan Mathavarajah, Carter Van Iderstine, and Graham Dellaire. "PML isoform expression and DNA break location relative to PML nuclear bodies impacts the efficiency of homologous recombination." Biochemistry and Cell Biology 98, no. 3 (2020): 314–26. http://dx.doi.org/10.1139/bcb-2019-0115.

Full text

Abstract:

Promyelocytic leukemia nuclear bodies (PML NBs) are nuclear subdomains that respond to genotoxic stress by increasing in number via changes in chromatin structure. However, the role of the PML protein and PML NBs in specific mechanisms of DNA repair has not been fully characterized. Here, we have directly examined the role of PML in homologous recombination (HR) using I-SceI extrachromosomal and chromosome-based homology-directed repair (HDR) assays, and in HDR by CRISPR/Cas9-mediated gene editing. We determined that PML loss can inhibit HR in an extrachromosomal HDR assay but had less of an e

APA, Harvard, Vancouver, ISO, and other styles

30

Shams, Forough, Hadi Bayat, Omid Mohammadian, et al. "Advance trends in targeting homology-directed repair for accurate gene editing: An inclusive review of small molecules and modified CRISPR-Cas9 systems." BioImpacts 12, no. 4 (2022): 371–91. http://dx.doi.org/10.34172/bi.2022.23871.

Full text

Abstract:

Introduction: Clustered regularly interspaced short palindromic repeat and its associated protein (CRISPR-Cas)-based technologies generate targeted modifications in host genome by inducing site-specific double-strand breaks (DSBs) that can serve as a substrate for homology-directed repair (HDR) in both in vitro and in vivo models. HDR pathway could enhance incorporation of exogenous DNA templates into the CRISPR-Cas9-mediated DSB site. Owing to low rate of HDR pathway, the efficiency of accurate genome editing is diminished. Enhancing the efficiency of HDR can provide fast, easy, and accurate

APA, Harvard, Vancouver, ISO, and other styles

31

Luo, Xianjin, Eric Weidinger, Tobias Burghardt, Miriam Höhn, and Ernst Wagner. "CRISPR/Cas9 Ribonucleoprotein Delivery Enhanced by Lipo-Xenopeptide Carriers and Homology-Directed Repair Modulators: Insights from Reporter Cell Lines." International Journal of Molecular Sciences 26, no. 9 (2025): 4361. https://doi.org/10.3390/ijms26094361.

Full text

Abstract:

CRISPR-Cas9 genome editing is a versatile platform for studying and treating various diseases. Homology-directed repair (HDR) with DNA donor templates serves as the primary pathway for gene correction in therapeutic applications, but its efficiency remains a significant challenge. This study investigates strategies to enhance gene correction efficiency using a T-shaped lipo-xenopeptide (XP)-based Cas9 RNP/ssDNA delivery system combined with various HDR enhancers. Nu7441, a known DNA-PKcs inhibitor, was found to be most effective in enhancing HDR-mediated gene correction. An over 10-fold increa

APA, Harvard, Vancouver, ISO, and other styles

32

Xu, Wanqing, Qingxia Zuo, Dongyan Feng, et al. "Validation Study to Determine the Accuracy of Widespread Promoterless EGFP Reporter at Assessing CRISPR/Cas9-Mediated Homology Directed Repair." Current Issues in Molecular Biology 44, no. 4 (2022): 1688–700. http://dx.doi.org/10.3390/cimb44040116.

Full text

Abstract:

An accurate visual reporter system to assess homology-directed repair (HDR) is a key prerequisite for evaluating the efficiency of Cas9-mediated precise gene editing. Herein, we tested the utility of the widespread promoterless EGFP reporter to assess the efficiency of CRISPR/Cas9-mediated homologous recombination by fluorescence expression. We firstly established a promoterless EGFP reporter donor targeting the porcine GAPDH locus to study CRISPR/Cas9-mediated homologous recombination in porcine cells. Curiously, EGFP was expressed at unexpectedly high levels from the promoterless donor in po

APA, Harvard, Vancouver, ISO, and other styles

33

Danner, Eric, Mikhail Lebedin, Kathrin de la Rosa, and Ralf Kühn. "A homology independent sequence replacement strategy in human cells using a CRISPR nuclease." Open Biology 11, no. 1 (2021): 200283. http://dx.doi.org/10.1098/rsob.200283.

Full text

Abstract:

Precision genomic alterations largely rely on homology directed repair (HDR), but targeting without homology using the non-homologous end-joining (NHEJ) pathway has gained attention as a promising alternative. Previous studies demonstrated precise insertions formed by the ligation of donor DNA into a targeted genomic double-strand break in both dividing and non-dividing cells. Here, we demonstrate the use of NHEJ repair to replace genomic segments with donor sequences; we name this method ‘Replace’ editing ( R ational e nd-joining p rotocol de l ivering a targeted sequen c e e xchange). Using

APA, Harvard, Vancouver, ISO, and other styles

34

Eki, Rebeka, Jane She, Mahmut Parlak, et al. "A robust CRISPR–Cas9-based fluorescent reporter assay for the detection and quantification of DNA double-strand break repair." Nucleic Acids Research 48, no. 21 (2020): e126-e126. http://dx.doi.org/10.1093/nar/gkaa897.

Full text

Abstract:

Abstract DNA double-strand breaks (DSBs) are highly cytotoxic lesions that can lead to chromosome rearrangements, genomic instability and cell death. Consequently, cells have evolved multiple mechanisms to efficiently repair DSBs to preserve genomic integrity. We have developed a DSB repair assay system, designated CDDR (CRISPR–Cas9-based Dual-fluorescent DSB Repair), that enables the detection and quantification of DSB repair outcomes in mammalian cells with high precision. CDDR is based on the introduction and subsequent resolution of one or two DSB(s) in an intrachromosomal fluorescent repo

APA, Harvard, Vancouver, ISO, and other styles

35

Zhao, Xiaoying, Kunli Qu, Benedetta Curci, et al. "Comparison of In-Frame Deletion, Homology-Directed Repair, and Prime Editing-Based Correction of Duchenne Muscular Dystrophy Mutations." Biomolecules 13, no. 5 (2023): 870. http://dx.doi.org/10.3390/biom13050870.

Full text

Abstract:

Recent progress in CRISPR gene editing tools has substantially increased the opportunities for curing devastating genetic diseases. Here we compare in-frame deletion by CRISPR-based non-homologous blunt end joining (NHBEJ), homology-directed repair (HDR), and prime editing (PE, PE2, and PE3)-based correction of two Duchenne Muscular Dystrophy (DMD) loss-of-function mutations (c.5533G>T and c.7893delC). To enable accurate and rapid evaluation of editing efficiency, we generated a genomically integrated synthetic reporter system (VENUS) carrying the DMD mutations. The VENUS contains a modifie

APA, Harvard, Vancouver, ISO, and other styles

36

Salsman, Jayme, and Graham Dellaire. "Precision genome editing in the CRISPR era." Biochemistry and Cell Biology 95, no. 2 (2017): 187–201. http://dx.doi.org/10.1139/bcb-2016-0137.

Full text

Abstract:

With the introduction of precision genome editing using CRISPR–Cas9 technology, we have entered a new era of genetic engineering and gene therapy. With RNA-guided endonucleases, such as Cas9, it is possible to engineer DNA double strand breaks (DSB) at specific genomic loci. DSB repair by the error-prone non-homologous end-joining (NHEJ) pathway can disrupt a target gene by generating insertions and deletions. Alternatively, Cas9-mediated DSBs can be repaired by homology-directed repair (HDR) using an homologous DNA repair template, thus allowing precise gene editing by incorporating genetic c

APA, Harvard, Vancouver, ISO, and other styles

37

Sundarraj, Jayakumar, Gillian C. A. Taylor, Alex von Kriegsheim, and Madapura M. Pradeepa. "H3K36me3 and PSIP1/LEDGF associate with several DNA repair proteins, suggesting their role in efficient DNA repair at actively transcribing loci." Wellcome Open Research 2 (September 14, 2021): 83. http://dx.doi.org/10.12688/wellcomeopenres.11589.4.

Full text

Abstract:

Background: Trimethylation at histone H3 at lysine 36 (H3K36me3) is associated with expressed gene bodies and recruit proteins implicated in transcription, splicing and DNA repair. PC4 and SF2 interacting protein (PSIP1/LEDGF) is a transcriptional coactivator, possesses an H3K36me3 reader PWWP domain. Alternatively spliced isoforms of PSIP1 binds to H3K36me3 and suggested to function as adaptor proteins to recruit transcriptional modulators, splicing factors and proteins that promote homology-directed repair (HDR), to H3K36me3 chromatin. Methods: We performed chromatin immunoprecipitation of H

APA, Harvard, Vancouver, ISO, and other styles

38

Sundarraj, Jayakumar, Gillian C. A. Taylor, Alex von Kriegsheim, and Madapura M. Pradeepa. "H3K36me3 and PSIP1/LEDGF associate with several DNA repair proteins, suggesting their role in efficient DNA repair at actively transcribing loci." Wellcome Open Research 2 (August 16, 2021): 83. http://dx.doi.org/10.12688/wellcomeopenres.11589.3.

Full text

Abstract:

Background: Trimethylation at histone H3 at lysine 36 (H3K36me3) is associated with expressed gene bodies and recruit proteins implicated in transcription, splicing and DNA repair. PC4 and SF2 interacting protein (PSIP1/LEDGF) is a transcriptional coactivator, possesses an H3K36me3 reader PWWP domain. Alternatively spliced isoforms of PSIP1 binds to H3K36me3 and suggested to function as adaptor proteins to recruit transcriptional modulators, splicing factors and proteins that promote homology-directed repair (HDR), to H3K36me3 chromatin. Methods: We performed chromatin immunoprecipitation of H

APA, Harvard, Vancouver, ISO, and other styles

39

Allen, Daniel, Nechama Kalter, Michael Rosenberg, and Ayal Hendel. "Homology-Directed-Repair-Based Genome Editing in HSPCs for the Treatment of Inborn Errors of Immunity and Blood Disorders." Pharmaceutics 15, no. 5 (2023): 1329. http://dx.doi.org/10.3390/pharmaceutics15051329.

Full text

Abstract:

Genome engineering via targeted nucleases, specifically CRISPR-Cas9, has revolutionized the field of gene therapy research, providing a potential treatment for diseases of the blood and immune system. While numerous genome editing techniques have been used, CRISPR-Cas9 homology-directed repair (HDR)-mediated editing represents a promising method for the site-specific insertion of large transgenes for gene knock-in or gene correction. Alternative methods, such as lentiviral/gammaretroviral gene addition, gene knock-out via non-homologous end joining (NHEJ)-mediated editing, and base or prime ed

APA, Harvard, Vancouver, ISO, and other styles

40

Nakayama, Takuya, Robert M. Grainger, and Sang-Wook Cha. "Homology-Directed Repair by CRISPR–Cas9 Mutagenesis inXenopusUsing Long Single-Stranded Donor DNA Templates via Simple Microinjection of Embryos." Cold Spring Harbor Protocols 2022, no. 12 (2022): pdb.prot107599. http://dx.doi.org/10.1101/pdb.prot107599.

Full text

Abstract:

We describe a step-by-step procedure to perform homology-directed repair (HDR)-mediated precise gene editing inXenopusembryos using long single-stranded DNA (lssDNA) as a donor template for HDR in conjunction with the CRISPR–Cas9 system. A key advantage of this method is that it relies on simple microinjection of fertilizedXenopuseggs, resulting in high yield of healthy founder embryos. These embryos are screened for those animals carrying the precisely mutated locus to then generate homozygous and/or heterozygous mutant lines in the F1generation. Therefore, we can avoid the more challenging “

APA, Harvard, Vancouver, ISO, and other styles

41

Meng, Yuan, Changwei Liu, Lei Shen, et al. "TRAF6 mediates human DNA2 polyubiquitination and nuclear localization to maintain nuclear genome integrity." Nucleic Acids Research 47, no. 14 (2019): 7564–79. http://dx.doi.org/10.1093/nar/gkz537.

Full text

Abstract:

Abstract The multifunctional human DNA2 (hDNA2) nuclease/helicase is required to process DNA ends for homology-directed recombination repair (HDR) and to counteract replication stress. To participate in these processes, hDNA2 must localize to the nucleus and be recruited to the replication or repair sites. However, because hDNA2 lacks the nuclear localization signal that is found in its yeast homolog, it is unclear how its migration into the nucleus is regulated during replication or in response to DNA damage. Here, we report that the E3 ligase TRAF6 binds to and mediates the K63-linked polyub

APA, Harvard, Vancouver, ISO, and other styles

42

Ang, Joshua Xin De, Katherine Nevard, Rebekah Ireland, et al. "Considerations for homology-based DNA repair in mosquitoes: Impact of sequence heterology and donor template source." PLOS Genetics 18, no. 2 (2022): e1010060. http://dx.doi.org/10.1371/journal.pgen.1010060.

Full text

Abstract:

The increasing prevalence of insecticide resistance and the ongoing global burden of vector-borne diseases have encouraged new efforts in mosquito control. For Aedes aegypti, the most important arboviral vector, integration rates achieved in Cas9-based knock-ins so far have been rather low, highlighting the need to understand gene conversion patterns and other factors that influence homology-directed repair (HDR) events in this species. In this study, we report the effects of sequence mismatches or donor template forms on integration rates. We found that modest sequence differences between con

APA, Harvard, Vancouver, ISO, and other styles

43

Borphukan, Bhabesh, Muslima Khatun, Dhirendra Fartyal, Donald James, and Malireddy K. Reddy. "A Gemini Virus-Derived Autonomously Replicating System for HDR-Mediated Genome Editing of the EPSP Synthase Gene in Indica Rice." Plants 14, no. 3 (2025): 477. https://doi.org/10.3390/plants14030477.

Full text

Abstract:

CRISPR/Cas9-mediated homology-directed repair (HDR) is a powerful tool for precise genome editing in plants, but its efficiency remains low, particularly for targeted amino acid substitutions or gene knock-ins. Successful HDR requires the simultaneous presence of Cas9, guide RNA, and a repair template (RT) in the same cell nucleus. Among these, the timely availability of the RT at the double-strand break (DSB) site is a critical bottleneck. To address this, we developed a sequential transformation strategy incorporating a deconstructed wheat dwarf virus (dWDV)-based autonomously replicating de

APA, Harvard, Vancouver, ISO, and other styles

44

Prill, Kendal, and John F. Dawson. "Homology-Directed Repair in Zebrafish: Witchcraft and Wizardry?" Frontiers in Molecular Biosciences 7 (December 7, 2020). http://dx.doi.org/10.3389/fmolb.2020.595474.

Full text

Abstract:

Introducing desired mutations into the genome of model organisms is a priority for all research focusing on protein function and disease modeling. The need to create stable mutant lines has resulted in the rapid advancement of genetic techniques over the last few decades from chemical mutagenesis and zinc finger nucleases to clustered regularly interspaced short palindromic repeats (CRISPR) and homology-directed repair (HDR). However, achieving consistently high success rates for direct mutagenesis in zebrafish remains one of the most sought-after techniques in the field. Several genes have be

APA, Harvard, Vancouver, ISO, and other styles

45

Schubert, Mollie S., Bernice Thommandru, Jessica Woodley, et al. "Optimized design parameters for CRISPR Cas9 and Cas12a homology-directed repair." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-98965-y.

Full text

Abstract:

AbstractCRISPR–Cas proteins are RNA-guided nucleases used to introduce double-stranded breaks (DSBs) at targeted genomic loci. DSBs are repaired by endogenous cellular pathways such as non-homologous end joining (NHEJ) and homology-directed repair (HDR). Providing an exogenous DNA template during repair allows for the intentional, precise incorporation of a desired mutation via the HDR pathway. However, rates of repair by HDR are often slow compared to the more rapid but less accurate NHEJ-mediated repair. Here, we describe comprehensive design considerations and optimized methods for highly e

APA, Harvard, Vancouver, ISO, and other styles

46

Kokemüller, Lara, Dhanya Ramachandran, Peter Schürmann, et al. "Germline variants of homology‐directed repair or mismatch repair genes in cervical cancer." International Journal of Cancer, October 23, 2024. http://dx.doi.org/10.1002/ijc.35221.

Full text

Abstract:

AbstractWhile cervical cancer is associated with a persistent human papillomavirus (HPV) infection, the progression to cancer is influenced by genomic risk factors that have remained largely obscure. Pathogenic variants in genes of the homology‐directed repair (HDR) or mismatch repair (MMR) are known to predispose to diverse tumour entities including breast and ovarian cancer (HDR) or colon and endometrial cancer (MMR). We here investigate the spectrum of HDR and MMR germline variants in cervical cancer, with particular focus on the HPV status and histological subgroups. We performed targeted

APA, Harvard, Vancouver, ISO, and other styles

47

VanDusen, Nathan J., Yanjiang Zheng, Catalina E. Butler, Qing Ma, Justin S. King, and William T. Pu. "Abstract 106: Efficient In Vivo Homology-Directed Repair Within Cardiomyocytes." Circulation Research 129, Suppl_1 (2021). http://dx.doi.org/10.1161/res.129.suppl_1.106.

Full text

Abstract:

CRISPR/Cas9-based genome editing technologies provide powerful tools for genetic manipulation. Delivery of Cas9 and a homology directed repair (HDR) template using adeno-associated virus (AAV; CASAAV-HDR), was recently shown to enable creation of precise genomic edits, even within postmitotic cells. Here we studied CASAAV-HDR in cardiomyocytes. We constructed an AAV9 vector containing a gRNA targeting the ventricle specific Myl2 gene, and a promoterless HDR template that replaces the native Myl2 stop codon with a self-cleaving 2A peptide followed by mScarlet, a red fluorescent protein. When th

APA, Harvard, Vancouver, ISO, and other styles

48

Petković, Igor, Johannes Bischof, Thomas Kocher, et al. "COL17A1 editing via homology-directed repair in junctional epidermolysis bullosa." Frontiers in Medicine 9 (August 25, 2022). http://dx.doi.org/10.3389/fmed.2022.976604.

Full text

Abstract:

BackgroundEpidermolysis bullosa (EB), a severe genetic disorder characterized by blister formation in skin, is caused by mutations in genes encoding dermal-epidermal junction proteins that function to hold the skin layers together. CRISPR/Cas9-induced homology-directed repair (HDR) represents a promising tool for editing causal mutations in COL17A1 in the treatment of junctional epidermolysis bullosa (JEB).MethodsIn this study, we treated primary type XVII collagen (C17)-deficient JEB keratinocytes with either Cas9 nuclease or nickase (Cas9n) ribonucleoproteins (RNP) and a single-stranded olig

APA, Harvard, Vancouver, ISO, and other styles

49

Li, Guoling, Xiaohui Yang, Xinxin Luo, Zhenfang Wu, and Huaqiang Yang. "Modulation of cell cycle increases CRISPR-mediated homology-directed DNA repair." Cell & Bioscience 13, no. 1 (2023). http://dx.doi.org/10.1186/s13578-023-01159-4.

Full text

Abstract:

Abstract Background Gene knock‐in (KI) in animal cells via homology‐directed repair (HDR) is an inefficient process, requiring a laborious work for screening from few modified cells. HDR tends to occur in the S and G2/M phases of cell cycle; therefore, strategies that enhance the proportion of cells in these specific phases could improve HDR efficiency. Results We used various types of cell cycle inhibitors to synchronize the cell cycle in S and G2/M phases in order to investigate their effect on regulating CRISPR/Cas9-mediated HDR. Our results indicated that the four small molecules—docetaxel

APA, Harvard, Vancouver, ISO, and other styles

50

Möller, Lukas, Eric J. Aird, Markus S. Schröder, et al. "Recursive Editing improves homology-directed repair through retargeting of undesired outcomes." Nature Communications 13, no. 1 (2022). http://dx.doi.org/10.1038/s41467-022-31944-7.

Full text

Abstract:

AbstractCRISPR-Cas induced homology-directed repair (HDR) enables the installation of a broad range of precise genomic modifications from an exogenous donor template. However, applications of HDR in human cells are often hampered by poor efficiency, stemming from a preference for error-prone end joining pathways that yield short insertions and deletions. Here, we describe Recursive Editing, an HDR improvement strategy that selectively retargets undesired indel outcomes to create additional opportunities to produce the desired HDR allele. We introduce a software tool, named REtarget, that enabl

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!