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

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Academic literature on the topic 'Homology-directed repair (HDR)'

Author: Grafiati
Published: 5 June 2025
Last updated: 2 August 2025

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

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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.

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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
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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.

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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
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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.

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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
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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.

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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
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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.

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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
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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.

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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
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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.

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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
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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.

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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.

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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.
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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.

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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
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Book chapters on the topic "Homology-directed repair (HDR)"

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S. Elton, Terry, Md Ismail Hossain, Jessika Carvajal-Moreno, Xinyi Wang, Dalton J. Skaggs, and Jack C. Yalowich. "Maximizing the Efficacy of CRISPR/Cas Homology-Directed Repair Gene Targeting." In CRISPR Technology - Recent Advances [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.109051.

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Clustered regularly interspaced short palindromic repeats/CRISPR-associated system (CRISPR/Cas) is a powerful gene editing tool that can introduce double-strand breaks (DSBs) at precise target sites in genomic DNA. In mammalian cells, the CRISPR/Cas-generated DSBs can be repaired by either template-free error-prone end joining (e.g., non-homologous end joining/microhomology-mediated end joining [NHEJ]/[MMEJ]) or templated error-free homology-directed repair (HDR) pathways. CRISPR/Cas with NHEJ/MMEJ DNA repair results in various length insertions/deletion mutations (indels), which can cause fra
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Gaur, Anjali, and Saurabh Pandey. "GENOME EDITING IN PLANTS CRISPR/CAS-9." In Futuristic Trends in Biotechnology Volume 3 Book 12. Iterative International Publishers, Selfypage Developers Pvt Ltd, 2024. http://dx.doi.org/10.58532/v3bjbt12p5ch2.

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The prokaryotes' genome is shielded against infectious viruses and plasmids by the RNA represent as CRISPR and Cas proteins. This is a tool for site-specific alteration, genome engineering, crop improvement, and molecular therapy because of its low cost, versatility, less time consuming, and efficiently modify endogenous genes in a wide variety of cell types and in organisms that are being manipulated genetically. Therefore, CRISPR-Cas 9 offers a quick and effective way to introduce specific mutations into a target DNA strand with high accuracy and efficacy. RNA-guided nuclease Cas 9 induce do
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Conference papers on the topic "Homology-directed repair (HDR)"

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Carvajal-Moreno, Jessika, Xinyi Wang, Victor A. Hernandez, Jack C. Yalowich та Terry Elton. "Use of CRISPR/Cas9 with Homology-Directed Repair (HDR) to Gene-Edit Topoisomerase IIβ in Human Leukemia K562 Cells: Generation of a Resistance Phenotype". У ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.181860.

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Reports on the topic "Homology-directed repair (HDR)"

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Yang, Shih-Hsin E. Targeting Homology-Directed Recombinational Repair (HDR) of Chromosomal Breaks to Sensitize Prostate Cancer Cells to Poly (ADP-Ribose) Polymerase (PARP) Inhibition. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada566394.

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Yang, Shih-Hsin E. Targeting Homology-Directed Recombinational Repair (HDR) of Chromosomal Breaks to Sensitize Prostate Cancer Cells to Poly (ADP-Ribose) Polymerase (PARP) Inhibition. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada590934.

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