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Relevant bibliographies by topics / DNA Single-strand Repair Pathway

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Academic literature on the topic 'DNA Single-strand Repair Pathway'

Author: Grafiati

Published: 6 September 2023

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Journal articles on the topic "DNA Single-strand Repair Pathway"

1

Pandya, Gagan A., In-Young Yang, Arthur P. Grollman, and Masaaki Moriya. "Escherichia coli Responses to a Single DNA Adduct." Journal of Bacteriology 182, no. 23 (December 1, 2000): 6598–604. http://dx.doi.org/10.1128/jb.182.23.6598-6604.2000.

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ABSTRACT To study the mechanisms by which Escherichia colimodulates the genotoxic effects of DNA damage, a novel system has been developed which permits quantitative measurements of various E. coli pathways involved in mutagenesis and DNA repair. Events measured include fidelity and efficiency of translesion DNA synthesis, excision repair, and recombination repair. Our strategy involves heteroduplex plasmid DNA bearing a single site-specific DNA adduct and several mismatched regions. The plasmid replicates in a mismatch repair-deficient host with the mismatches serving as strand-specific markers. Analysis of progeny plasmid DNA for linkage of the strand-specific markers identifies the pathway from which the plasmid is derived. Using this approach, a single 1,N 6-ethenodeoxyadenosine adduct was shown to be repaired inefficiently by excision repair, to inhibit DNA synthesis by approximately 80 to 90%, and to direct the incorporation of correct dTMP opposite this adduct. This approach is especially useful in analyzing the damage avoidance-tolerance mechanisms. Our results also show that (i) progeny derived from the damage avoidance-tolerance pathway(s) accounts for more than 15% of all progeny; (ii) this pathway(s) requires functional recA, recF,recO, and recR genes, suggesting the mechanism to be daughter strand gap repair; (iii) the ruvABC genes or the recG gene is also required; and (iv) the RecG pathway appears to be more active than the RuvABC pathway. Based on these results, the mechanism of the damage avoidance-tolerance pathway is discussed.

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Zhao, Lei, Chengyu Bao, Yuxuan Shang, Xinye He, Chiyuan Ma, Xiaohua Lei, Dong Mi, and Yeqing Sun. "The Determinant of DNA Repair Pathway Choices in Ionising Radiation-Induced DNA Double-Strand Breaks." BioMed Research International 2020 (August 25, 2020): 1–12. http://dx.doi.org/10.1155/2020/4834965.

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Ionising radiation- (IR-) induced DNA double-strand breaks (DSBs) are considered to be the deleterious DNA lesions that pose a serious threat to genomic stability. The major DNA repair pathways, including classical nonhomologous end joining, homologous recombination, single-strand annealing, and alternative end joining, play critical roles in countering and eliciting IR-induced DSBs to ensure genome integrity. If the IR-induced DNA DSBs are not repaired correctly, the residual or incorrectly repaired DSBs can result in genomic instability that is associated with certain human diseases. Although many efforts have been made in investigating the major mechanisms of IR-induced DNA DSB repair, it is still unclear what determines the choices of IR-induced DNA DSB repair pathways. In this review, we discuss how the mechanisms of IR-induced DSB repair pathway choices can operate in irradiated cells. We first briefly describe the main mechanisms of the major DNA DSB repair pathways and the related key repair proteins. Based on our understanding of the characteristics of IR-induced DNA DSBs and the regulatory mechanisms of DSB repair pathways in irradiated cells and recent advances in this field, We then highlight the main factors and associated challenges to determine the IR-induced DSB repair pathway choices. We conclude that the type and distribution of IR-induced DSBs, chromatin state, DNA-end structure, and DNA-end resection are the main determinants of the choice of the IR-induced DNA DSB repair pathway.

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Yan, Hong, Thomas Toczylowski, Jill McCane, Chinyi Chen, and Shuren Liao. "Replication protein A promotes 5′→3′ end processing during homology-dependent DNA double-strand break repair." Journal of Cell Biology 192, no. 2 (January 24, 2011): 251–61. http://dx.doi.org/10.1083/jcb.201005110.

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Replication protein A (RPA), the eukaryotic single-strand deoxyribonucleic acid (DNA [ss-DNA])–binding protein, is involved in DNA replication, nucleotide damage repair, mismatch repair, and DNA damage checkpoint response, but its function in DNA double-strand break (DSB) repair is poorly understood. We investigated the function of RPA in homology-dependent DSB repair using Xenopus laevis nucleoplasmic extracts as a model system. We found that RPA is required for single-strand annealing, one of the homology-dependent DSB repair pathways. Furthermore, RPA promotes the generation of 3′ single-strand tails (ss-tails) by stimulating both the Xenopus Werner syndrome protein (xWRN)–mediated unwinding of DNA ends and the subsequent Xenopus DNA2 (xDNA2)–mediated degradation of the 5′ ss-tail. Purified xWRN, xDNA2, and RPA are sufficient to carry out the 5′-strand resection of DNA that carries a 3′ ss-tail. These results provide strong biochemical evidence to link RPA to a specific DSB repair pathway and reveal a novel function of RPA in the generation of 3′ ss-DNA for homology-dependent DSB repair.

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Li, Jinbao, Huize Sun, Yulin Huang, Yali Wang, Yuyan Liu, and Xuefeng Chen. "Pathways and assays for DNA double-strand break repair by homologous recombination." Acta Biochimica et Biophysica Sinica 51, no. 9 (July 10, 2019): 879–89. http://dx.doi.org/10.1093/abbs/gmz076.

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AbstractDouble strand breaks (DSBs) are the most detrimental type of DNA damage that must be repaired to ensure genome integrity and cell survival. Unrepaired or improperly repaired DSBs can potentially cause tumorigenesis or cell death. DSBs are primarily repaired by non-homologous end joining or homologous recombination (HR). The HR pathway is initiated by processing of the 5′-end of DSBs to generate 3′-end single-strand DNA (ssDNA). Furthermore, the intermediate is channeled to one of the HR sub-pathways, including: (i) double Holliday junction (dHJ) pathway, (ii) synthesis-dependent strand annealing (SDSA), (iii) break-induced replication (BIR), and (iv) single-strand annealing (SSA). In the dHJ sub-pathway, the 3′-ssDNA coated with Rad51 recombinase performs homology search and strand invasion, forming a displacement loop (D-loop). Capture of the second end by the D-loop generates a dHJ intermediate that is subsequently dissolved by DNA helicase or resolved by nucleases, producing non-crossover or crossover products. In SDSA, the newly synthesized strand is displaced from the D-loop and anneals to the end on the other side of the DSBs, producing non-crossovers. In contrast, BIR repairs one-end DSBs by copying the sequence up to the end of the template chromosome, resulting in translocation or loss of heterozygosity. SSA takes place when resection reveals flanking homologous repeats that can anneal, leading to deletion of the intervening sequences. A variety of reporter assays have been developed to monitor distinct HR sub-pathways in both Saccharomyces cerevisiae and mammals. Here, we summarize the principles and representative assays for different HR sub-pathways with an emphasis on the studies in the budding yeast.

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Preston, Christine R., William Engels, and Carlos Flores. "Efficient Repair of DNA Breaks in Drosophila: Evidence for Single-Strand Annealing and Competition With Other Repair Pathways." Genetics 161, no. 2 (June 1, 2002): 711–20. http://dx.doi.org/10.1093/genetics/161.2.711.

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Abstract We show evidence that DNA double-strand breaks induced in the Drosophila germ line can be repaired very efficiently by the single-strand annealing (SSA) mechanism. A double-strand break was made between two copies of a 1290-bp direct repeat by mobilizing a P transposon. In >80% of the progeny that acquired this chromosome, repair resulted in loss of the P element and loss of one copy of the repeat, as observed in SSA. The frequency of this repair was much greater than seen for gene conversion using an allelic template, which is only ∼7%. A similar structure, but with a smaller duplication of only 158 bp, also yielded SSA-like repair events, but at a reduced frequency, and gave rise to some products by repair pathways other than SSA. The 1290-bp repeats carried two sequence polymorphisms that were examined in the products. The allele nearest to a nick in the putative heteroduplex intermediate was lost most often. This bias is predicted by the SSA model, although other models could account for it. We conclude that SSA is the preferred repair pathway in Drosophila for DNA breaks between sequence repeats, and it competes with gene conversion by the synthesis-dependent strand annealing (SDSA) pathway.

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Lin, Yunfeng, Jude Raj, Jia Li, Anh Ha, Md Akram Hossain, Christine Richardson, Pinku Mukherjee, and Shan Yan. "APE1 senses DNA single-strand breaks for repair and signaling." Nucleic Acids Research 48, no. 4 (December 12, 2019): 1925–40. http://dx.doi.org/10.1093/nar/gkz1175.

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Abstract DNA single-strand breaks (SSBs) represent the most abundant type of DNA damage. Unrepaired SSBs impair DNA replication and transcription, leading to cancer and neurodegenerative disorders. Although PARP1 and XRCC1 are implicated in the SSB repair pathway, it remains unclear how SSB repair and SSB signaling pathways are coordinated and regulated. Using Xenopus egg extract and in vitro reconstitution systems, here we show that SSBs are first sensed by APE1 to initiate 3′–5′ SSB end resection, followed by APE2 recruitment to continue SSB end resection. Notably, APE1’s exonuclease activity is critical for SSB repair and SSB signaling pathways. An APE1 exonuclease-deficient mutant identified in somatic tissue from a cancer patient highlighted the significance of APE1 exonuclease activity in cancer etiology. In addition, APE1 interacts with APE2 and PCNA, although PCNA is dispensable for APE1’s exonuclease activity. Taken together, we propose a two-step APE1/APE2-mediated mechanism for SSB end resection that couples DNA damage response with SSB repair in a eukaryotic system.

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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 (February 20, 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 can proceed by a pathway dependent upon canonical HDR factors RAD51 and BRCA2; or by an efficient alternative pathway that uses either ssDNA or nicked dsDNA donors and that is strongly inhibited by RAD51 and BRCA2. Nicks generated by either I-AniI or the CRISPR/Cas9D10A nickase are repaired by the alternative HDR pathway with little accompanying mutagenic end-joining, so this pathway may be usefully applied to genome engineering. These results suggest that alternative HDR at nicks may be stimulated in physiological contexts in which canonical RAD51/BRCA2-dependent HDR is compromised or down-regulated, which occurs frequently in tumors.

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Fernandes, Margret S., Mamatha M. Reddy, Jeffrey R. Gonneville, Scott C. DeRoo, Klaus Podar, James D. Griffin, David M. Weinstock, and Martin Sattler. "BCR-ABL promotes the frequency of mutagenic single-strand annealing DNA repair." Blood 114, no. 9 (August 27, 2009): 1813–19. http://dx.doi.org/10.1182/blood-2008-07-172148.

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Intracellular oxidative stress in cells transformed by the BCR-ABL oncogene is associated with increased DNA double-strand breaks. Imprecise repair of these breaks can result in the accumulation of mutations, leading to therapy-related drug resistance and disease progression. Using several BCR-ABL model systems, we found that BCR-ABL specifically promotes the repair of double-strand breaks through single-strand annealing (SSA), a mutagenic pathway that involves sequence repeats. Moreover, our results suggest that mutagenic SSA repair can be regulated through the interplay between BCR-ABL and extrinsic growth factors. Increased SSA activity required Y177 in BCR-ABL, as well as a functional PI3K and Ras pathway downstream of this site. Furthermore, our data hint at a common pathway for DSB repair whereby BCR-ABL, Tel-ABL, Tel-PDGFR, FLT3-ITD, and Jak2V617F all increase mutagenic repair. This increase in SSA may not be sufficiently suppressed by tyrosine kinase inhibitors in the stromal microenvironment. Therefore, drugs that target growth factor receptor signaling represent potential therapeutic agents to combat tyrosine kinase-induced genomic instability.

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An, Liwei, Chao Dong, Junshi Li, Jie Chen, Jingsong Yuan, Jun Huang, Kui Ming Chan, Cheng-han Yu, and Michael S. Y. Huen. "RNF169 limits 53BP1 deposition at DSBs to stimulate single-strand annealing repair." Proceedings of the National Academy of Sciences 115, no. 35 (August 13, 2018): E8286—E8295. http://dx.doi.org/10.1073/pnas.1804823115.

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Unrestrained 53BP1 activity at DNA double-strand breaks (DSBs) hampers DNA end resection and upsets DSB repair pathway choice. RNF169 acts as a molecular rheostat to limit 53BP1 deposition at DSBs, but how this fine balance translates to DSB repair control remains undefined. In striking contrast to 53BP1, ChIP analyses of AsiSI-induced DSBs unveiled that RNF169 exhibits robust accumulation at DNA end-proximal regions and preferentially targets resected, RPA-bound DSBs. Accordingly, we found that RNF169 promotes CtIP-dependent DSB resection and favors homology-mediated DSB repair, and further showed that RNF169 dose-dependently stimulates single-strand annealing repair, in part, by alleviating the 53BP1-imposed barrier to DSB end resection. Our results highlight the interplay of RNF169 with 53BP1 in fine-tuning choice of DSB repair pathways.

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JOSEPH JERRY, D., NICHOLAS B. GRINER, and LUWEI TAO. "TUMOR SUPPRESSOR PATHWAYS AND CELLULAR ORIGINS OF BREAST CANCER: NEW COMPLEXITIES AND NEW HOPES." Nano LIFE 01, no. 01n02 (March 2010): 1–16. http://dx.doi.org/10.1142/s179398441000002x.

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Heritable breast cancer syndromes have identified the recognition and processing of DNA double strand breaks as a fundamental vulnerability in the breast epithelium. The role of homology-directed DNA repair is particularly prominent, indicating that this repair pathway is rate-limiting. Although the activities of the tumor suppressor genes underlying heritable breast cancer act in a common pathway of DNA double strand break repair, the specific lesions result in surprisingly different patterns of biomarkers in the breast cancers, suggesting that they arise from different cell types that include the luminal, basal and progenitor cells within the breast epithelium. Therefore, each cell type appears to have distinct underlying vulnerabilities in repair of DNA double strand breaks. While the heterogeneity of targets poses a challenge to develop specific therapies, these pathways also render tumor cells sensitive to drugs targeting double strand break repair pathways offering new options for therapies. As double strand break repair is a common pathway underlying breast cancer risk, therapies that enhance the proficiency of this pathway offer a strategy for chemoprevention.

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Dissertations / Theses on the topic "DNA Single-strand Repair Pathway"

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Stephanou, Nicolas Constantinos. "Mycobacterial non-homologous end-joining : molecular mechanisms and components of a novel DNA double strand break repair pathway /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528973431&sid=21&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Demond, Marilen [Verfasser], and George [Akademischer Betreuer] Iliakis. "The influence of chromatin structure on DNA double strand break repair pathway choice / Marilen Demond ; Betreuer: George Iliakis." Duisburg, 2017. http://d-nb.info/1133478859/34.

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Caldecott, Keith. "Role of the xrs double strand break repair pathway in response to DNA damage induced by topoisomerase II-inhibiting antitumour drugs." Thesis, University College London (University of London), 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279158.

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Wang, Yu. "Mismatch ligation during non-homologous end joining pathway kinetic characterization of human DNA ligase IV/XRCC4 complex /." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1179947467.

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Saitou, Yuuichirou. "Regulatory mechanism of damage-dependent homologous recombination." Kyoto University, 2015. http://hdl.handle.net/2433/199392.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(人間・環境学)
甲第19068号
人博第721号
新制||人||173(附属図書館)
26||人博||721(吉田南総合図書館)
32019
京都大学大学院人間・環境学研究科相関環境学専攻
(主査)教授小松賢志, 教授宮下英明, 准教授三浦智行
学位規則第4条第1項該当

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Jaffary, Syed Ali Naqi Raza. "The human single-stranded DNA binding protein 2 (HSSB2) and its novel role in the base excision repair pathway." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/119175/1/Syed%20Ali%20Naqi%20Raza_Jaffary_Thesis.pdf.

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Genetic instability is the driver of cancer initiation and progression. The human single stranded DNA binding protein 2 is known to be involved in the prevention of such genetic instability. This project has highlighted how human single stranded DNA binding protein 2 is involved in a particular DNA repair pathway called, base excision repair. The researcher identified the role of human single stranded DNA binding protein 2 in the removal of uracils that have been added by mistake to the human genome. This project details the mechanism by which uracils are removed from the genome, shedding light on the evolution of the cancer genome and the mechanism through which genetic stability can occur.

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Dean, Philip John. "Double strand break repair and DNA damage signalling pathways in Arabidopsis." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487719.

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The external environment and internal cellular processes generate DNA double strand breaks (DSBs), a particularly toxic form of DNA damage that can result in chromosome fragmentation, replication failure, mutagenesis and cell death. Cells have evolved effective mechanisms to preserve the mtegrity of the genome including DNA damage signalling, cell cycle checkpoint activation and DNA repair.

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Zhang, Hongshan. "A single molecule perspective on DNA double-strand break repair mechanisms." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0177.

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Les cassures double brin de l'ADN altèrent l'intégrité physique du chromosome et constituent l'un des types les plus sévères de dommages à l'ADN. Pour préserver l'intégrité du génome contre les effets potentiellement néfastes des cassures double brin de l'ADN, les cellules humaines ont développé plusieurs mécanismes de réparation, dont la réparation par recombinaison de l'ADN et la jonction d'extrémités non-homologues (NHEJ), catalysés par des enzymes spécifiques. Pendant ma thèse, nous avons caractérisé la dynamique de certaines des interactions protéines/ADN impliquées dans ces mécanismes au niveau de la molécule unique. Dans ce but, nous avons combiné des pinces optiques et de la micro-fluidique avec de la microscopie de fluorescence à champ large afin de manipuler une ou deux molécules d'ADN individuelles et d'observer directement les protéines de la réparation marquées par fluorescence agissant sur l'ADN. Nous avons concentré notre analyse sur trois protéines/complexes essentiels impliqués dans la réparation de l'ADN: (i) la protéine humaine d’appariement de brin RAD52, (ii) les protéines humaines XRCC4, XLF et le complexe XRCC4/Ligase IV de la NHEJ et (iii) le complexe humain MRE11/RAD50/NBS1
DNA double-strand breaks disrupt the physical continuity of the chromosome and are one of the most severe types of DNA damage. To preserve genome integrity against the potentially deleterious effects of DNA double-strand breaks, human cells have evolved several repair mechanisms including DNA recombinational repair and Non-Homologous End Joining (NHEJ), each catalyzed by specific enzymes. In this thesis we aimed at unraveling the dynamics of protein/DNA transactions involved in DNA double-strand break repair mechanisms at single molecule level. To do this, we combined optical tweezers and microfluidics with wide-field fluorescence microscopy, which allowed us to manipulate individual DNA molecules while directly visualize fluorescently-labeled DNA repair proteins acting on them. We focused the study on three crucial proteins/complexes involved in DNA repair: (i) the human DNA annealing protein RAD52, (ii) the non-homologous end joining human proteins XRCC4 and XLF and the complex XRCC4/Ligase IV, and (iii) the human MRE11/RAD50/NBS1 complex

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Iles, Natasha J. "The role of a divergent FHA domain in DNA single-strand break repair." Thesis, University of Sussex, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487930.

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XRCC1 plays a major role in the repair of these lesions in mammalian cells by binding and/or activating many components of the single-strand break repair (SSBR) pathway. One such component is polynucleotide kinase (PNK) which possesses a divergent forkhead associated (FHA) domain that binds CK2-phosphorylated XRCC1. Aprataxin has a similar divergent FHA domain that also interacts with XRCC1 and which has been implicated in SSBR. In this thesis, yeast two-hybrid analysis indicated that PNK interacted with the pro-apoptotic protein Hippi in a manner dependent on the PNK FHA domain. In addition, a novel protein containing a similar FHA domain to PNK and aprataxin was identified and denoted APLF (Aprataxin and PNK-Like Factor). APLF was also shown to bind XRCC1 in a manner dependent on its FHA domain. Furthermore, this interaction was greatly stimulated by CK2-phosphorylation of XRCC1. APLF interacted with the double-strand break repair (DSBR) factor XRCC4. APLF was modified following DNA damage, presumably by phosphorylation. Nuclear localisation of YFP-APLF was promoted by the presence of XRCC1. Moreover, YFP-APLF colocalised with RFP-XRCC1 in DNA damage-induced nuclear foci following H₂O₂ treatment. Novel interaction partners of APLF identified by employing a yeast two-hybrid library screen included Ku86/XRCC5 and KEAP1. These data suggest a role for APLF in the cellular response to DNA strand breaks.

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Breslin, Claire. "Investigating the importance of XRCC1 binding partners in DNA single-strand break repair." Thesis, University of Sussex, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439658.

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Books on the topic "DNA Single-strand Repair Pathway"

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Stauropoulos, Dimitrios James. An analysis of the interplay between telomeric factors and DNA repair proteins, in the human ALT pathway and cellular response to genomic double strand breaks. 2005.

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Sherif Mohamed Faruk Ahmed El-Khamisy. Biochemical characterisation of a novel DNA single-strand break repair process and its defect in a neurodegenerative disease. 2005.

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Book chapters on the topic "DNA Single-strand Repair Pathway"

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Dutta, Arijit, Joy Mitra, Pavana M. Hegde, Sankar Mitra, and Muralidhar L. Hegde. "Characterizing the Repair of DNA Double-Strand Breaks: A Review of Surrogate Plasmid-Based Reporter Methods." In Base Excision Repair Pathway, 173–82. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3373-1_11.

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Hang, Bo. "A DNA Cleavage Assay Using Synthetic Oligonucleotide Containing a Single Site-Directed Lesion for In Vitro Base Excision Repair Study." In Base Excision Repair Pathway, 77–90. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3373-1_5.

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Böhringer, Michael, and Lisa Wiesmüller. "Fluorescence-Based Quantification of Pathway-Specific DNA Double-Strand Break Repair Activities: A Powerful Method for the Analysis of Genome Destabilizing Mechanisms." In Subcellular Biochemistry, 297–306. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3471-7_15.

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Caldecott, Keith W. "Chromosomal Single-Strand Break Repair." In The DNA Damage Response: Implications on Cancer Formation and Treatment, 261–84. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2561-6_12.

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Marceau, Aimee H. "Functions of Single-Strand DNA-Binding Proteins in DNA Replication, Recombination, and Repair." In Single-Stranded DNA Binding Proteins, 1–21. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-032-8_1.

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Michael, Barry D., Susan Davies, and Kathryn D. Held. "Ultrafast Chemical Repair of DNA Single and Double Strand Break Precursors in Irradiated V79 Cells." In Mechanisms of DNA Damage and Repair, 89–100. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-9462-8_10.

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Dynan, William S., Shuyi Li, Raymond Mernaugh, Stephanie Wragg, John Barrett, and Yoshihiko Takeda. "Visualization of DNA Double-Strand Break Repair at the Single-Molecule Level." In ACS Symposium Series, 351–73. Washington, DC: American Chemical Society, 2005. http://dx.doi.org/10.1021/bk-2005-0904.ch016.

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Wollman, Adam J. M., Aisha H. Syeda, Peter McGlynn, and Mark C. Leake. "Single-Molecule Observation of DNA Replication Repair Pathways in E. coli." In Biophysics of Infection, 5–16. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32189-9_2.

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Lin, Yunfeng, Anh Ha, and Shan Yan. "Methods for Studying DNA Single-Strand Break Repair and Signaling in Xenopus laevis Egg Extracts." In Methods in Molecular Biology, 161–72. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9500-4_9.

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Cantoni, O., and F. Cattabeni. "Chemical Inhibition of the Repair of DNA Single Strand Breaks Produced by X-irradiation or Hydrogen Peroxide in Cultured Mammalian Cells." In Radiation Carcinogenesis and DNA Alterations, 297–304. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5269-3_20.

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Conference papers on the topic "DNA Single-strand Repair Pathway"

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Chen, Guo, Ke Xu, Maohua Xie, Taofeek K. Owonikoko, Suresh S. Ramalingam, Paul W. Doetsch, and Xingming Deng. "Abstract 2757: Mcl-1 dictates DNA double-strand break repair pathway choice." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2757.

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Ito, Tatsuo, Shigehisa Kitano, Hediye Erdjument-Bromage, and Marc Ladanyi. "Abstract 437: Novel function of the BAP1 nuclear deubiquitinase in the non-homologous end joining (NHEJ) pathway of double strand DNA repair." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-437.

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Chen, F., L. Tang, and J. Huang. "Abstract P1-08-03: Association analysis of single-nucleotide polymorphisms in FANCD2-DNA damage repair pathway genes with breast cancer risk." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p1-08-03.

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Seo, Yuji, Keita Yoshizaki, Keisuke Tamari, Yutaka Takahashi, Keisuke Otani, Masahiko Koizumi, and Kazuhiko Ogawa. "Abstract 5205: Poly(ADP-ribose) polymerase inhibitors induce β-radiosensitization through an altered selection of DNA double-strand break repair pathways." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5205.

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Ghosh, Rajib, Sanchita Roy, Francoise Dantzer, and Sonia Franco. "Abstract 3850: Understanding PARP inhibitor sensitivity: Analyses of the genetic interactions between specific PARP inhibitor targets and DNA double-strand repair pathways." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3850.

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Sears, Catherine R., and John J. Turchi. "Repair Of DNA Double-Strand Breaks By Non-Homologous End-Joining Is Independent Of Cisplatin-Induced Checkpoint Activation And Downstream Damage Response Pathways In A Non-Small Cell Lung Cancer Cell Culture Model." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5064.

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Reports on the topic "DNA Single-strand Repair Pathway"

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Wilson, Thomas E., Avraham A. Levy, and Tzvi Tzfira. Controlling Early Stages of DNA Repair for Gene-targeting Enhancement in Plants. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7697124.bard.

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Gene targeting (GT) is a much needed technology as a tool for plant research and for the precise engineering of crop species. Recent advances in this field have shown that the presence of a DNA double-strand break (DSB) in a genomic locus is critical for the integration of an exogenous DNA molecule introduced into this locus. This integration can occur via either non-homologous end joining (NHEJ) into the break or homologous recombination (HR) between the broken genomic DNA and the introduced vector. A bottleneck for DNA integration via HR is the machinery responsible for homology search and strand invasion. Important proteins in this pathway are Rad51, Rad52 and Rad54. We proposed to combine our respective expertise: on the US side, in the design of zincfinger nucleases (ZFNs) for the induction of DNA DSBs at any desired genomic locus and in the integration of DNA molecules via NHEJ; and on the Israeli side in the HR events, downstream of the DSB, that lead to homology search and strand invasion. We sought to test three major pathways of targeted DNA integration: (i) integration by NHEJ into DSBs induced at desired sites by specially designed ZFNs; (ii) integration into DSBs induced at desired sites combined with the use of Rad51, Rad52 and Rad54 proteins to maximize the chances for efficient and precise HR-mediated vector insertion; (iii) stimulation of HR by Rad51, Rad52 and Rad54 in the absence of DSB induction. We also proposed to study the formation of dsT-DNA molecules during the transformation of plant cells. dsT-DNA molecules are an important substrate for HR and NHEJ-mediatedGT, yet the mode of their formation from single stranded T-DNA molecules is still obscure. In addition we sought to develop a system for assembly of multi-transgene binary vectors by using ZFNs. The latter may facilitate the production of binary vectors that may be ready for genome editing in transgenic plants. ZFNs were proposed for the induction of DSBs in genomic targets, namely, the FtsH2 gene whose loss of function can easily be identified in somatic tissues as white sectors, and the Cruciferin locus whose targeting by a GFP or RFP reporter vectors can give rise to fluorescent seeds. ZFNs were also proposed for the induction of DSBs in artificial targets and for assembly of multi-gene vectors. We finally sought to address two important cell types in terms of relevance to plant transformation, namely GT of germinal (egg) cells by floral dipping, and GT in somatic cells by root and leave transformation. To be successful, we made use of novel optimized expression cassettes that enable coexpression of all of the genes of interest (ZFNs and Rad genes) in the right tissues (egg or root cells) at the right time, namely when the GT vector is delivered into the cells. Methods were proposed for investigating the complementation of T-strands to dsDNA molecules in living plant cells. During the course of this research, we (i) designed, assembled and tested, in vitro, a pair of new ZFNs capable of targeting the Cruciferin gene, (ii) produced transgenic plants which expresses for ZFN monomers for targeting of the FtsH2 gene. Expression of these enzymes is controlled by constitutive or heat shock induced promoters, (iii) produced a large population of transgenic Arabidopsis lines in which mutated mGUS gene was incorporated into different genomic locations, (iv) designed a system for egg-cell-specific expression of ZFNs and RAD genes and initiate GT experiments, (v) demonstrated that we can achieve NHEJ-mediated gene replacement in plant cells (vi) developed a system for ZFN and homing endonuclease-mediated assembly of multigene plant transformation vectors and (vii) explored the mechanism of dsTDNA formation in plant cells. This work has substantially advanced our understanding of the mechanisms of DNA integration into plants and furthered the development of important new tools for GT in plants.

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Wright, Adam, Marija Milacic, Karen Rothfels, Joel Weiser, Quang Trinh, Bijay Jassal, Robin Haw, and Lincoln Stein. Evaluating the Predictive Accuracy of Reactome's Curated Biological Pathways. Reactome, November 2022. http://dx.doi.org/10.3180/poster/20221109wright.

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Reactome is a database of human biological pathways manually curated from the primary literature and peer-reviewed by experts. To evaluate the utility of Reactome pathways for predicting functional consequences of genetic perturbations, we compared predictions of perturbation effects based on Reactome pathways against published empirical observations. Ten cancer-relevant Reactome pathways, representing diverse biological processes such as signal transduction, cell division, DNA repair, and transcriptional regulation, were selected for testing. For each pathway, root input nodes and key pathway outputs were defined. We then used pathway-diagram-derived logic graphs to predict, either by inspection by biocurators or using a novel algorithm MP-BioPath, the effects of bidirectional perturbations (upregulation/activation or downregulation/inhibition) of single root inputs on the status of key outputs. These predictions were then compared to published empirical tests.

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Tzfira, Tzvi, Michael Elbaum, and Sharon Wolf. DNA transfer by Agrobacterium: a cooperative interaction of ssDNA, virulence proteins, and plant host factors. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7695881.bard.

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Agrobacteriumtumefaciensmediates genetic transformation of plants. The possibility of exchanging the natural genes for other DNA has led to Agrobacterium’s emergence as the primary vector for genetic modification of plants. The similarity among eukaryotic mechanisms of nuclear import also suggests use of its active elements as media for non-viral genetic therapy in animals. These considerations motivate the present study of the process that carries DNA of bacterial origin into the host nucleus. The infective pathway of Agrobacterium involves excision of a single-stranded DNA molecule (T-strand) from the bacterial tumor-inducing plasmid. This transferred DNA (T-DNA) travels to the host cell cytoplasm along with two virulence proteins, VirD2 and VirE2, through a specific bacteriumplant channel(s). Little is known about the precise structure and composition of the resulting complex within the host cell and even less is known about the mechanism of its nuclear import and integration into the host cell genome. In the present proposal we combined the expertise of the US and Israeli labs and revealed many of the biophysical and biological properties of the genetic transformation process, thus enhancing our understanding of the processes leading to nuclear import and integration of the Agrobacterium T-DNA. Specifically, we sought to: I. Elucidate the interaction of the T-strand with its chaperones. II. Analyzing the three-dimensional structure of the T-complex and its chaperones in vitro. III. Analyze kinetics of T-complex formation and T-complex nuclear import. During the past three years we accomplished our goals and made the following major discoveries: (1) Resolved the VirE2-ssDNA three-dimensional structure. (2) Characterized VirE2-ssDNA assembly and aggregation, along with regulation by VirE1. (3) Studied VirE2-ssDNA nuclear import by electron tomography. (4) Showed that T-DNA integrates via double-stranded (ds) intermediates. (5) Identified that Arabidopsis Ku80 interacts with dsT-DNA intermediates and is essential for T-DNA integration. (6) Found a role of targeted proteolysis in T-DNA uncoating. Our research provide significant physical, molecular, and structural insights into the Tcomplex structure and composition, the effect of host receptors on its nuclear import, the mechanism of T-DNA nuclear import, proteolysis and integration in host cells. Understanding the mechanical and molecular basis for T-DNA nuclear import and integration is an essential key for the development of new strategies for genetic transformation of recalcitrant plant species. Thus, the knowledge gained in this study can potentially be applied to enhance the transformation process by interfering with key steps of the transformation process (i.e. nuclear import, proteolysis and integration). Finally, in addition to the study of Agrobacterium-host interaction, our research also revealed some fundamental insights into basic cellular mechanisms of nuclear import, targeted proteolysis, protein-DNA interactions and DNA repair.

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