Relevant bibliographies by topics / NHEJ [Non Homologous End joining]

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  2. Dissertations / Theses
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Academic literature on the topic 'NHEJ [Non Homologous End joining]'

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Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "NHEJ [Non Homologous End joining]"

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Pastwa, Elzbieta, and Janusz Błasiak. "Non-homologous DNA end joining." Acta Biochimica Polonica 50, no. 4 (2003): 891–908. http://dx.doi.org/10.18388/abp.2003_3622.

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DNA double-strand breaks (DSBs) are a serious threat for the cell and when not repaired or misrepaired can result in mutations or chromosome rearrangements and eventually in cell death. Therefore, cells have evolved a number of pathways to deal with DSB including homologous recombination (HR), single-strand annealing (SSA) and non-homologous end joining (NHEJ). In mammals DSBs are primarily repaired by NHEJ and HR, while HR repair dominates in yeast, but this depends also on the phase of the cell cycle. NHEJ functions in all kinds of cells, from bacteria to man, and depends on the structure of DSB termini. In this process two DNA ends are joined directly, usually with no sequence homology, although in the case of same polarity of the single stranded overhangs in DSBs, regions of microhomology are utilized. The usage of microhomology is common in DNA end-joining of physiological DSBs, such as at the coding ends in V(D)J (variable(diversity) joining) recombination. The main components of the NHEJ system in eukaryotes are the catalytic subunit of DNA protein kinase (DNA-PK(cs)), which is recruited by DNA Ku protein, a heterodimer of Ku70 and Ku80, as well as XRCC4 protein and DNA ligase IV. A complex of Rad50/Mre11/Xrs2, a family of Sir proteins and probably other yet unidentified proteins can be also involved in this process. NHEJ and HR may play overlapping roles in the repair of DSBs produced in the S phase of the cell cycle or at replication forks. Aside from DNA repair, NHEJ may play a role in many different processes, including the maintenance of telomeres and integration of HIV-1 genome into a host genome, as well as the insertion of pseudogenes and repetitive sequences into the genome of mammalian cells. Inhibition of NHEJ can be exploited in cancer therapy in radio-sensitizing cancer cells. Identification of all key players and fundamental mechanisms underlying NHEJ still requires further research.
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Shibata, Atsushi, and Penny A. Jeggo. "Canonical DNA non-homologous end-joining; capacity versus fidelity." British Journal of Radiology 93, no. 1115 (2020): 20190966. http://dx.doi.org/10.1259/bjr.20190966.

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The significance of canonical DNA non-homologous end-joining (c-NHEJ) for DNA double strand break (DSB) repair has increased from lower organisms to higher eukaryotes, and plays the predominant role in human cells. Ku, the c-NHEJ end-binding component, binds DSBs with high efficiency enabling c-NHEJ to be the first choice DSB repair pathway, although alternative pathways can ensue after regulated steps to remove Ku. Indeed, radiation-induced DSBs are repaired rapidly in human cells. However, an important question is the fidelity with which radiation-induced DSBs are repaired, which is essential for assessing any harmful impacts caused by radiation exposure. Indeed, is compromised fidelity a price we pay for high capacity repair. Two subpathways of c-NHEJ have been revealed; a fast process that does not require nucleases or significant chromatin changes and a slower process that necessitates resection factors, and potentially more significant chromatin changes at the DSB. Recent studies have also shown that DSBs within transcriptionally active regions are repaired by specialised mechanisms, and the response at such DSBs encompasses a process of transcriptional arrest. Here, we consider the limitations of c-NHEJ that might result in DSB misrepair. We consider the common IR-induced misrepair events and discuss how they might arise via the distinct subpathways of c-NHEJ.
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Brissett, Nigel C., and Aidan J. Doherty. "Repairing DNA double-strand breaks by the prokaryotic non-homologous end-joining pathway." Biochemical Society Transactions 37, no. 3 (2009): 539–45. http://dx.doi.org/10.1042/bst0370539.

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The NHEJ (non-homologous end-joining) pathway is one of the major mechanisms for repairing DSBs (double-strand breaks) that occur in genomic DNA. In common with eukaryotic organisms, many prokaryotes possess a conserved NHEJ apparatus that is essential for the repair of DSBs arising in the stationary phase of the cell cycle. Although the bacterial NHEJ complex is much more minimal than its eukaryotic counterpart, both pathways share a number of common mechanistic features. The relative simplicity of the prokaryotic NHEJ complex makes it a tractable model system for investigating the cellular and molecular mechanisms of DSB repair. The present review describes recent advances in our understanding of prokaryotic end-joining, focusing primarily on biochemical, structural and cellular aspects of the mycobacterial NHEJ repair pathway.
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Ensminger, Michael, and Markus Löbrich. "One end to rule them all: Non-homologous end-joining and homologous recombination at DNA double-strand breaks." British Journal of Radiology 93, no. 1115 (2020): 20191054. http://dx.doi.org/10.1259/bjr.20191054.

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Double-strand breaks (DSBs) represent the most severe type of DNA damage since they can lead to genomic rearrangements, events that can initiate and promote tumorigenic processes. DSBs arise from various exogenous agents that induce two single-strand breaks at opposite locations in the DNA double helix. Such two-ended DSBs are repaired in mammalian cells by one of two conceptually different processes, non-homologous end-joining (NHEJ) and homologous recombination (HR). NHEJ has the potential to form rearrangements while HR is believed to be error-free since it uses a homologous template for repair. DSBs can also arise from single-stranded DNA lesions if they lead to replication fork collapse. Such DSBs, however, have only one end and are repaired by HR and not by NHEJ. In fact, the majority of spontaneously arising DSBs are one-ended and HR has likely evolved to repair one-ended DSBs. HR of such DSBs demands the engagement of a second break end that is generated by an approaching replication fork. This HR process can cause rearrangements if a homologous template other than the sister chromatid is used. Thus, both NHEJ and HR have the potential to form rearrangements and the proper choice between them is governed by various factors, including cell cycle phase and genomic location of the lesion. We propose that the specific requirements for repairing one-ended DSBs have shaped HR in a way which makes NHEJ the better choice for the repair of some but not all two-ended DSBs.
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Kotnis, Ashwin, Likun Du, Chonghai Liu, Sergey W. Popov, and Qiang Pan-Hammarström. "Non-homologous end joining in class switch recombination: the beginning of the end." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1517 (2008): 653–65. http://dx.doi.org/10.1098/rstb.2008.0196.

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Immunoglobulin class switch recombination (CSR) is initiated by a B-cell-specific factor, activation-induced deaminase, probably through deamination of deoxycytidine residues within the switch (S) regions. The initial lesions in the S regions are subsequently processed, resulting in the production of DNA double-strand breaks (DSBs). These breaks will then be recognized, edited and repaired, finally leading to the recombination of the two S regions. Two major repair pathways have been implicated in CSR, the predominant non-homologous end joining (NHEJ) and the alternative end-joining (A-EJ) pathways. The former requires not only components of the ‘classical’ NHEJ machinery, i.e. Ku70/Ku80, DNA-dependent protein kinase catalytic subunit, DNA ligase IV and XRCC4, but also a number of DNA-damage sensors or adaptors, such as ataxia–telangiectasia mutated, γH2AX, 53BP1, MDC1, the Mre11–Rad50–NBS1 complex and the ataxia telangiectasia and Rad3-related protein (ATR). The latter pathway is not well characterized yet and probably requires microhomologies. In this review, we will focus on the current knowledge of the predominant NHEJ pathway in CSR and will also give a perspective on the A-EJ pathway.
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Wojewódzka, Maria, Marcin Kruszewski, Iwona Buraczewska, et al. "Sirtuin inhibition increases the rate of non-homologous end-joining of DNA double strand breaks." Acta Biochimica Polonica 54, no. 1 (2007): 63–69. http://dx.doi.org/10.18388/abp.2007_3270.

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Sirtuins (type III histone deacetylases) are an important member of a group of enzymes that modify chromatin conformation. We investigated the role of sirtuin inhibitor, GPI 19015, in double strand break (DSB) repair in CHO-K1 wt and xrs-6 mutant cells. The latter is defective in DNA-dependent protein kinase (DNA-PK)-mediated non-homologous end-joining (D-NHEJ). DSB were estimated by the neutral comet assay and histone gammaH2AX foci formation. We observed a weaker effect of GPI 19015 treatment on the repair kinetics in CHO wt cells than in xrs6. In the latter cells the increase in DNA repair rate was most pronounced in G1 phase and practically absent in S and G2 cell cycle phases. The decrease in the number of histone gammaH2AX foci was faster in xrs6 than in CHO-K1 cells. The altered repair rate did not affect survival of X-irradiated cells. Since in G1 xrs6 cells DNA-PK-dependent non-homologous end-joining, D-NHEJ, does not operate, these results indicate that inhibition of sirtuins modulates DNA-PK-independent (backup) non-homologous end-joining, B-NHEJ, to a greater extent than the other DSB repair system, D-NHEJ.
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Hristova, Dayana B., Katharina B. Lauer, and Brian J. Ferguson. "Viral interactions with non-homologous end-joining: a game of hide-and-seek." Journal of General Virology 101, no. 11 (2020): 1133–44. http://dx.doi.org/10.1099/jgv.0.001478.

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There are extensive interactions between viruses and the host DNA damage response (DDR) machinery. The outcome of these interactions includes not only direct effects on viral nucleic acids and genome replication, but also the activation of host stress response signalling pathways that can have further, indirect effects on viral life cycles. The non-homologous end-joining (NHEJ) pathway is responsible for the rapid and imprecise repair of DNA double-stranded breaks in the nucleus that would otherwise be highly toxic. Whilst directly repairing DNA, components of the NHEJ machinery, in particular the DNA-dependent protein kinase (DNA-PK), can activate a raft of downstream signalling events that activate antiviral, cell cycle checkpoint and apoptosis pathways. This combination of possible outcomes results in NHEJ being pro- or antiviral depending on the infection. In this review we will describe the broad range of interactions between NHEJ components and viruses and their consequences for both host and pathogen.
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Caracciolo, Daniele, Caterina Riillo, Maria Teresa Di Martino, Pierosandro Tagliaferri, and Pierfrancesco Tassone. "Alternative Non-Homologous End-Joining: Error-Prone DNA Repair as Cancer’s Achilles’ Heel." Cancers 13, no. 6 (2021): 1392. http://dx.doi.org/10.3390/cancers13061392.

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Error-prone DNA repair pathways promote genomic instability which leads to the onset of cancer hallmarks by progressive genetic aberrations in tumor cells. The molecular mechanisms which foster this process remain mostly undefined, and breakthrough advancements are eagerly awaited. In this context, the alternative non-homologous end joining (Alt-NHEJ) pathway is considered a leading actor. Indeed, there is experimental evidence that up-regulation of major Alt-NHEJ components, such as LIG3, PolQ, and PARP1, occurs in different tumors, where they are often associated with disease progression and drug resistance. Moreover, the Alt-NHEJ addiction of cancer cells provides a promising target to be exploited by synthetic lethality approaches for the use of DNA damage response (DDR) inhibitors and even as a sensitizer to checkpoint-inhibitors immunotherapy by increasing the mutational load. In this review, we discuss recent findings highlighting the role of Alt-NHEJ as a promoter of genomic instability and, therefore, as new cancer’s Achilles’ heel to be therapeutically exploited in precision oncology.
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Pastwa, Elzbieta, Tomasz Poplawski, Agnieszka Czechowska, Mariusz Malinowski, and Janusz Blasiak. "Non-homologous DNA End Joining Repair in Normal and Leukemic Cells Depends on the Substrate Ends." Zeitschrift für Naturforschung C 60, no. 5-6 (2005): 493–500. http://dx.doi.org/10.1515/znc-2005-5-619.

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Double-strand breaks (DSBs) are the most serious DNA damage which, if unrepaired or misrepaired, may lead to cell death, genomic instability or cancer transformation. In human cells they can be repaired mainly by non-homologous DNA end joining (NHEJ). The efficacy of NHEJ pathway was examined in normal human lymphocytes and K562 myeloid leukemic cells expressing the BCR/ABL oncogenic tyrosine kinase activity and lacking p53 tumor suppressor protein. In our studies we employed a simple and rapid in vitro DSB end joining assay based on fluorescent detection of repair products. Normal and cancer cells were able to repair DNA damage caused by restriction endonucleases, but the efficiency of the end joining was dependent on the type of cells and the structure of DNA ends. K562 cells displayed decreased NHEJ activity in comparison to normal cells for 5′ complementary DNA overhang. For blunt-ended DNA there was no significant difference in end joining activity. Both kinds of cells were found about 10-fold more efficient for joining DNA substrates with compatible 5′ overhangs than those with blunt ends. Our recent findings have shown that stimulation of DNA repair could be involved in the drug resistance of BCR/ABL-positive cells in anticancer therapy. For the first time the role of STI571 was investigated, a specific inhibitor of BCR/ABL oncogenic protein approved for leukemia treatment in the NHEJ pathway. Surprisingly, STI571 did not change the response of BCR/ABL-positive K562 cells in terms of NHEJ for both complementary and blunt ends. Our results suggest that the various responses of the cells to DNA damage via NHEJ can be correlated with the differences in the genetic constitution of human normal and cancer cells. However, the role of NHEJ in anticancer drug resistance in BCR/ABL-positive cells is questionable.
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Du, Wei, Surya Amarachintha, Wilson Andrew, and Qishen Pang. "Hyper-Active Non-Homologous End Joining Selects for Synthetic Lethality Resistant and Pathological Hematopoietic Stem Cells." Blood 126, no. 23 (2015): 5400. http://dx.doi.org/10.1182/blood.v126.23.5400.5400.

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Abstract The prominent role of Fanconi anemia (FA) proteins involves homologous recombination (HR) repair. Poly[ADP-ribose] polymerase1 (PARP1) functions in multiple cellular processes including DNA repair and PARP inhibition is an emerging targeted therapy for cancer patients deficient in HR. Here we show that PARP1 activation in hematopoietic stem and progenitor cells (HSPCs) in response to genotoxic or oxidative stress attenuates HSPC exhaustion. Mechanistically, PARP1 controls the balance between HR and non-homologous end joining (NHEJ) in double strand break (DSB) repair by preventing excessive NHEJ. Disruption of the FA core complex skews PARP1 function in DSB repair and led to hyper-active NHEJ in Fanca-/- or Fancc-/- HSPCs. Re-expression of PARP1 rescues the hyper-active NHEJ phenotype in Brca1-/-Parp1-/- but less effective in Fanca-/-Parp1-/- cells. Inhibition of NHEJ prevents myeloid/erythroid pathologies associated with "synthetic lethality" and reduces human engraftment. Our results suggest that hyper-active NHEJ may select for "synthetic lethality" resistant and pathological HSPCs. Disclosures No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "NHEJ [Non Homologous End joining]"

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Deville, Sara Sofia. "The intermediate filament synemin promotes non-homologous end joining in an ATM-dependent manner." Technische Universität Dresden, 2019. https://tud.qucosa.de/id/qucosa%3A72378.

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Background: Therapy resistance is a great challenge in cancer treatment. Among numerous factors, cell adhesion to extracellular matrix is a well-known determinant of radiochemo-resistance. It has been shown that targeting focal adhesion proteins (FAPs), e.g. β1 integrin, enhances tumor cell radio(chemo)sensitivity in various entities such as head and neck squamous cell carcinoma (HNSCC), lung carcinoma, glioblastoma, breast carcinoma and leukemia. Previous studies demonstrated a functional crosstalk between specific FAPs and DNA repair processes; however, the molecular circuitry underlying this crosstalk remains largely unsolved. Hence, this study in HNSCC aimed to identify alternative FAPs associated with DNA damage repair mechanisms and radioresistance. Materials and Methods: A novel 3D High Throughput RNAi Screen (3DHT-RNAi-S) using laminin-rich extracellular matrix (lrECM) was established to determine radiation-induced re-sidual DNA double strand breaks (DSBs; foci assay) and clonogenic radiation survival. In the screen, we used UTSCC15 HNSSC cells stably expressing the DSB marker protein 53BP1 tagged to pEGFP. Validations were performed in 10 additional HNSCC cell lines (Cal33, FaDu, SAS, UTSCC5, UTSCC8, UTSCC14, UTSCC15, UTSCC45 and XF354fl2) grown in 3D lrECM. Immunofluorescence staining, immunoblotting, chromatin fractionation were utilized to evaluate protein expression, dynamics and kinetics post irradiation. Investigations of molecular mechanisms of DNA repair and radio(chemo)resistance employed DSB repair reporter assays for non-homologous end joining (NHEJ) and homologous recombination (HR), cell cycle analysis, chromatin fractionation levels evaluation and kinase activity profiling (PamGene) upon protein knockdown in combination with/-out X-ray exposure. Foci assay and clonogenic survival assay were performed after single or multiple knockdowns of synemin and associated proteins such as DNA-PKcs and c-Abl. Protein-protein interactions between synemin and associated proteins were determined using immunoprecipitation and proximity ligation assay. Mutant/depletion constructs of synemin (ΔLink-Tail, ΔHead-Link, Synemin_301-961, Synemin_962-1565, S1114A and S1159A) were generated in order to identify essential synemin’s sites controlling DNA repair functions. Results: Among the targets found in the 3DHT-RNAi-S, synemin was one of the most promising FAP candidates to determine HNSCC cell survival and DNA damage repair. Synemin silencing radiosensitized HNSCC cells, while its exogenous overexpression induced radio-protection. Radiation induced an increased synemin/chromatin interaction and a marked ac-cumulation of synemin in the perinuclear area. Intriguingly, synemin depletion elicited a 40% reduction in NHEJ activity without affecting HR or Alt-EJ. In line, ATM, DNA-PKcs and c-Abl phosphorylation as well as Ku70 expression strongly declined in synemin depleted and irra-diated cells relative to controls, whereas an opposite effect was observed under synemin overexpression. Single, double and triple depletion of synemin, DNA-PKcs and c-Abl resulted in a similar radiosensitizing effect and DSB levels as detected upon single knockdown of synemin, describing its upstream role. In kinome analysis, tyrosine kinases showed signifi-cantly reduced activity after synemin silencing relative to controls. Furthermore, immunoprecipitation assays revealed a protein complex formed between synemin, DNA-PKcs and c-Abl under pre- and post-irradiation conditions. This protein complex dispersed when ATM was pharmacologically inhibited, implying synemin function to be dependent on ATM kinase activity. By means of the different mutation/deletion constructs of synemin, the phosphorylation site at serine 1114 located on the distal portion of synemin’s tail was identified as essential protein-protein interaction site for synemin’s function in DNA repair. Conclusions: The established 3DHT-RNAi-S provides a robust screening platform for identifying novel targets involved in therapy resistance. Based on this screen and detailed mechanistic analyses, the intermediate filament synemin was discovered as a novel important determinant of DNA repair, tyrosine kinase activity and radiochemoresistance of HNSCC cells. These results further support the notion that DNA repair is controlled by cooperative interactions between nuclear and cytoplasmic proteins.
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Karlsson, Karin. "Role of Non-Homologous End-Joining in Repair of Radiation-Induced DNA Double-Strand Breaks." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7219.

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Chayot, Romain. "Réparation des causes double brin de l'ADN par le mécanisme de non homologous end joining : des bactéries aux cellules souches." Paris 6, 2009. http://www.theses.fr/2009PA066028.

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Les travaux de thèse présentés dans ce manuscrit ont contribué à démontrer que la réparation des cassures double brin (CDBs) de l’ADN par End Joining (raboutage des extrémités) est un mécanisme flexible, qui s’est adapté aux contraintes des organismes et également à celles des types cellulaires. Le Proto End Joining, que nous avons mis en évidence chez Escherichia coli, est hautement mutagène. C’est un mécanisme de secours, qui utilise des protéines également employées lors de la Recombinaison Homologue (recBCD) et vraisemblablement lors de la réplication de l’ADN (LigA). Ceci fait naître des interrogations, d’un point de vue évolutif, sur l’origine ou la co-origine des mécanismes de réplication/réparation. Le minimalisme et la flexibilité des protéines du PEJ bactérien contrastent avec la panoplie de protéines hautement spécialisées utilisées par le NHEJ chez les mammifères. Nous savions que la polymérase µ, une polymérase de la famille X, n’était pas indispensable pour l’organisme. Néanmoins, nous démontrons que cette protéine perfectionne la machinerie du NHEJ. Elle rend le complexe synaptique plus efficace et accélère la réparation des CDBs. Les conséquences de ce perfectionnement se manifestent par une meilleure réponse de la cellule aux dommages de l’ADN et finalement par une sénescence cellulaire moins accentuée. Enfin, les données préliminaires sur les cellules satellites du muscle squelettique murin, cellules indifférenciées en charge du maintien de l’homéostasie du tissu, indiquent que le NHEJ est optimisé, extrêmement rapide et très efficace. Il reste à savoir si cette plus grande efficacité est également associée à une plus grande fidélité du NHEJ.
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Dupuy, Pierre. "Réparation des cassures double-brin chez la bactérie symbiotique Sinorhizobium meliloti : caractérisation du mécanisme de non-homologous end-joining." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30153.

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Les cassures double-brin (CDBs) de l'ADN sont décrites comme étant les lésions de l'ADN les plus délétères puisqu'elles conduisent systématiquement à la mort de la cellule si elles ne sont pas réparées. Les CDBs peuvent être réparées par différents mécanismes et notamment par Non-Homologous End-Joining (NHEJ). Chez les eucaryotes, les protéines centrales de la NHEJ, Ku70 et Ku80, forment un hétérodimère capable de se lier aux extrémités de l'ADN générées par la cassure. Par la suite, Ku70 et Ku80 recrutent de nombreuses autres protéines permettant la modification des extrémités et la réparation de la CDB par ligation. La NHEJ a également été caractérisée chez un nombre limité de bactéries chez qui le mécanisme semble moins complexe que chez les eucaryotes. Chez les bactéries, la NHEJ nécessite seulement deux protéines : un homodimère de Ku, et la protéine multifonctionnelle LigD capable de modifier les extrémités et d'effectuer la ligation. La majorité des études faites sur la NHEJ ont été menées chez des bactéries ne possédant qu'une seule paire des gènes ku/ligD. Cependant, de nombreux autres génomes bactériens possèdent plusieurs copies de ces deux gènes et le fonctionnement de la NHEJ chez ces organismes est inconnu. Le génome de la bactérie symbiotique Sinorhizobium meliloti code quatre Ku putatives (ku1-4) et quatre LigD putatives (ligD1-4). A ce jour, une seule étude a été menée chez ce modèle bactérien montrant que chacun des simples mutants ku est plus sensible que la souche sauvage à un traitement aux rayonnements ionisants, suggérant que chacune des Ku joue un rôle dans la réparation des CDBs par NHEJ. Par l'utilisation de différentes approches in vivo, nous avons mené une caractérisation génétique de la NHEJ chez S. meliloti permettant de clarifier les contributions relatives des gènes ku et ligD dans le mécanisme. Pour la première fois chez une bactérie, nous avons pu obtenir des résultats montrant la présence de plusieurs systèmes indépendants de NHEJ chez S. meliloti, et suggérant l'existence d'un possible hétérodimère de Ku. Nous avons également mis en évidence que la NHEJ est activée dans différentes conditions de stress, telles que le stress thermique et la carence nutritive, et qu'une partie de cette réparation est sous le contrôle du régulateur central de la réponse générale au stress RpoE2. Par ailleurs, nous avons montré que la NHEJ, et plus généralement les mécanismes de réparation des CDBs sont impliqués dans la résistance à la dessiccation chez S. meliloti. Enfin, nous avons généré la première preuve expérimentale d'une implication de la NHEJ dans le transfert horizontal de gène chez les bactéries. Dans leur ensemble, ces travaux enrichissent nos connaissances sur les mécanismes de réparation des CDBs chez les bactéries possédant plusieurs orthologues de Ku et LigD. Ils suggèrent également que la NHEJ pourrait contribuer à l'évolution des génomes, en particulier en condition de stress, non seulement en raison du caractère mutagène de ce type de réparation mais également en participant à l'acquisition d'ADN exogène originaire de bactéries distantes<br>DNA double-strand breaks (DSBs) are described as the most deleterious DNA damages as they can lead to cell death if they are not repaired. DSBs can be repaired through several mechanisms, including Non-Homologous End-Joining (NHEJ). In eukaryotes, the main NHEJ proteins, Ku70 and Ku80, bind DNA ends as a heterodimer, and then recruit several additional proteins including enzymes which catalyze the processing and ligation of DNA ends. NHEJ has also been characterized in a limited number of bacteria, where the repair mechanism appears to be less complex than in eukaryotes. Indeed, only two proteins are required: a homodimeric Ku protein, and a multifunctional LigD enzyme able to process and ligate the DNA ends. However, most studies were performed on bacterial species encoding a single pair of ku/ligD. Actually, many bacterial species encode multiple copies of these genes, whose relative contributions to NHEJ in vivo are so far unknown. The Sinorhizobium meliloti genome encodes four putative Ku (ku1-4) and four putative LigD (ligD1-4). To date, a single study conducted on this model bacterium showed that every ku single mutant is more sensitive than the wild type strain to ionizing radiations showing that all ku genes are involved in NHEJ repair of DSBs in this organism. Here, using several in vivo approaches, we performed a comprehensive genetic characterization of NHEJ repair in S. meliloti, and clarified the respective contributions of the various ku and ligD genes. For the first time in bacteria, we obtained results showing the presence of several independent NHEJ systems in S. meliloti and suggesting the existence of a putative heterodimeric form of Ku. We also demonstrated that NHEJ repair is activated under various stress conditions, including heat and nutrient starvation, and that part of this repair is under the control of the general stress response regulator RpoE2. We showed that NHEJ and more generally DSB repair mechanisms are involved in desiccation resistance in S. meliloti. Finally, for the first time in bacteria, we provided evidence that NHEJ not only repairs DSBs, but can also erroneously integrate heterologous DNA molecules into the breaks. Altogether, our data provide new insights into the mechanisms of DSB repair in bacteria which encode multiple Ku and LigD orthologues. It also suggest that NHEJ might contribute to the evolution of bacterial genomes under adverse environmental conditions not only through error-prone repair of DSB by its mutagenesis repair characteristic but also by participating in the acquisition of foreign DNA from distantly related organisms during horizontal gene transfer events
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Bordelet, Hélène. "Régulation de la résection aux cassures double-brin par l'hétérochromatine SIR dépendante." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS300.

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L'hétérochromatine est une caractéristique conservée des chromosomes eucaryotes, avec des rôles centraux dans la régulation de l'expression des gènes et le maintien de la stabilité du génome. Comment la réparation de l'ADN est régulée par l'hétérochromatine reste mal compris. Chez Saccharomyces cerevisiae, le complexe SIR (Silent Information Regulator) assemble une fibre de chromatine compacte. La chromatine SIR limite la résection aux cassures double-brin (DSB) protégeant les extrémités chromosomiques endommagées contre la perte d'informations génétiques. Toutefois, lesquels des trois complexes de résection redondants, MRX-Sae2, Exo1 et Sgs1-Dna2 sont inhibés et par quel(s) mécanisme(s) reste à decouvrir. Nous montrons que Sir3, le facteur de fixation des histones de l’hétérochromatine de Saccharomyces cerevisiae, interagit physiquement avec Sae2 et inhibe toutes ses fonctions. Cette interaction limite notamment la résection médiée par Sae2, stabilise MRX à la DSB et augmente le Non-Homologous End Joining (NHEJ). De plus, la chromatine répressive SIR inhibe partiellement les deux voies de résection extensive médiées par Exo1 et Sgs1-Dna2 par des mécanismes distincts. L'inhibition par les SIR de la résection extensive et de Sae2 favorise la NHEJ et limite le Break-Induced Replication (BIR), prévenant ainsi de la perte d'hétérozygotie au niveau des subtélomères<br>Heterochromatin is a conserved feature of eukaryotic chromosomes, with central roles in regulation of gene expression and maintenance of genome stability. How DNA repair occurs in heterochromatin remains poorly described. In Saccharomyces cerevisiae, the Silent Information Regulator (SIR) complex assembles a compact chromatin fibre. SIR-mediated repressive chromatin limits Double Strand Break (DSB) resection protecting damaged chromosome ends against the loss of genetic information. However, which of the three redundant resection complexes, MRX-Sae2, Exo1 and Sgs1-Dna2 are inhibited and by which mechanism remains to be deciphered. We show that Sir3, the histone-binding factor of yeast heterochromatin, physically interacts with Sae2-mediated resection and inhibits all its functions. Notably, this interaction limits Sae2-mediated resection, delays MRX removal from DSB ends and promotes Non-Homologous End Joining (NHEJ). In addition, SIR-mediated repressive chromatin partially inhibits the two long range resection pathways mediated by Exo1 and Sgs1-Dna2 by distinct mechanisms. Altogether SIR mediated inhibition of extensive resection and of Sae2 promotes NHEJ and limits Break-Induced Replication (BIR) preventing loss of heterozygosity at subtelomeres
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Tsouroula, Aikaterini. "Double strand break repair within constitutive heterochromatin." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ036/document.

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L'hétérochromatine, de nature compacte et répétitive, limite l’accès à l'ADN et fait de la réparation des DSBs un processus difficile que les cellules doivent surmonter afin de maintenir leur intégrité génomique. Pour y étudier la réparation des DSBs, nous avons conçu un système CRISPR / Cas9 dans lequel les DSB peuvent être efficacement et spécifiquement induites dans l'hétérochromatine de fibroblastes de souris NIH3T3. En développant un système CRISPR / Cas9 hautement spécifique et robuste pour cibler l'hétérochromatine péricentrique, nous avons montré que les DSB en G1 sont positionnellement stables et réparés par NHEJ. En S / G2, ils se déplacent vers la périphérie de ce domaine pour être réparés par HR. Ce processus de relocalisation dépend de la résection et de l'exclusion de RAD51 du domaine central de l'hétérochromatine. Si ces cassures ne se relocalisent pas, elles sont réparées dans le cœur du domaine de l'hétérochromatine par NHEJ ou SSA. D'autre part, les DSBs dans l'hétérochromatine centromérique activent NHEJ et HR tout au long du cycle cellulaire. Nos résultats révèlent le choix de la voie de réparation différentielle entre l'hétérochromatine centromérique et péricentrique, ce qui régule également la position des DSBs<br>Heterochromatin is the tightly packed form of repetitive DNA, essential for cell viability. Its highly compacted and repetitive nature renders DSB repair a challenging process that cells need to overcome in order to maintain their genome integrity. Developing a highly specific and robust CRISPR/Cas9 system to target pericentric heterochromatin, we showed that DSBs in G1 are positionally stable and repaired by NHEJ. In S/G2, they relocate to the periphery of this domain to be repaired by HR. This relocation process is dependent of resection and RAD51 exclusion from the core domain of heterochromatin. If these breaks fail to relocate, they are repaired within heterochromatin by NHEJ or SSA. On the other hand, DSBs in centromeric heterochromatin activate both NHEJ and HR throughout the cell cycle. Our results reveal the differential repair pathway choice between centromeric and pericentric heterochromatin that also regulates the DSB position
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De, Melo Abinadabe Jackson. "Molecular basis for the structural role of human DNA ligase IV." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4040.

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Les défauts dans la réparation des cassures double-brin de l'ADN (DSBs) peuvent avoir d'importantes conséquences pouvant entrainer une instabilité génomique et conduire à la mort cellulaire ou au développement de cancers. Dans la plupart des cellules mammifères, le mécanisme de Jonction des Extrémités Non Homologues (NHEJ) est le principal mécanisme de réparation des DSBs. L'ADN Ligase IV (LigIV) est une protéine unique dans sa capacité à promouvoir la NHEJ classique. Elle s'associe avec deux autres protéines structuralement similaires, XRCC4 et XLF (ou Cernunnos). LigIV interagit directement avec XRCC4 pour former un complexe stable, tandis que l'interaction entre XLF et ce complexe est médiée par XRCC4. XLF stimule fortement l'activité de ligation du complexe LigIV/XRCC4 par un mécanisme encore indéterminé. Récemment, un rôle structurel non catalytique a été attribué à LigIV (Cottarel et al., 2013). Dans le travail de thèse présenté ici, nous avons reconstitué l'étape de ligation de la NHEJ en utilisant des protéines recombinantes produites dans des bactéries afin d’une part, d'explorer les bases moléculaires du rôle structural de LigIV, d’autre part de comprendre le mécanisme par lequel XLF stimule le complexe de ligation, et enfin de mieux comprendre comment ces trois protéines coopèrent au cours de la NHEJ. Nos analyses biochimiques suggèrent que XLF via son interaction avec XRCC4 lié à LigIV, pourrait induire un changement conformationnel dans la LigIV. Ce réarrangement de la ligase exposerait son interface de liaison à l'ADN ce qui lui permettrait alors de ponter deux molécules indépendantes d'ADN, une capacité indépendante de l'activité catalytique de LigIV<br>Failure to repair DNA double-strand breaks (DSBs) may have deleterious consequences inducing genomic instability and even cell death. In most mammalian cells, Non-Homologous End Joining (NHEJ) is a prominent DSB repair pathway. DNA ligase IV (LigIV) is unique in its ability to promote classical NHEJ. It associates with two structurally related proteins called XRCC4 and XLF (aka Cernunnos). LigIV directly interacts with XRCC4 forming a stable complex while the XLF interaction with this complex is mediated by XRCC4. XLF strongly stimulates the ligation activity of the LigIV/XRCC4 complex by an unknown mechanism. Recently, a structural noncatalytic role of LigIV has been uncovered (Cottarel et al., 2013). Here, we have reconstituted the end joining ligation step using recombinant proteins produced in bacteria to explore not only the molecular basis for the structural role of LigIV, but also to understand the mechanism by which XLF stimulates the ligation complex, and how these three proteins work together during NHEJ. Our biochemical analysis suggests that XLF, through interactions with LigIV/XRCC4 complex, could induce a conformational change in LigIV. Rearrangement of the LigIV would expose its DNA binding interface that is able to bridge two independent DNA molecules. This bridging ability is fully independent of LigIV’s catalytic activity. We have mutated this interface in order to attempt to disrupt the newly identified DNA bridging ability. In vitro analysis of this LigIV mutant will be presented as well as a preliminary in vivo analysis
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Li, Yi. "Structural biology in DNA repair : non-homologous end-joining." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612519.

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Cecillon, Sophie M. "Characterisation of non-homologous end-joining in xenopus egg extracts." Thesis, University of Sussex, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.536988.

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Tonkin, Louise Mary. "Characterisation of the non-homologous end joining DNA repair system from Mycobacterium tuberculosis." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615245.

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Book chapters on the topic "NHEJ [Non Homologous End joining]"

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Menon, Vijay, and Lawrence Povirk. "Involvement of p53 in the Repair of DNA Double Strand Breaks: Multifaceted Roles of p53 in Homologous Recombination Repair (HRR) and Non-Homologous End Joining (NHEJ)." In Subcellular Biochemistry. Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9211-0_17.

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Nagaria, Pratik, and Feyruz V. Rassool. "Alternative Non-homologous End-Joining: Mechanisms and Targeting Strategies in Cancer." In Cancer Drug Discovery and Development. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75836-7_15.

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Arentshorst, Mark, Arthur F. J. Ram, and Vera Meyer. "Using Non-homologous End-Joining-Deficient Strains for Functional Gene Analyses in Filamentous Fungi." In Plant Fungal Pathogens. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-501-5_9.

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Steinert, Jeannette, Carla Schmidt, and Holger Puchta. "Use of the Cas9 Orthologs from Streptococcus thermophilus and Staphylococcus aureus for Non-Homologous End-Joining Mediated Site-Specific Mutagenesis in Arabidopsis thaliana." In Methods in Molecular Biology. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7286-9_27.

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Lucchesi, John C. "DNA repair and genomic stability." In Epigenetics, Nuclear Organization & Gene Function. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.003.0015.

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A number of pathways have evolved in order to repair DNA. Mismatch repair (MMR) operates when an improper nucleotide is used or when an insertion or deletion occurs during replication. Nucleotide excision repair (NER) repairs damage that distorts the DNA helix such as the presence of pyrimidine dimers induced by ultraviolet light. Base excision repair (BER) removes damaged or altered DNA bases that do not result in a conformational change in the chromatin. Single-strand break repair (SSBR) uses the same enzymatic steps as BER. Double-strand break (DSB) repair can involve either non-homologous end-joining (NHEJ) or homologous recombination (HR). In NHEJ, the broken DNA ends are joined directly. HR requires that one of the strands of the broken DNA molecule participates in the strand invasion of the sister chromatid. The site of the DSB must be modified to allow access to the repair machinery. This modification involves remodeling complexes, as well as histone-modifying enzymes.
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Kumar Sharma, Ajay, Priyanka Shaw, Aman Kalonia, et al. "Recent Perspectives in Radiation-Mediated DNA Damage and Repair: Role of NHEJ and Alternative Pathways." In DNA - Damages and Repair Mechanisms. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96374.

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Radiation is one of the causative agents for the induction of DNA damage in biological systems. There is various possibility of radiation exposure that might be natural, man-made, intentional, or non-intentional. Published literature indicates that radiation mediated cell death is primarily due to DNA damage that could be a single-strand break, double-strand breaks, base modification, DNA protein cross-links. The double-strand breaks are lethal damage due to the breakage of both strands of DNA. Mammalian cells are equipped with strong DNA repair pathways that cover all types of DNA damage. One of the predominant pathways that operate DNA repair is a non-homologous end-joining pathway (NHEJ) that has various integrated molecules that sense, detect, mediate, and repair the double-strand breaks. Even after a well-coordinated mechanism, there is a strong possibility of mutation due to the flexible nature in joining the DNA strands. There are alternatives to NHEJ pathways that can repair DNA damage. These pathways are alternative NHEJ pathways and single-strand annealing pathways that also displayed a role in DNA repair. These pathways are not studied extensively, and many reports are showing the relevance of these pathways in human diseases. The chapter will very briefly cover the radiation, DNA repair, and Alternative repair pathways in the mammalian system. The chapter will help the readers to understand the basic and applied knowledge of radiation mediated DNA damage and its repair in the context of extensively studied NHEJ pathways and unexplored alternative NHEJ pathways.
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Beying, Natalja, Carla Schmidt, and Holger Puchta. "Double strand break (DSB) repair pathways in plants and their application in genome engineering." In Genome editing for precision crop breeding. Burleigh Dodds Science Publishing, 2021. http://dx.doi.org/10.19103/as.2020.0082.04.

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In genome engineering, after targeted induction of double strand breaks (DSBs) researchers take advantage of the organisms’ own repair mechanisms to induce different kinds of sequence changes into the genome. Therefore, understanding of the underlying mechanisms is essential. This chapter will review in detail the two main pathways of DSB repair in plant cells, non-homologous end joining (NHEJ) and homologous recombination (HR) and sum up what we have learned over the last decades about them. We summarize the different models that have been proposed and set these into relation with the molecular outcomes of different classes of DSB repair. Moreover, we describe the factors that have been identified to be involved in these pathways. Applying this knowledge of DSB repair should help us to improve the efficiency of different types of genome engineering in plants.
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Vladislavov Ostoich, Peter, Michaela Beltcheva, and Roumiana Metcheva. "Nefarious, but in a Different Way: Comparing the Ecotoxicity, Gene Toxicity and Mutagenicity of Lead (Pb) and Cadmium (Cd) in the Context of Small Mammal Ecotoxicology." In Genotoxicity and Mutagenicity - Mechanisms and Test Methods [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.89850.

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Lead and cadmium are long established toxic and carcinogenic metals. Still, the mechanisms of their interaction with eukaryotic DNA are not unequivocally understood. New data provide evidence on the influence of both metals on DNA repair, particularly non-homologous end joining (NHEJ) and mismatch repair (MMR). This may help explain the weak direct mutagenicity of both Pb2+ and Cd2+ ions in the Ames test, as opposed to the proven carcinogenicity of both metals; it has long been proposed that lead and cadmium may induce an imbalance in mammalian systems of DNA damage repair and promote genomic instability. While new evidence for mechanistic interactions of metals with DNA repair emerges, some of the old questions involving dose distribution, pathways of exposure and bioaccumulation/detoxification kinetics still remain valid. To help place the current state of the art in the genetic toxicology of lead and cadmium within the context of ecotoxicology, the current authors propose an integrative approach and offer a review of other authors’ work as well as some of their own data on systemic and organ-specific toxicities in laboratory mice. The current chapter is a comparative analysis of the state of the art in the specific toxicity and genotoxicity of Pb and Cd, presenting some new and little-known information.
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"Non-Homologous End Joining." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4111.

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Jeggo, Penny A. "Non-Homologous End Joining." In Encyclopedia of Biological Chemistry. Elsevier, 2004. http://dx.doi.org/10.1016/b0-12-443710-9/00432-4.

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Conference papers on the topic "NHEJ [Non Homologous End joining]"

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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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Sears, Catherine R., Katherine S. Pawelczak, and John J. Turchi. "Cisplatin Sensitizes DNA To Ionizing Radiation By Impairing Non-Homologous End-Joining." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3475.

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Caracciolo, Daniele, Martina Montesano, Emanuela Altomare, et al. "Abstract 2827: Alternative non-homologous end joining DNA repair as therapeutic target in multiple myeloma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2827.

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Allen, Brittany N., Michal Masternak, and Mark Muller. "Abstract A43: DNA repair by non-homologous end joining induced gene silencing via DNA hypermethylation." In Abstracts: AACR Special Conference: Chromatin and Epigenetics in Cancer; September 24-27, 2015; Atlanta, GA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.chromepi15-a43.

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Oike, Takahiro, Hideaki Ogiwara, Takashi Nakano, Jun Yokota, and Takashi Kohno. "Abstract 5721: Garcinol, a histone acetyltransferase inhibitor, radiosensitizes cancer cells by inhibiting non-homologous end joining." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5721.

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Zhang, Yongwei, Marie Regairaz, Jennifer Seiler, Keli Agama, James Doroshow, and Yves Pommier. "Abstract 2973: Poly(ADP)ribose inhibition forces the repair of topoisomerase I cleavage complexes through homologous recombination and non-homologous end joining." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2973.

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Steinberg, Ruchama C., Jianyong Liu, Ajay Vaghasia, et al. "Abstract 2383: RepairSwitch: a novel cell-based functional assay for simultaneous measurement of homologous recombination and non-homologous end joining mediated DNA repair." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2383.

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Head, PamelaSara E., Nagaraju P. Ganji, Shi-Ya Wang, et al. "Abstract 2561: DNA-PKCS deacetylation by SIRT2 promotes DNA double-strand break repair by non-homologous end joining." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2561.

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Sears, Catherine R., and John J. Turchi. "Cisplatin-IR Synergy In NSCLC Is A Function Of DNA-Cisplatin Lesions Causing Impaired Non-Homologous End-Joining." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6289.

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Deraska, Peter V., Colin O’Leary, Jean-Bernard Lazaro, Christopher J. Sweeney, Alan D. D’Andrea та David Kozono. "Abstract 1644: NF-κB inhibitor DMAPT blocks non-homologous end-joining repair of radiation-induced DSBs in NSCLC". У 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.am2016-1644.

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Reports on the topic "NHEJ [Non Homologous End joining]"

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Yin, Hong. Identify in Breast Cancer Stem Cell-Like Cells the Proteins Involved in Non- Homologous End Joining DNA Repair. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada493642.

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