Relevant bibliographies by topics / DNA interstrand crosslinks

Academic literature on the topic 'DNA interstrand crosslinks'

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Published: 6 September 2023

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Journal articles on the topic "DNA interstrand crosslinks"

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ZHAO, LIJIAO, RUGANG ZHONG, and YAN ZHEN. "AN ONIOM STUDY ON THE CROSSLINKED BASE PAIRS IN DNA REACTED WITH CHLOROETHYLNITROSOUREAS." Journal of Theoretical and Computational Chemistry 06, no. 03 (September 2007): 631–39. http://dx.doi.org/10.1142/s0219633607003283.

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Chloroethylnitrosoureas (CENUs) are clinically useful anticancer agents. Their cytotoxicity is associated with the generation of DNA interstrand crosslinks. QM/MM computations are carried out to investigate DNA crosslinks by CENUs with ONIOM hybrid method. The crosslinked DNA are subdivided into three layers, each of which are described at B3LYP/6-311+G(d,p), AM1, and UFF level of theory, respectively. The result shows that the deformation of DNA with dG ( N 1)– dC ( N 3) crosslink is much less than the other crosslinks, which indicate that the most favorable crosslink is between the N1 atom of guanine and the N3 atom of the complementary cytosine.
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Mladenova, Veronika, and George Russev. "DNA Interstrand Crosslinks Repair in Mammalian Cells." Zeitschrift für Naturforschung C 63, no. 3-4 (April 1, 2008): 289–96. http://dx.doi.org/10.1515/znc-2008-3-421.

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We studied the formation of double strand breaks (DSBs) as intermediates in the repair of DNA interstrand crosslinks (ICLs) by homologous recombination (HR). The plasmid EGFP-N1 was crosslinked with trioxsalen to give one ICL per plasmid on average. HeLa cells were transfected with the crosslinked plasmids and the ICL repair was monitored by following the restoration of the GFP expression. It was accompanied by γ-H2AX foci formation suggesting that DSBs were formed during the process. However, the same amount of γ-H2AX foci was observed when cells were transfected with native plasmid, which indicated that γ-H2AX foci appearance could not be used to determine the amount of DSBs connected with the ICL repair in this system. For this reason we further monitored the DSB formation by determining the amount of linearized plasmids, since having one crosslink per plasmid on average, any ICL-driven DSB formation would lead to plasmid linearization. Native and crosslinked plasmids were incubated in repair-competent cell-free extracts from G1 and S phase HeLa cells. Although a considerable part of the ICLs was repaired, no linearization of the plasmids was observed in the extracts, which was interpreted that DSBs were not formed as intermediates in the process of ICL repair. In another set of experiments HRproficient HeLa and HR-deficient irs3 cells were transfected with native and crosslinked plasmids, and 6 h and 12 h later the plasmid DNA was isolated and analyzed by electrophoresis. The same amount of linear plasmid molecules was observed in both cell lines, regardless of whether they were transfected with native or crosslinked pEGFP-N1, which further confirmed that DSB formation was not an obligatory step in the process of ICL repair by HR
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Bezalel-Buch, Rachel, Young K. Cheun, Upasana Roy, Orlando D. Schärer, and Peter M. Burgers. "Bypass of DNA interstrand crosslinks by a Rev1–DNA polymerase ζ complex." Nucleic Acids Research 48, no. 15 (July 7, 2020): 8461–73. http://dx.doi.org/10.1093/nar/gkaa580.

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Abstract DNA polymerase ζ (Pol ζ) and Rev1 are essential for the repair of DNA interstrand crosslink (ICL) damage. We have used yeast DNA polymerases η, ζ and Rev1 to study translesion synthesis (TLS) past a nitrogen mustard-based interstrand crosslink (ICL) with an 8-atom linker between the crosslinked bases. The Rev1–Pol ζ complex was most efficient in complete bypass synthesis, by 2–3 fold, compared to Pol ζ alone or Pol η. Rev1 protein, but not its catalytic activity, was required for efficient TLS. A dCMP residue was faithfully inserted across the ICL-G by Pol η, Pol ζ, and Rev1–Pol ζ. Rev1–Pol ζ, and particularly Pol ζ alone showed a tendency to stall before the ICL, whereas Pol η stalled just after insertion across the ICL. The stalling of Pol η directly past the ICL is attributed to its autoinhibitory activity, caused by elongation of the short ICL-unhooked oligonucleotide (a six-mer in our study) by Pol η providing a barrier to further elongation of the correct primer. No stalling by Rev1–Pol ζ directly past the ICL was observed, suggesting that the proposed function of Pol ζ as an extender DNA polymerase is also required for ICL repair.
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Williams, Hannah L., Max E. Gottesman, and Jean Gautier. "Replication-Independent Repair of DNA Interstrand Crosslinks." Molecular Cell 47, no. 1 (July 2012): 140–47. http://dx.doi.org/10.1016/j.molcel.2012.05.001.

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Chang, Chun-Ling, Dmitri Y. Lando, Alexander S. Fridman, and Chin-Kun Hu. "Thermal stability of DNA with interstrand crosslinks." Biopolymers 97, no. 10 (July 13, 2012): 807–17. http://dx.doi.org/10.1002/bip.22077.

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Enderle, Janina, Annika Dorn, and Holger Puchta. "DNA- and DNA-Protein-Crosslink Repair in Plants." International Journal of Molecular Sciences 20, no. 17 (September 3, 2019): 4304. http://dx.doi.org/10.3390/ijms20174304.

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DNA-crosslinks are one of the most severe types of DNA lesions. Crosslinks (CLs) can be subdivided into DNA-intrastrand CLs, DNA-interstrand CLs (ICLs) and DNA-protein crosslinks (DPCs), and arise by various exogenous and endogenous sources. If left unrepaired before the cell enters S-phase, ICLs and DPCs pose a major threat to genomic integrity by blocking replication. In order to prevent the collapse of replication forks and impairment of cell division, complex repair pathways have emerged. In mammals, ICLs are repaired by the so-called Fanconi anemia (FA) pathway, which includes 22 different FANC genes, while in plants only a few of these genes are conserved. In this context, two pathways of ICL repair have been defined, each requiring the interaction of a helicase (FANCJB/RTEL1) and a nuclease (FAN1/MUS81). Moreover, homologous recombination (HR) as well as postreplicative repair factors are also involved. Although DPCs possess a comparable toxic potential to cells, it has only recently been shown that at least three parallel pathways for DPC repair exist in plants, defined by the protease WSS1A, the endonuclease MUS81 and tyrosyl-DNA phosphodiesterase 1 (TDP1). The importance of crosslink repair processes are highlighted by the fact that deficiencies in the respective pathways are associated with diverse hereditary disorders.
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Behmand, B., A. M. Noronha, C. J. Wilds, J.-L. Marignier, M. Mostafavi, J. R. Wagner, D. J. Hunting, and L. Sanche. "Hydrated electrons induce the formation of interstrand cross-links in DNA modified by cisplatin adducts." Journal of Radiation Research 61, no. 3 (March 25, 2020): 343–51. http://dx.doi.org/10.1093/jrr/rraa014.

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Abstract Double-stranded oligonucleotides containing cisplatin adducts, with and without a mismatched region, were exposed to hydrated electrons generated by gamma-rays. Gel electrophoresis analysis demonstrates the formation of cisplatin-interstrand crosslinks from the cisplatin-intrastrand species. The rate constant per base for the reaction between hydrated electrons and the double-stranded oligonucleotides with and without cisplatin containing a mismatched region was determined by pulse radiolysis to be 7 × 109 and 2 × 109 M−1 s−1, respectively. These results provide a better understanding of the radiosensitizing effect of cisplatin adducts in hypoxic tumors and of the formation of interstrand crosslinks, which are difficult for cells to repair.
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Liang, Chih-Chao, and Martin A. Cohn. "UHRF1 is a sensor for DNA interstrand crosslinks." Oncotarget 7, no. 1 (December 17, 2015): 3–4. http://dx.doi.org/10.18632/oncotarget.6647.

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Murina, Olga, Christine von Aesch, Ufuk Karakus, Lorenza P. Ferretti, Hella A. Bolck, Kay Hänggi, and Alessandro A. Sartori. "FANCD2 and CtIP Cooperate to Repair DNA Interstrand Crosslinks." Cell Reports 7, no. 4 (May 2014): 1030–38. http://dx.doi.org/10.1016/j.celrep.2014.03.069.

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van Rosmalen, Anne, Carleen Cullinane, Suzanne M. Cutts, and Don R. Phillips. "Stability of adriamycin-induced DNA adducts and interstrand crosslinks." Nucleic Acids Research 23, no. 1 (1995): 42–50. http://dx.doi.org/10.1093/nar/23.1.42.

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Dissertations / Theses on the topic "DNA interstrand crosslinks"

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Vare, Daniel. "Interstrand Crosslinks - Induction and repair." Doctoral thesis, Stockholms universitet, Institutionen för genetik, mikrobiologi och toxikologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-78797.

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DNA crosslinking agents exhibit a variety of DNA lesions, such as monoadducts, DNA-DNA interstrand or intrastrand crosslinks or DNA-protein crosslinks. Agents that produce interstrand crosslinks (ICLs) exist naturally and are widely used in chemotherapy. Therefore, it is important to understand how the lesions induced by these agents are repaired. In bacteria, the repair is mainly dependent on nucleotide excision repair (NER) together with homologous recombination (HR) or translesion synthesis (TLS). In human cells, it is not clear how these lesions are repaired, and it is believed to be a more complicated process in which NER does not play as important a role as in prokaryotes. Here, we investigated the repair mechanisms mainly after treatment with psoralen but also with acetaldehyde, cisplatin and mitomycin C in some studies. As expected from studies on plasmids and in bacteria, we used new techniques to confirm that various ICL-inducing agents block replication fork elongation in mammalian cells. We also found that the replication fork was unable to bypass these lesions. We confirmed that ERCC1/XPF and the HR proteins BRCA2 and XRCC2/3 are vital for protection against ICL treatments. These proteins were also found to be equally important for the repair of monoadducts. To better understand ICL repair in mammalian cells, we developed a method to study the induction and unhooking of ICL in human fibroblasts. We found that ICLs were repaired and that 50% of the induced ICLs were unhooked within 3 hours following exposure. Additionally, we determined that XPA, but not XPE, is involved in ICL unhooking, although not affecting lethality. A step in ICL repair is the formation of double-strand breaks (DSBs), and we identified a replication-dependent formation of DSBs following ICL treatment. Furthermore, ERCC1/XPF was not necessary for DSB formation. The repair of these DSBs was performed by HR and involved ERCC1/XPF. Additionally, we were able to quantify the ICL unhooking in human fibroblasts and found that they can unhook ~2500 ICL/h. We also determined that a dose of approximately 400 ICL/cell is lethal to 50% of the cells, indicating that ICL unhooking is not the most critical step during the repair process.
DNA-skadande ämnen är vanligt i cancerbehandling, då snabbt växande celler, såsom cancerceller är betydligt känsligare än normala celler för DNA skador. En grupp av ämnen som vanligen används i cancerbehandling är korsbindare av DNA. Dessa ämnen kommer reagera två gånger med DNA och skapa två bindningar mitt emot varandra. DNA strängen, som består av två delar, måste kunna separeras och kopieras (replikation) på ett tillförlitligt sätt för att cellerna ska kunna dela sig och bli flera. DNA strängen måste också kunna dela sig och bli avläst rätt för att nya proteiner ska kunna bildas (transkription). När korsbindarna har bundit till DNA strängarna, hindrar detta deras separation och därigenom förhindras även avläsningen och kopieringen.  För att göra undersökningarna av DNA korsbindande ämnen ännu lite svårare, så ger korsbindare flera olika typer av skador. Dels kan det bli flera olika typer av korsbindningar, både mellan två DNA-strängar (ICL) vilket är den farligaste och mest svårreparerade typen, men det kan också ske inom samma DNA-sträng (intrastrand crosslink) eller mellan en DNA-sträng och ett protein (DNA-protein crosslink). Korsbindare kan även bilda enbindningsskador (monoaddukt), vilket innebär den bara binder en gång till DNA. För att cellen ska kunna överleva, så måste den reparera skadorna och ta bort korsbindningen eller monoaddukten. Hur detta sker i människor är inte helt klarlagt men det verkar som det sker i flera steg. Till att börja med klipps DNA sönder i ena strängen på båda sidorna om korsbindningen, detta gör att den kvarvarande delen av korsbindningen kan böjas bort. Därefter kommer cellen att skapa nytt DNA för att fylla mellanrummet som bildats. Cellen använder sig av den andra DNA strängen som mall för att sätta in rätt DNA baser, men i fallet med korsbindande ämnen så är även den strängen skadad och därför finns det en stor risk för att fel DNA baser sätts in och då uppstår mutationer. Nästa steg är att klippa den kvarvarande delen av korsbindningen, även denna gång skapas ett mellanrum som måste fyllas med nya baser. Den första artikeln i avhandlingen handlar om att försöka reda ut om det är ICLen eller monoaddukten som är orsak till olika effekter som påträffas efter behandling med korsbindande ämnen. Det vi fann var att även om det bara var från ICLs som vi kunde mäta en effekt på replikationen, så fick vi nästan lika stark effekt från monoaddukterna, som från ICL, för en av de vanligast använda markörerna (kännetecknen) för båda DNA strängarna var brutna på samma ställe (dubbelstränsbrott). Detta berodde dock inte på att även monoaddukterna skapade dubbelsträngsbrott, utan på att markören vi använde var ospecifik. Vi fann även att även om ICLs har mycket större effekt än monoaddukten på cellens överlevnad m.m., så kan man inte bortse ifrån effekten av monoaddukten och att den troligen har en betydande roll för de korsbindande ämnen som endast ger en liten del ICLs. I artikel två har vi utvecklat en ny metod, som gör det möjligt att mäta hur många ICLs som bildas vid en viss dos av de korsbindande ämnen vi undersöker. Vi kan även mäta hur fort ICLerna kan repareras i mänskliga celler med hjälp av metoden. Tack vare en kombination av våra mätningar och med hjälp av datorsimuleringar, kunde vi räkna ut hur många ICLs som bildades per dos för tre vanliga korsbindare. Vi kunde även visa att 50 % av ICLen har påbörjat reparationen och kommit så långt att de var bortklippta från ena stängen inom 3 timmar efter behandlingen. I artikel tre undersöker vi vilka proteiner som är inblandade i den tidiga delen av ICL reparationen, alltså fram till och med att celler klipper ut korsbindningen på båda sidorna om skadan i ena strängen. Här visar vi att celler som är defekta i reparationsprotein kallat XPA, har en betydligt långsammare borttagning av ICLer än vad båda normala celler och celler defekta i reparationsprotein XPE har. Vi visar även att detta inte påverkar cellens replikationshastighet, eller har någon effekt på cellens överlevnad. Den fjärde artikeln handlar om acetaldehyd, som bildas när alkohol förbränns i kroppen. Acetaldehyd har föreslagits bilda ICL och därför undersökte vi vilka effekter den har på cellerna. Vi visar i den här artikeln att det krävs nysyntes av DNA för att acetaldehyd ska leda till dubbelsträngsbrott. Celler kan reparera dessa dubbelsträngsbrott med hjälp av reparationssystem, som kallas homolog rekombination, men att reparationen ibland blir felaktig. I den femte och sista artikeln i avhandligen undersöker vi ett av de vanligast föreslagna proteinen för att sköta klippningen av DNA (ERCC1/XPF) och hur den är inblandad i reparationen av korsbindningar. Vi kan här visa att även det krosbindande ämnet mitomycin C bromsar replikationshastigheter och att ERCC1/XPF är nödvändigt för att kunna fullfölja homolog rekombination av ICLs.

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 1: Submitted. Paper 2: Manuscript. Paper 3: Manuscript. Paper 4: Submitted.

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Dangeti, Venkata Srinivas Mohan Nimai. "Processing of Cisplatin Interstrand crosslinks (ICLs) by DNA repair proteins." University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1352833172.

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Gruver, Aaron Matthew. "Cellular Analyses of the RAD51-related Homologous Recombination Repair Proteins." University of Toledo Health Science Campus / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=mco1127144634.

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Cattell, Emma. "The role of the human SNM1A gene in the repaire of DNA interstrand crosslinks." Thesis, Oxford Brookes University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493405.

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Shamai, Pamela Win. "Repair of DNA interstrand crosslinks as a mechanism of clinical resistance to platinum drugs in ovarian cancer." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445841/.

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Despite improvements in tumour response and survival following platinum based therapy in ovarian cancer, both intrinsic and acquired drug resistance remain a significant problem. Mechanisms of acquired drug resistance have been studied extensively in ovarian cancer cells in culture following repeated drug exposure however the relevance of these mechanisms to the clinical situation still needs to be clearly defined. Studies in clinical material have been hampered by the unavailability of sensitive methods to detect the critical drug-induced effects in individual cells. Recently, a modification of the single cell gel electrophoresis (comet) assay has been developed which allows for the first time the sensitive detection of DNA interstrand crosslinks in both tumour and normal cells derived directly from clinical material. In this study the role of DNA crosslink repair as a potential mechanism of clinical resistance to platinum drugs has been examined. Methods for isolating ovarian tumour cells and mesothelial (normal) cells from ascitic fluid, and to prepare a single cell suspension from primary ovarian tumour tissue from surgery have been established. Cells treated ex vivo with cisplatin were examined for crosslink formation and repair (unhooking) using the comet assay. No significant difference in the peak level of crosslinking was observed between tumour and mesothelial cells from an individual patient, or between patients either untreated or previously treated with platinum-based therapy. In the majority of tumours from nine untreated patients little or no repair of crosslinks was evident at 24 hours (mean of 13.6% repair) with seven patients showing less than 10% repair. In contrast, in the majority of ten treated patients a high level of repair was observed in tumour cells (mean 46.5%), with greater than 70% repair in four at 24 hours. Increased interstrand crosslink repair was also observed in a cisplatin acquired resistant human ovarian tumour cell line. Differences in gene expression pattern between the sensitive and resistant cell lines were compared using microarray analysis. The expression of a number of genes, including ERCC1, were consistently elevated in the resistant cell line, which was confirmed using RT-PCR.
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Menon, Vijay. "CYTOTOXIC PROPERTIES OF NOVEL PLATINUM COMPOUNDS, BBR3610-DACH AND TRANS-4-NBD IN TUMOR CELLS: CELLULAR EFFECTS OF 1, 2-DACH AND NBD LIGANDS." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3001.

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Platinum-based chemotherapeutics are used for the treatment of a wide range of cancers and a number of attempts have been made toward developing compounds with better cellular stability and similar or enhanced cytotoxicity as compared to their predecessors. The first part of the work reported here focuses on the cellular effects of the metabolically stable dinuclear platinum compound, BBR3610-DACH. Comet assay showed this compound to form interstrand crosslinks, a highly toxic DNA lesion in HCT116 cells, at equimolar concentrations to its parental compound, BBR3610. Cell cycle studies showed that BBR3610-DACH causes G1/S and G2/M cell cycle arrest with S phase depletion, which was p21 dependent and partially p53 dependent in contrast to BBR3610 which showed initial S phase accumulation followed by a classical G2/M arrest. BBR3610-DACH-induced G1/S and G2/M cell cycle arrest interestingly was found to be independent of the DNA damage response mediated via the activation of ATM and ATR kinases. Also, the cell cycle arrest culminated in apoptosis, although apparently through a non-canonical pathway. The second project explores the cellular effects of trans-4-NBD which is a fluorescent derivative of transplatin. Like cisplatin, trans-4-NBD induced interstrand crosslinks in HCT116 cells as detected by the comet assay. Treatment with trans-4-NBD showed a G2/M arrest in HCT116 cells and a transient S phase accumulation in A2780 cells, with a marked increase in p53 and p21 protein levels. A robust apoptotic response is also seen via caspase activation and PARP cleavage in both the cell lines. Finally, the focus is shifted toward the nucleolar targeting platinum complex, TriplatinNC. Confocal studies in TriplatinNC-treated HCT116 and A2780 cells showed disruption of rRNA transcription as an early event followed by a robust G1 cell cycle arrest. Apoptotic induction was observed with the onset of cellular morphological changes and apparent caspase activation which was independent of the p53 status of the cells. Overall, these studies explore novel platinum based compounds that show promising anti-cancer activities by affecting various facets of cellular signaling.
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Kumar, Ambika. "DNA interstrand crosslink repair in Trypanosoma brucei." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/36675.

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Genomes are constantly challenged by agents that promote DNA damage, with interstrand crosslinks (ICLs) representing a particularly dangerous lesion. Ongoing work in the Wilkinson laboratory aimed at identifying novel agents that target Trypanosoma brucei, the causative agent of African trypanosomiasis, identified several prodrugs that once activated form ICLs in this protozoan parasite. To understand the complexity of ICL repair systems that T. brucei employs to resolve such damage, a variety of null mutant lines were generated that lack activities postulated to fix such lesions. Phenotypic screens using various DNA damaging agents revealed that TbMRE11, TbEXO1, TbCSB, TbCHL1, TbFAN1, TbBRCA2 and TbRAD51 all help to resolve ICLs, implicating components of the homologous recombination, nucleotide excision repair and mismatch repair pathways in resolving this form of damage: This approach demonstrated that components of the translesion synthesis pathway (TbREV2 and TbREV3) do not play a significant role in ICL repair. In many organisms, nucleases belonging to the SNM1/PSO2 family play a key and specific role in the repair of ICLs with this property extending to the T. brucei homologue, TbSNM1. To assess whether there is a functional linkage between the DNA repair factors noted above and TbSNM1, a series of double null mutants were constructed and the susceptibility of these lines to ICL inducing agents determined. Identification of their epistatic/non-epistatic interactions revealed that T. brucei expresses at least two ICL repair systems with one pathway involving the concerted activities of TbSNM1/TbCSB/TbEXO1, that we postulate functions to repair ICLs encountered by the transcriptional machinery, while the other is centred upon TbMRE11/TbFAN1/TbEXO1 that may help resolve lesions which cause stalling of DNA replication forks. By unravelling how T. brucei repairs ICLs, specific inhibitors against key components of these pathways could be developed and used in combination with DNA damaging agents to target trypanosomal infections.
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Zhang, Jieqiong. "Mechanism of Replication-Coupled DNA Interstrand Crosslink Repair." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:26718742.

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DNA interstrand crosslinks (ICLs) can be induced by multiple crosslinking agents and are a severe form of DNA damage that prevents strand separation during DNA replication and transcription. Failure to repair endogenous ICLs in S phase is thought to underlie the bone marrow failure syndrome Fanconi anemia, and up-regulation of ICL repair is one of the causes of tumor chemoresistance against widely used cancer drugs. In metazoans, a major pathway of ICL repair is coupled to DNA replication and requires the Fanconi anemia pathway. In most current models, collision of a single DNA replication fork with an ICL is sufficient to initiate repair. In contrast, we show that in Xenopus egg extracts, two DNA replication forks must converge on an ICL to trigger repair. When only one fork reaches the ICL, the replicative DNA helicase, CMG, fails to unload from the stalled fork, and repair is blocked. Arrival of a second fork, even when substantially delayed, rescues repair. We conclude that ICL repair requires a replication-induced X-shaped DNA structure surrounding the lesion, and we speculate how this requirement helps maintain genomic stability in S phase. Next, we focus on how psoralen-induced ICLs are repaired. Although psoralen-ICL repair still requires replication fork convergence, downstream repair events are completely different. Unlike cisplatin-ICLs, which are resolved via incisions in the parental strands with formation of double-strand breaks (DSBs), psoralen-ICLs are resolved via cleavage of a N-glycosyl bond that forms part of the ICL. Unlike cisplatin-ICL repair, psoralen-ICL repair does not require CMG helicase unloading or FANCI-FANCD2. When N-glycosyl bond cleavage is inhibited, the psoralen-ICL is repaired via FANCI-FANCD2-dependent incisions. Our work identifies a novel S phase ICL repair mechanism that is independent of the Fanconi anemia pathway and avoids DSBs.
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Harwood, Eric Alexander. "Chemical synthesis and structural characterization of a nitrous acid interstrand cross-linked duplex DNA /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8702.

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Hain, Karolina Ottilia. "Characterisation of human SLX4/FANCP, a coordinator of DNA repair nucleases." Thesis, University of Dundee, 2012. https://discovery.dundee.ac.uk/en/studentTheses/bf9a5ba3-7cea-4d25-8e8c-aa4cd5de3fae.

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Budding yeast Slx4 binds to the structure-specific DNA repair nucleases Slx1 and Rad1XPF-Rad10ERCC1, and it was reported that Slx4 is essential for DNA flap cleavage by Rad1XPF-Rad10ERCC1 during certain types of DNA repair in yeast. At the outset of this thesis, bioinformatic analyses identified the uncharacterised protein BTBD12 in higher eukaryotes as a putative orthologue of yeast Slx4. In the first results chapter of this thesis, I describe the identification of BTBD12-interacting proteins, including XPF-ERCC1 and SLX1. These findings led me to refer to BTBD12 as human SLX4. I found that SLX4 binds to another structure-specific nuclease MUS81-EME1, and other proteins involved in telomere maintenance and cell cycle progression. The remainder of this chapter describes detailed biochemical analysis of the nuclease activities associated with the SLX4 complex isolated from human cells. Work from this lab and others revealed that depletion of SLX4 from human cells using siRNAs causes defects in the repair of DNA interstrand crosslinks (ICLs). Inherited mutations in humans that reduce the efficiency of ICL repair cause Fanconi anaemia (FA). The cellular sensitivity of SLX4 depleted cells to ICLs prompted me to investigate SLX4 as a candidate FA gene. Dr. Johan de Winter (VU University Medical Center, Amsterdam) and Dr. Detlev Schindler (University of Wurzburg) had identified several patients with unclassified FA that was not caused by mutations in the FA genes known at the time. In the second results I describe characterisation of SLX4, and the SLX4 holo-complex, in cells from some of these FA patients who had bi-allelic SLX4 mutations. In three of the patients SLX4 was expressed at normal levels but was missing part of the first, and all of the second, UBZ-type putative ubiquitin-binding domain. This prompted me to investigate the function of the SLX4 UBZ domains. I found that the first, but not the second, UBZ domain of SLX4 binds to ubiquitin in vitro and targets SLX4 to sites of DNA damage in vivo. Furthermore, the first but not the second SLX4 UBZ domain appears to be required for ICL repair, demonstrating the important of correctly localising SLX4 for DNA repair. In the final chapter, I present preliminary data which suggests that SLX4 is regulated in an unusual manner in during S-phase of the cell cycle, and that SLX4 interacts with the PLK1 kinase in a phosphorylation-dependent manner.
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Books on the topic "DNA interstrand crosslinks"

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Kato, Niyo. The Molecular Mechanism of Replication Independent Repair of DNA Interstrand Crosslinks. [New York, N.Y.?]: [publisher not identified], 2018.

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Book chapters on the topic "DNA interstrand crosslinks"

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Legerski, Randy J., and Christopher Richie. "Mechanisms of Repair of Interstrand Crosslinks in DNA." In Cancer Treatment and Research, 109–28. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1173-1_6.

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Wu, Jian Hong, and Nigel J. Jones. "Assessment of DNA Interstrand Crosslinks Using the Modified Alkaline Comet Assay." In Methods in Molecular Biology, 165–81. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-421-6_9.

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"DNA-Interstrand Crosslinks." In Encyclopedia of Cancer, 1147. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1679.

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James, Ryan C., Marina A. Bellani, Jing Zhang, Jing Huang, Althaf Shaik, Durga Pokharel, Himabindu Gali, Julia Gichimu, Arun K. Thazhathveetil, and Michael M. Seidman. "Visualizing replication fork encounters with DNA interstrand crosslinks." In Methods in Enzymology, 53–75. Elsevier, 2021. http://dx.doi.org/10.1016/bs.mie.2021.08.015.

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Aqeel, Amna, Javaria Zafar, Naureen Ehsan, Qurat-Ul-Ain, Mahnoor Tariq, and Abdul Hannan. "Interstrand Crosslink Repair: New Horizons of DNA Damage Repair." In DNA - Damages and Repair Mechanisms. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97551.

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Abstract:
Since the dawn of civilization, living organisms are unceasingly exposed to myriads of DNA damaging agents that can temper the ailments and negatively influence the well-being. DNA interstrand crosslinks (ICLs) are spawned by various endogenous and chemotherapeutic agents, thus posing a somber menace to genome solidity and cell endurance. However, the robust techniques of damage repair including Fanconi anemia pathway, translesion synthesis, nucleotide excision and homologous recombination repair faithfully protect the DNA by removing or tolerating damage to ensure the overall survival. Aberrations in such repair mechanisms adverse the pathophysiological states of several hereditary disorders i.e. Fanconi Anemia, xeroderma pigmentosum, cerebro-oculo-facio-skeletal syndrome and cockayne syndrome etc. Although, the recognition of ICL lesions during interphase have opened the new horizons of research in the field of genetics but still the detailed analysis of conditions in which repair should occur is largely elusive.
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G., Tsvetan, Marie-Eve Dextraze, and Darel J. "DNA Radiosensitization: The Search for Repair Refractive Lesions Including Double Strand Breaks and Interstrand Crosslinks." In Selected Topics in DNA Repair. InTech, 2011. http://dx.doi.org/10.5772/23886.

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Blackburn, G. Michael. "Covalent Modifications of Nucleic Acids and Their Repair." In Nucleic Acids in Chemistry and Biology, 421–76. The Royal Society of Chemistry, 2022. http://dx.doi.org/10.1039/9781837671328-00421.

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The main DNA repair processes in humans involve direct repair (DR), base excision repair (BER), nucleotide excision repair (NER), interstrand crosslink repair (ICR) and base mismatch repair (BMR), as have been described in other chapters, in addition to homologous recombination (HR) and non-homologous end-joining (NHEJ). Studies on human repair systems have advanced rapidly, especially into UV damage, and recent studies have shown that human DNA polymerase η (Pol η) modulates susceptibility to skin cancer by promoting DNA synthesis past sunlight-induced cyclobutane pyrimidine dimers that have escaped nucleotide excision repair (NER). This bypass has low fidelity, meaning that in normal people, and especially in individuals with xeroderma pigmentosum who accumulate photodimers because they are NER-defective, the errors made by Pol η during dimer bypass may contribute to mutagenesis and to skin cancer. The depth of understanding that is now being achieved on the covalent modification of nucleic acids is awesome, both for adventitious (exogenous) and evolutionarily evolved (endogenous) modification. It is uncovering new questions and posing new challenges. A clear manifestation of this is the range of targets that have now been explored using cutting-edge methodologies that were unimaginable in earlier years. Above all, the advances made have brought us face-to-face with the amazing complexity of repair systems for our nucleic acids that supremely have made viable life on our planet.
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O’Rourke, J. J., and A. J. Deans. "The FANCA to FANCZ of DNA interstrand crosslink repair: Lessons from Fanconi anemia." In DNA Repair in Cancer Therapy, 353–81. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-803582-5.00012-7.

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Conference papers on the topic "DNA interstrand crosslinks"

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Zhao, Li-Jiao, Ru-Gang Zhong, and Yan Zhen. "ONIOM Study on the DNA Interstrand Crosslinks by the Chloroethylnitrosoureas." In 2007 IEEE/ICME International Conference on Complex Medical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/iccme.2007.4381733.

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Weng, Mao Wen, Yi Zheng, Vijay P. Jasti, Elise Champeil, Maria Tomasz, Yin sheng Wang, Ashis K. Basu, and Moon Shong Tang. "Abstract 1967: UvrABC excision of interstrand crosslink mitomycin C-DNA lesion induces double-stranded DNA breaks." 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.am10-1967.

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Zhang, Pan, Utz Herbig, and Muriel W. Lambert. "Abstract 2121: Nonerythroid alpha spectrin prevents telomere fragility after DNA interstrand crosslink damage." 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.am2012-2121.

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Ren, Ting, Li-Jiao Zhao, Wei Tang, Da-Wei Zheng, and Ru-Gang Zhong. "Quantitative Analysis of DNA Interstrand Crosslink Induced by Chloroethylnitrosoureas with Real-Time Fluorometric Assay." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5518256.

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Lambert, Muriel W., Deepa Sridharan, and Pan Zhang. "Abstract 3018: FANCF, a Fanconi anemia core protein, functions outside of monoubiquitinating FANCD2 in DNA interstrand crosslink repair." 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.am2015-3018.

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Valentine, Helen, Emily Dixon, John A. Hartley, and Konstantinos Kiakos. "Abstract C51: Chemosensitisation to cisplatin by STAT3 inhibitors is mediated through the inhibition of DNA interstrand crosslink unhooking." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-c51.

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Lambert, Muriel W., Deepa Sridharan, and Pan Zhang. "Abstract 2380: Separate but important roles of αSpII and FANCD2 in the FA pathway after DNA interstrand crosslink damage." 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.am2014-2380.

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Zhang, Pan, and Muriel W. Lambert. "Abstract 621: XPF, a DNA interstrand crosslink (ICL) repair protein, localizes to telomeres after DNA ICL damage in normal but not Fanconi anemia cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-621.

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Lambert, Muriel W., Deepa Sridharan, and Pan Zhang. "Abstract 2758: FANCF, a Fanconi anemia core complex protein involved in monoubiquitination of FANCD2, also has a role with nuclear alpha spectrin in DNA interstrand crosslink repair." 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.am2016-2758.

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