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Journal articles on the topic 'DNA interstrand crosslinks'

Author: Grafiati

Published: 6 September 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Mladenova, Veronika, and George Russev. "Enhanced repair of DNA interstrand crosslinks in S phase." FEBS Letters 580, no. 6 (February 17, 2006): 1631–34. http://dx.doi.org/10.1016/j.febslet.2006.02.009.

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12

Jones, Martin, and Ann Rose. "A DOG’s View of Fanconi Anemia: Insights fromC. elegans." Anemia 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/323721.

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C. elegansprovides an excellent model system for the study of the Fanconi Anemia (FA), one of the hallmarks of which is sensitivity to interstrand crosslinking agents. Central to our understanding of FA has been the investigation of DOG-1, the functional ortholog of the deadbox helicaseFANCJ. Here we review the current understanding of the unique role of DOG-1 in maintaining stability of G-rich DNA inC. elegansand explore the question of why DOG-1 animals are crosslink sensitive. We propose a dynamic model in which noncovalently linked G-rich structures form and un-form in the presence of DOG-1. When DOG-1 is absent but crosslinking agents are present the G-rich structures are readily covalently crosslinked, resulting in increased crosslinks formation and thus giving increased crosslink sensitivity. In this interpretation DOG-1 is neither upstream nor downstream in the FA pathway, but works alongside it to limit the availability of crosslink substrates. This model reconciles the crosslink sensitivity observed in the absence of DOG-1 function with its unique role in maintaining G-Rich DNA and will help to formulate experiments to test this hypothesis.

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13

Woźniak, Katarzyna, and Janusz Błasiak. "Recognition and repair of DNA-cisplatin adducts." Acta Biochimica Polonica 49, no. 3 (September 30, 2002): 583–96. http://dx.doi.org/10.18388/abp.2002_3768.

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Anticancer activity of cisplatin (cis-diamminedichloroplatinum) is believed to result from its interaction with DNA. The drug reacts with nucleophilic sites in DNA forming monoadducts as well as intra- and interstrand crosslinks. DNA-cisplatin adducts are specifically recognized by several proteins. They can be divided into two classes. One constitutes proteins which recognize DNA damage as an initial step of the nucleotide excision and mismatch repair pathways. The other class contains proteins stabilizing cellular DNA-protein and protein-protein complexes, including non-histone proteins from the HMG (high-mobility-group) family. They specifically recognize 1,2-interstrand d(GpG) and d(ApG) crosslinks of DNA-cisplatin adducts and inhibit their repair. Many HMG-domain proteins can function as transcription factors, e.g. UBF, an RNA polymerase I transcription factor, the mammalian testis-determining factor SRY and the human mitochondrial transcription factor mtTFA. Moreover, it seems that some proteins, which probably recognize DNA-cisplatin adducts non-specifically, e.g. actin and other nuclear matrix proteins, can disturb the structural and functional organization of the nucleus and whole cell. The formation of complexes between DNA and proteins in the presence of cisplatin and the changes in the cell architecture may account for the drug cytotoxicity.

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14

Koba, Marcin, and Jerzy Konopa. "Interactions of antitumor triazoloacridinones with DNA." Acta Biochimica Polonica 54, no. 2 (April 19, 2007): 297–306. http://dx.doi.org/10.18388/abp.2007_3250.

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Triazoloacridinones (TA) are a new group of potent antitumor compounds, from which the most active derivative, C-1305, has been selected for extended preclinical trials. This study investigated the mechanism of TA binding to DNA. Initially, for selected six TA derivatives differing in chemical structures as well as cytotoxicity and antitumor activity, the capability of noncovalent DNA binding was analyzed. We showed that all triazoloacridinones studied stabilized the DNA duplex at a low-concentration buffer but not at a salt concentration corresponding to that in cells. DNA viscometric studies suggested that intercalation to DNA did not play a major role in the mechanism of the cytotoxic action of TA. Studies involving cultured cells revealed that triazoloacridinone C-1305 after previous metabolic activation induced the formation of interstrand crosslinks in DNA of some tumor and fibroblast cells in a dose dependent manner. However, the detection of crosslink formation was possible only when the activity of topoisomerase II in cells was lowered. Furthermore, it was impossible to validate the relevance of the ability to crosslink DNA to biological activity of TA derivatives.

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15

Vos, J. M., and E. L. Wauthier. "Differential introduction of DNA damage and repair in mammalian genes transcribed by RNA polymerases I and II." Molecular and Cellular Biology 11, no. 4 (April 1991): 2245–52. http://dx.doi.org/10.1128/mcb.11.4.2245-2252.1991.

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We have developed a general quantitative method for comparing the levels of drug-induced DNA crosslinking in specific mammalian genes. We observed a dramatic difference between the efficiency of the removal of both psoralen monoadducts and interstrand crosslinks from the rRNA genes and the efficiency of their removal from the dihydrofolate reductase (DHFR) gene in cultured human and hamster cells. While 90% of the interstand crosslinks were removed from the human DHFR gene in 48 h, less than 25% repair occurred in the rRNA genes. Similarly, in Chinese hamster ovary cells, 85% repair of interstrand crosslinks occurred within 8 h in the DHFR gene versus only 20% repair in the rRNA genes. The preferential repair of the DHFR gene relative to that of the rRNA genes was also observed for psoralen monoadducts in cells from both mammalian species. In human-mouse hybrid cells, the active mouse rRNA genes were five times more susceptible to psoralen modification than are the silent rRNA human genes, but adduct removal was similarly inefficient for both classes. We conclude that the repair of chemical damage such as psoralen photoadducts in an expressed mammalian gene may depend upon the class of transcription to which it belongs.

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16

Vos, J. M., and E. L. Wauthier. "Differential introduction of DNA damage and repair in mammalian genes transcribed by RNA polymerases I and II." Molecular and Cellular Biology 11, no. 4 (April 1991): 2245–52. http://dx.doi.org/10.1128/mcb.11.4.2245.

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We have developed a general quantitative method for comparing the levels of drug-induced DNA crosslinking in specific mammalian genes. We observed a dramatic difference between the efficiency of the removal of both psoralen monoadducts and interstrand crosslinks from the rRNA genes and the efficiency of their removal from the dihydrofolate reductase (DHFR) gene in cultured human and hamster cells. While 90% of the interstand crosslinks were removed from the human DHFR gene in 48 h, less than 25% repair occurred in the rRNA genes. Similarly, in Chinese hamster ovary cells, 85% repair of interstrand crosslinks occurred within 8 h in the DHFR gene versus only 20% repair in the rRNA genes. The preferential repair of the DHFR gene relative to that of the rRNA genes was also observed for psoralen monoadducts in cells from both mammalian species. In human-mouse hybrid cells, the active mouse rRNA genes were five times more susceptible to psoralen modification than are the silent rRNA human genes, but adduct removal was similarly inefficient for both classes. We conclude that the repair of chemical damage such as psoralen photoadducts in an expressed mammalian gene may depend upon the class of transcription to which it belongs.

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17

Huang, Jing, Shuo Liu, Marina A. Bellani, Arun Kalliat Thazhathveetil, Chen Ling, Johan P. de Winter, Yinsheng Wang, Weidong Wang, and Michael M. Seidman. "The DNA Translocase FANCM/MHF Promotes Replication Traverse of DNA Interstrand Crosslinks." Molecular Cell 52, no. 3 (November 2013): 434–46. http://dx.doi.org/10.1016/j.molcel.2013.09.021.

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18

Kothandapani, Anbarasi, and Steve M. Patrick. "Evidence for base excision repair processing of DNA interstrand crosslinks." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 743-744 (March 2013): 44–52. http://dx.doi.org/10.1016/j.mrfmmm.2012.11.007.

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19

McHugh, Peter J., Victoria J. Spanswick, and John A. Hartley. "Repair of DNA interstrand crosslinks: molecular mechanisms and clinical relevance." Lancet Oncology 2, no. 8 (August 2001): 483–90. http://dx.doi.org/10.1016/s1470-2045(01)00454-5.

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20

Lopez-Martinez, David, Chih-Chao Liang, and Martin A. Cohn. "Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway." Cellular and Molecular Life Sciences 73, no. 16 (April 19, 2016): 3097–114. http://dx.doi.org/10.1007/s00018-016-2218-x.

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21

Socha, Anna, Di Yang, Alicja Bulsiewicz, Kelvin Yaprianto, Marian Kupculak, Chih-Chao Liang, Andreas Hadjicharalambous, Ronghu Wu, Steven P. Gygi, and Martin A. Cohn. "WRNIP1 Is Recruited to DNA Interstrand Crosslinks and Promotes Repair." Cell Reports 32, no. 1 (July 2020): 107850. http://dx.doi.org/10.1016/j.celrep.2020.107850.

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22

McNeill, Daniel R., Manikandan Paramasivam, Jakita Baldwin, Jing Huang, Vaddadi N. Vyjayanti, Michael M. Seidman, and David M. Wilson. "NEIL1 Responds and Binds to Psoralen-induced DNA Interstrand Crosslinks." Journal of Biological Chemistry 288, no. 18 (March 18, 2013): 12426–36. http://dx.doi.org/10.1074/jbc.m113.456087.

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23

Koba, Marcin, Alicja Szostek, and Jerzy Konopa. "Limitation of usage of PicoGreen dye in quantitative assays of double-stranded DNA in the presence of intercalating compounds." Acta Biochimica Polonica 54, no. 4 (December 10, 2007): 883–86. http://dx.doi.org/10.18388/abp.2007_3193.

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PicoGreen is a very sensitive fluorescent dye for quantitative assays of double-stranded DNA (dsDNA) in solution and is used in several analytical protocols in which sensitive and precise DNA detection is needed, also for examination of drug-DNA interactions. The data shown in this paper indicate that compounds intercalating to DNA influence the applicability of PicoGreen dye for quantitative measurements of dsDNA, and for this reason PicoGreen dye is not suitable for examination of drug-DNA interactions, especially interstrand DNA crosslinks.

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24

Singh, Jatinder, Laura C. Bridgewater, and Steven R. Patierno. "Differential Sensitivity of Chromium-Mediated DNA Interstrand Crosslinks and DNA-Protein Crosslinks to Disruption by Alkali and EDTA." Toxicological Sciences 45, no. 1 (1998): 72–76. http://dx.doi.org/10.1093/toxsci/45.1.72.

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25

Singh, J. "Differential Sensitivity of Chromium-Mediated DNA Interstrand Crosslinks and DNA–Protein Crosslinks to Disruption by Alkali and EDTA." Toxicological Sciences 45, no. 1 (September 1998): 72–76. http://dx.doi.org/10.1006/toxs.1998.2489.

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26

Taylor, Sarah J., Mark J. Arends, and Simon P. Langdon. "Inhibitors of the Fanconi anaemia pathway as potential antitumour agents for ovarian cancer." Exploration of Targeted Anti-tumor Therapy 1, no. 1 (February 29, 2020): 26–52. http://dx.doi.org/10.37349/etat.2020.00003.

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The Fanconi anaemia (FA) pathway is an important mechanism for cellular DNA damage repair, which functions to remove toxic DNA interstrand crosslinks. This is particularly relevant in the context of ovarian and other cancers which rely extensively on interstrand cross-link generating platinum chemotherapy as standard of care treatment. These cancers often respond well to initial treatment, but reoccur with resistant disease and upregulation of DNA damage repair pathways. The FA pathway is therefore of great interest as a target for therapies that aim to improve the efficacy of platinum chemotherapies, and reverse tumour resistance to these. In this review, we discuss recent advances in understanding the mechanism of interstrand cross-link repair by the FA pathway, and the potential of the component parts as targets for therapeutic agents. We then focus on the current state of play of inhibitor development, covering both the characterisation of broad spectrum inhibitors and high throughput screening approaches to identify novel small molecule inhibitors. We also consider synthetic lethality between the FA pathway and other DNA damage repair pathways as a therapeutic approach.

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27

Shugalii, A. V. "The quantitative estimation of induced DNA interstrand crosslinks in nanomoles interval." Biopolymers and Cell 12, no. 5 (September 20, 1996): 34–37. http://dx.doi.org/10.7124/bc.000446.

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28

Liu, Y., R. S. Nairn, and K. M. Vasquez. "Processing of triplex-directed psoralen DNA interstrand crosslinks by recombination mechanisms." Nucleic Acids Research 36, no. 14 (June 27, 2008): 4680–88. http://dx.doi.org/10.1093/nar/gkn438.

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29

Perrin, L. C., C. Cullinane, D. R. Phillips, and K. i. Kimura. "Barminomycin forms GC-specific adducts and virtual interstrand crosslinks with DNA." Nucleic Acids Research 27, no. 8 (April 1, 1999): 1781–87. http://dx.doi.org/10.1093/nar/27.8.1781.

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30

Ho, The Vinh, Angelo Guainazzi, Semsi Burak Derkunt, Milica Enoiu, and Orlando D. Schärer. "Structure-dependent bypass of DNA interstrand crosslinks by translesion synthesis polymerases." Nucleic Acids Research 39, no. 17 (June 11, 2011): 7455–64. http://dx.doi.org/10.1093/nar/gkr448.

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31

Guo, Chuanxin, Sefan Asamitsu, Gengo Kashiwazaki, Shinsuke Sato, Toshikazu Bando, and Hiroshi Sugiyama. "DNA Interstrand Crosslinks by H-pin Polyamide (S )-seco -CBI Conjugates." ChemBioChem 18, no. 2 (November 30, 2016): 166–70. http://dx.doi.org/10.1002/cbic.201600425.

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32

Sun, Huabing, Heli Fan, Hyeyoung Eom, and Xiaohua Peng. "Coumarin-Induced DNA Ligation, Rearrangement to DNA Interstrand Crosslinks, and Photorelease of Coumarin Moiety." ChemBioChem 17, no. 21 (September 21, 2016): 2046–53. http://dx.doi.org/10.1002/cbic.201600240.

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33

Schärer, Orlando D. "DNA Interstrand Crosslinks: Natural and Drug-Induced DNA Adducts that Induce Unique Cellular Responses." ChemBioChem 6, no. 1 (January 7, 2005): 27–32. http://dx.doi.org/10.1002/cbic.200400287.

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34

Rohleder, Florian, Jing Huang, Yutong Xue, Jochen Kuper, Adam Round, Michael Seidman, Weidong Wang, and Caroline Kisker. "FANCM interacts with PCNA to promote replication traverse of DNA interstrand crosslinks." Nucleic Acids Research 44, no. 7 (January 28, 2016): 3219–32. http://dx.doi.org/10.1093/nar/gkw037.

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35

Zheng, Xiaotong, Xuechai Chen, Linna Zhao, Minjun Guo, and Rugang Zhong. "Assessment of DNA interstrand crosslinks in NIH/3T3 cells induced by Chloroethylnitrosoureas." BIO Web of Conferences 8 (2017): 01019. http://dx.doi.org/10.1051/bioconf/20170801019.

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36

Pumuye, Paul P., Benny J. Evison, Shyam K. Konda, J. Grant Collins, Celine Kelso, Jelena Medan, Brad E. Sleebs, Keith Watson, Don R. Phillips, and Suzanne M. Cutts. "Formaldehyde-activated WEHI-150 induces DNA interstrand crosslinks with unique structural features." Bioorganic & Medicinal Chemistry 28, no. 3 (February 2020): 115260. http://dx.doi.org/10.1016/j.bmc.2019.115260.

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37

Atanassov, Boyko, Anastas Gospodinov, Ivaylo Stoimenov, Emil Mladenov, George Russev, Irina Tsaneva, and Boyka Anachkova. "Repair of DNA interstrand crosslinks may take place at the nuclear matrix." Journal of Cellular Biochemistry 96, no. 1 (2005): 126–36. http://dx.doi.org/10.1002/jcb.20518.

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38

Kato, Niyo, Yoshitaka Kawasoe, Hannah Williams, Elena Coates, Upasana Roy, Yuqian Shi, Lorena S. Beese, et al. "Sensing and Processing of DNA Interstrand Crosslinks by the Mismatch Repair Pathway." Cell Reports 21, no. 5 (October 2017): 1375–85. http://dx.doi.org/10.1016/j.celrep.2017.10.032.

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39

Ishiai, Masamichi. "Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination." Genes 12, no. 11 (November 5, 2021): 1763. http://dx.doi.org/10.3390/genes12111763.

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The Fanconi anemia (FA) DNA repair pathway coordinates a faithful repair mechanism for stalled DNA replication forks caused by factors such as DNA interstrand crosslinks (ICLs) or replication stress. An important role of FA pathway activation is initiated by monoubiquitination of FANCD2 and its binding partner of FANCI, which is regulated by the ATM-related kinase, ATR. Therefore, regulation of the FA pathway is a good example of the contribution of ATR to genome stability. In this short review, we summarize the knowledge accumulated over the years regarding how the FA pathway is activated via phosphorylation and monoubiquitination.

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40

Lambert, W. Clark, and Monique M. Brown. "A Potential Novel Therapeutic Approach for Fanconi Anemia." Blood 112, no. 11 (November 16, 2008): 1040. http://dx.doi.org/10.1182/blood.v112.11.1040.1040.

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Abstract Lymphoblastoid cells from normal subjects and from patients with the bone marrow failure and cancer prone inherited disease, Fanconi anemia (FA) were treated in culture with psoralen plus ultraviolet A radiation (PUVA) in a scheme shown to produce interstrand crosslinks in cellular DNA. Hypersensitivity to DNA interstrand crosslinks, with associated increased clastogenicity, is considered to be a diagnostic hallmark of the disease. Following this cells were treated with hydroxyurea, 5 fluorouracil, or high dose thymidine for 24 hours. Clastogenicity and cytotoxicity, measured as trypan blue exclusion, were then found to be markedly increased in FA cells but not in FA cells subsequently treated with any of these other agents. Similar results were also found when all drugs were removed after these treatments and the cells cultured for 10 days without any drug in colony forming ability assays. We propose that the mechanism is related to decrease in the rate of DNA synthesis, which we have shown occurs in normal but not FA cells following PUVA, and which is also produced by these other drugs in the concentrations used here. Hydroxyurea has been used for many years as a safe and effective treatment for sickle cell anemia. It is now proposed as a possible treatment for Fanconi anemia to delay or even prevent development of bone marrow failure and/or other complications, including leukemogenesis and carcinogenesis, with or without prior bone marrow transplantation.

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41

Hodson, Charlotte, and Helen Walden. "Towards a Molecular Understanding of the Fanconi Anemia Core Complex." Anemia 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/926787.

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Fanconi Anemia (FA) is a genetic disorder characterized by the inability of patient cells to repair DNA damage caused by interstrand crosslinking agents. There are currently 14 verified FA genes, where mutation of any single gene prevents repair of DNA interstrand crosslinks (ICLs). The accumulation of ICL damage results in genome instability and patients having a high predisposition to cancers. The key event of the FA pathway is dependent on an eight-protein core complex (CC), required for the monoubiquitination of each member of the FANCD2-FANCI complex. Interestingly, the majority of patient mutations reside in the CC. The molecular mechanisms underlying the requirement for such a large complex to carry out a monoubiquitination event remain a mystery. This paper documents the extensive efforts of researchers so far to understand the molecular roles of the CC proteins with regard to its main function in the FA pathway, the monoubiquitination of FANCD2 and FANCI.

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Guohui, Sun, Zhao Lijiao, and Zhong Rugang. "The Induction and Repair of DNA Interstrand Crosslinks and Implications in Cancer Chemotherapy." Anti-Cancer Agents in Medicinal Chemistry 16, no. 2 (November 17, 2015): 221–46. http://dx.doi.org/10.2174/1871520615666150824160421.

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Sasaki, M. S., M. Takata, E. Sonoda, A. Tachibana, and S. Takeda. "Recombination repair pathway in the maintenance of chromosomal integrity against DNA interstrand crosslinks." Cytogenetic and Genome Research 104, no. 1-4 (2004): 28–34. http://dx.doi.org/10.1159/000077463.

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Christensen, L. A., H. Wang, B. Van Houten, and K. M. Vasquez. "Efficient processing of TFO-directed psoralen DNA interstrand crosslinks by the UvrABC nuclease." Nucleic Acids Research 36, no. 22 (November 7, 2008): 7136–45. http://dx.doi.org/10.1093/nar/gkn880.

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45

Eder, J. P., B. A. Teicher, S. A. Holden, K. N. Cathcart, and L. E. Schnipper. "Novobiocin enhances alkylating agent cytotoxicity and DNA interstrand crosslinks in a murine model." Journal of Clinical Investigation 79, no. 5 (May 1, 1987): 1524–28. http://dx.doi.org/10.1172/jci112983.

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Standeven, Andrew M., and Karen E. Wetterhahn. "Chromium(VI) Toxicity: Uptake, Reduction, and DNA Damage." Journal of the American College of Toxicology 8, no. 7 (December 1989): 1275–83. http://dx.doi.org/10.3109/10915818909009118.

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Much recent data supports the “uptake-reduction” model explaining the carcinogenicity of chromium(VI) compounds and the lack of carcinogenicity of chromium(III) com pounds. Cr(VI) readily enters cells by diffusion through a nonspecific anion channel, whereas cells are relatively impermeable to Cr(III). Glutathione appears to facilitate Cr(VI) uptake by reducing Cr(VI) to Cr(III) after it enters the cell, presumably keeping intracellular Cr(VI) concentration low and allowing for further Cr(VI) uptake. Some other nonenzymatic factors, for example, ascorbate and riboflavin, as well as enzymes, such as cytochrome P-450, DT-diaphorase, and the mitochondrial electron transport chain complexes, are capable of reducing Cr(VI) in vitro, but their contribution in vivo is not clear. Cr(VI), once reduced intracellularly, produces various forms of DNA damage including DNA interstrand crosslinks, DNA-protein crosslinks, DNA strand breaks, and Cr-DNA adducts. The pathway of Cr(VI) metabolism in different tissues appears to influence the type of “reactive intermediates” produced, for example, Cr(V) and radical species, and thus the nature and extent of DNA damage. This DNA damage presumably accounts for observed functional changes in DNA replication and transcription which may be crucial to the carcinogenicity of chromium(VI) compounds.

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Li, Tonia T., and Karen M. Vasquez. "Multi-Faceted Roles of ERCC1-XPF Nuclease in Processing Non-B DNA Structures." DNA 2, no. 4 (October 11, 2022): 231–47. http://dx.doi.org/10.3390/dna2040017.

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Genetic instability can result from increases in DNA damage and/or alterations in DNA repair proteins and can contribute to disease development. Both exogenous and endogenous sources of DNA damage and/or alterations in DNA structure (e.g., non-B DNA) can impact genome stability. Multiple repair mechanisms exist to counteract DNA damage. One key DNA repair protein complex is ERCC1-XPF, a structure-specific endonuclease that participates in a variety of DNA repair processes. ERCC1-XPF is involved in nucleotide excision repair (NER), repair of DNA interstrand crosslinks (ICLs), and DNA double-strand break (DSB) repair via homologous recombination. In addition, ERCC1-XPF contributes to the processing of various alternative (i.e., non-B) DNA structures. This review will focus on the processing of alternative DNA structures by ERCC1-XPF.

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Woynarowski, Jan M., William G. Chapman, Cheryl Napier, and Maryanne C. S. Herzig. "Induction of AT-specific DNA-interstrand crosslinks by bizelesin in genomic and simian virus 40 DNA." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1444, no. 2 (February 1999): 201–17. http://dx.doi.org/10.1016/s0167-4781(99)00002-0.

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Abdullah, Ummi B., Joanna F. McGouran, Sanja Brolih, Denis Ptchelkine, Afaf H. El‐Sagheer, Tom Brown, and Peter J. McHugh. "RPA activates the XPF ‐ ERCC 1 endonuclease to initiate processing of DNA interstrand crosslinks." EMBO Journal 36, no. 14 (June 12, 2017): 2047–60. http://dx.doi.org/10.15252/embj.201796664.

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Wu, Qi, Laura A. Christensen, Randy J. Legerski, and Karen M. Vasquez. "Mismatch repair participates in error‐free processing of DNA interstrand crosslinks in human cells." EMBO reports 6, no. 6 (June 2005): 551–57. http://dx.doi.org/10.1038/sj.embor.7400418.

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