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Artykuły w czasopismach na temat „DNA damage”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 31 lipca 2024

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1

Chakarov, Stoyan, Rumena Petkova, George Russev i Nikolai Zhelev. "DNA damage and mutation. Types of DNA damage". BioDiscovery, nr 11 (23.02.2014): 1. http://dx.doi.org/10.7750/biodiscovery.2014.11.1.

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Yeung, ManTek, i Daniel Durocher. "Engineering a DNA damage response without DNA damage". Genome Biology 9, nr 7 (2008): 227. http://dx.doi.org/10.1186/gb-2008-9-7-227.

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3

Bagchi, Srilata, i Pradip Raychaudhuri. "Damaged-DNA Binding Protein-2 Drives Apoptosis Following DNA Damage". Cell Division 5, nr 1 (2010): 3. http://dx.doi.org/10.1186/1747-1028-5-3.

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4

Wallace, Bret D., i R. Scott Williams. "Ribonucleotide triggered DNA damage and RNA-DNA damage responses". RNA Biology 11, nr 11 (2.11.2014): 1340–46. http://dx.doi.org/10.4161/15476286.2014.992283.

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5

Nawy, Tal. "DNA variants or DNA damage?" Nature Methods 14, nr 4 (kwiecień 2017): 341. http://dx.doi.org/10.1038/nmeth.4254.

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6

Bush, Stephen P., Peter E. Hart i Eric M. Russell. "Investigating DNA Damage". American Biology Teacher 68, nr 5 (1.05.2006): 280–84. http://dx.doi.org/10.2307/4451989.

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7

Oksenych, Valentyn, i Denis E. Kainov. "DNA Damage Response". Biomolecules 11, nr 1 (19.01.2021): 123. http://dx.doi.org/10.3390/biom11010123.

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Bush, Stephen P., Peter E. Hart i Eric M. Russell. "Investigating DNA Damage". American Biology Teacher 68, nr 5 (2006): 280. http://dx.doi.org/10.1894/0038-4909(2006)68[280:idd]2.0.co;2.

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9

Skrypnyk, N. V., i O. O. Maslova. "Oxidative DNA damage". Biopolymers and Cell 23, nr 3 (20.05.2007): 202–14. http://dx.doi.org/10.7124/bc.000766.

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10

Giglia-Mari, G., A. Zotter i W. Vermeulen. "DNA Damage Response". Cold Spring Harbor Perspectives in Biology 3, nr 1 (27.10.2010): a000745. http://dx.doi.org/10.1101/cshperspect.a000745.

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11

Dabney, J., M. Meyer i S. Paabo. "Ancient DNA Damage". Cold Spring Harbor Perspectives in Biology 5, nr 7 (31.05.2013): a012567. http://dx.doi.org/10.1101/cshperspect.a012567.

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12

Lou, Kai-Jye. "DNA damage control". Science-Business eXchange 1, nr 38 (październik 2008): 916. http://dx.doi.org/10.1038/scibx.2008.916.

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13

Rossi, Harald H. "Interactive DNA Damage". Radiation Research 140, nr 2 (listopad 1994): 295. http://dx.doi.org/10.2307/3578915.

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14

Cadet, Jean, i Michael Weinfeld. "DETECTING DNA DAMAGE". Analytical Chemistry 65, nr 15 (sierpień 1993): 675A—682A. http://dx.doi.org/10.1021/ac00063a724.

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15

Alderton, Gemma K. "Secreted DNA damage?" Nature Reviews Cancer 13, nr 2 (24.01.2013): 77. http://dx.doi.org/10.1038/nrc3455.

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16

Coon, Elizabeth A., i Eduardo E. Benarroch. "DNA damage response". Neurology 90, nr 8 (19.01.2018): 367–76. http://dx.doi.org/10.1212/wnl.0000000000004989.

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17

Beshay, Victor E., i Orhan Bukulmez. "Sperm DNA damage". Current Opinion in Obstetrics and Gynecology 24, nr 3 (czerwiec 2012): 172–79. http://dx.doi.org/10.1097/gco.0b013e32835211b5.

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18

Friedman, Danielle. "DNA Damage Pathways". JAMA 304, nr 15 (20.10.2010): 1645. http://dx.doi.org/10.1001/jama.2010.1346.

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19

Branzei, Dana, i Ivan Psakhye. "DNA damage tolerance". Current Opinion in Cell Biology 40 (czerwiec 2016): 137–44. http://dx.doi.org/10.1016/j.ceb.2016.03.015.

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20

Pereira, Cristiana, Rosa Coelho, Daniela Grácio, Cláudia Dias, Marco Silva, Armando Peixoto, Pedro Lopes i in. "DNA Damage and Oxidative DNA Damage in Inflammatory Bowel Disease". Journal of Crohn's and Colitis 10, nr 11 (19.04.2016): 1316–23. http://dx.doi.org/10.1093/ecco-jcc/jjw088.

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21

Babazadeh, Zahra, Shahnaz Razavi, Marziyeh Tavalaee, Mohammad Reza Deemeh, Maryam Shahidi i Mohammad Hossein Nasr-Esfahani. "Sperm DNA damage and its relation with leukocyte DNA damage". Reproductive Toxicology 29, nr 1 (styczeń 2010): 120–24. http://dx.doi.org/10.1016/j.reprotox.2009.09.002.

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22

Popp, Kohl, Naumann, Flach, Brendel, Kleiner, Weiss i in. "DNA Damage and DNA Damage Response in Chronic Myeloid Leukemia". International Journal of Molecular Sciences 21, nr 4 (11.02.2020): 1177. http://dx.doi.org/10.3390/ijms21041177.

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DNA damage and alterations in the DNA damage response (DDR) are critical sources of genetic instability that might be involved in BCR-ABL1 kinase-mediated blastic transformation of chronic myeloid leukemia (CML). Here, increased DNA damage is detected by γH2AX foci analysis in peripheral blood mononuclear cells (PBMCs) of de novo untreated chronic phase (CP)-CML patients (n = 5; 2.5 γH2AX foci per PBMC ± 0.5) and blast phase (BP)-CML patients (n = 3; 4.4 γH2AX foci per PBMC ± 0.7) as well as CP-CML patients with loss of major molecular response (MMR) (n = 5; 1.8 γH2AX foci per PBMC ± 0.4) when compared to DNA damage in PBMC of healthy donors (n = 8; 1.0 γH2AX foci per PBMC ± 0.1) and CP-CML patients in deep molecular response or MMR (n = 26; 1.0 γH2AX foci per PBMC ± 0.1). Progressive activation of erroneous non-homologous end joining (NHEJ) repair mechanisms during blastic transformation in CML is indicated by abundant co-localization of γH2AX/53BP1 foci, while a decline of the DDR is suggested by defective expression of (p-)ATM and (p-)CHK2. In summary, our data provide evidence for the accumulation of DNA damage in the course of CML and suggest ongoing DNA damage, erroneous NHEJ repair mechanisms, and alterations in the DDR as critical mediators of blastic transformation in CML.

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23

Bouziane, M., F. Miao, N. Ye, G. Holmquist, G. Chyzak i T. R. O'Connor. "Repair of DNA alkylation damage." Acta Biochimica Polonica 45, nr 1 (31.03.1998): 191–202. http://dx.doi.org/10.18388/abp.1998_4333.

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Alkylation damage of DNA is one of the major types of insults which cells must repair to remain viable. One way alkylation damaged ring nitrogens are repaired is via the Base Excision Repair (BER) pathway. Examination of mutants in both BER and Nucleotide Excision Repair show that there is actually an overlap of repair by these two pathways for the removal of cytotoxic lesions in Escherichia coli. The enzymes removing damaged bases in the first step in the BER pathway are DNA glycosylases. The coding sequences for a number of methylpurine-DNA glycosylases (MPG proteins) were cloned, and a comparison of the amino-acid sequences shows that there are some similarities between these proteins, but nonetheless, compared to other DNA glycosylases, MPG proteins are more divergent. MPG proteins have been purified to homogeneity and used to identify their substrates ranging from methylating agents to deamination products to oxidatively damaged bases. The ligation-mediated polymerase chain reaction has been used to study the formation of alkylation damage, and its repair in mammalian cells. We have studied DNA damage in the PGK1 gene for a series of DNA alkylating agents including N-methyl-N'-nitro-N-nitrosoguanidine, Mechlorethamine, and Chlorambucil and shown that the damage observed in the PGK1 (phosphoglycerate kinase 1) gene depends on the alkylating agent used. This report reviews the literature on the MPG proteins, DNA glycosylases removing 3-methyladenine, and the use of these enzymes to detect DNA damage at the nucleotide level.

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24

BRYANT, P. E. "DNA damage, repair and chromosomal damage". International Journal of Radiation Biology 71, nr 6 (styczeń 1997): 675–80. http://dx.doi.org/10.1080/095530097143680.

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25

Stokes, Matthew P., Ruth Van Hatten, Howard D. Lindsay i W. Matthew Michael. "DNA replication is required for the checkpoint response to damaged DNA in Xenopus egg extracts". Journal of Cell Biology 158, nr 5 (2.09.2002): 863–72. http://dx.doi.org/10.1083/jcb.200204127.

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Alkylating agents, such as methyl methanesulfonate (MMS), damage DNA and activate the DNA damage checkpoint. Although many of the checkpoint proteins that transduce damage signals have been identified and characterized, the mechanism that senses the damage and activates the checkpoint is not yet understood. To address this issue for alkylation damage, we have reconstituted the checkpoint response to MMS in Xenopus egg extracts. Using four different indicators for checkpoint activation (delay on entrance into mitosis, slowing of DNA replication, phosphorylation of the Chk1 protein, and physical association of the Rad17 checkpoint protein with damaged DNA), we report that MMS-induced checkpoint activation is dependent upon entrance into S phase. Additionally, we show that the replication of damaged double-stranded DNA, and not replication of damaged single-stranded DNA, is the molecular event that activates the checkpoint. Therefore, these data provide direct evidence that replication forks are an obligate intermediate in the activation of the DNA damage checkpoint.

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26

Henkel, Ralf R., i Daniel R. Franken. "Sperm DNA Fragmentation: Origin and Impact on Human Reproduction". Journal of Reproductive and Stem Cell Biotechnology 2, nr 2 (grudzień 2011): 88–108. http://dx.doi.org/10.1177/205891581100200204.

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Sperm DNA can be damaged due to a multitude of different noxae, which include disease, and occupational and environmental factors. Depending on the magnitude of the damage, such lesions may be repaired by the oocyte or the embryo. If this is not possible, a permanent damage can be manifested leading to mutations of the male genome. In cases where the oocyte or the embryo does not counter these damages to the male genome in terms of repair or an early abortion, sperm DNA damage and fragmentation can be a cause of numerous diseases including childhood cancer.

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27

Basu, Ashis, Suse Broyde, Shigenori Iwai i Caroline Kisker. "DNA Damage, Mutagenesis, and DNA Repair". Journal of Nucleic Acids 2010 (2010): 1. http://dx.doi.org/10.4061/2010/182894.

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28

Griffin, Shaun. "DNA damage, DNA repair and disease". Current Biology 6, nr 5 (maj 1996): 497–99. http://dx.doi.org/10.1016/s0960-9822(02)00525-0.

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29

Kemp, Michael G., Laura A. Lindsey-Boltz i Aziz Sancar. "The DNA Damage Response Kinases DNA-dependent Protein Kinase (DNA-PK) and Ataxia Telangiectasia Mutated (ATM) Are Stimulated by Bulky Adduct-containing DNA". Journal of Biological Chemistry 286, nr 22 (12.04.2011): 19237–46. http://dx.doi.org/10.1074/jbc.m111.235036.

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A variety of environmental, carcinogenic, and chemotherapeutic agents form bulky lesions on DNA that activate DNA damage checkpoint signaling pathways in human cells. To identify the mechanisms by which bulky DNA adducts induce damage signaling, we developed an in vitro assay using mammalian cell nuclear extract and plasmid DNA containing bulky adducts formed by N-acetoxy-2-acetylaminofluorene or benzo(a)pyrene diol epoxide. Using this cell-free system together with a variety of pharmacological, genetic, and biochemical approaches, we identified the DNA damage response kinases DNA-dependent protein kinase (DNA-PK) and ataxia telangiectasia mutated (ATM) as bulky DNA damage-stimulated kinases that phosphorylate physiologically important residues on the checkpoint proteins p53, Chk1, and RPA. Consistent with these results, purified DNA-PK and ATM were directly stimulated by bulky adduct-containing DNA and preferentially associated with damaged DNA in vitro. Because the DNA damage response kinase ATM and Rad3-related (ATR) is also stimulated by bulky DNA adducts, we conclude that a common biochemical mechanism exists for activation of DNA-PK, ATM, and ATR by bulky adduct-containing DNA.

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30

Rzeszowska-Wolny, J., i P. Widłak. "Damaged DNA-binding proteins: recognition of N-acetoxy-acetylaminofluorene-induced DNA adducts." Acta Biochimica Polonica 46, nr 1 (31.03.1999): 173–80. http://dx.doi.org/10.18388/abp.1999_4195.

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Proteins which bind to the DNA damaged by genotoxic agents can be detected in all living organisms. Damage-recognition proteins are thought to be generally involved in DNA repair mechanisms. On the other hand, the relevance to DNA repair of some other proteins which show elevated affinity to damaged DNA (e.g. HMG-box containing proteins or histone H1) has not been established. Using the electrophoretic mobility-shift assay we have investigated damage-recognition proteins in nuclei from rat hepatocytes. We detected two different protein complexes which preferentially bound the DNA damaged by N-acetoxy-acetylaminofluorene. One of them also recognized the DNA damaged by benzo(a)pyrene diol epoxide (yet with much lower efficiency). The proteins which bind to damaged DNA are permanently present in rat cells and their level does not change after treatment of animals with the carcinogens. Differences in the affinity of the detected damage-recognition proteins to DNA lesion evoked by either carcinogen did not correlate with more efficient removal from hepatic DNA of 2-acetylaminofluorene-induced adducts than benzo(a)pyrene-induced ones.

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31

Guo, Peiyan, Ning Ma, Jingbo Shan, Techang Chen, Yujie Zhang, Sa Zhou i Wenjian Ma. "Exogenous damage causes cell DNA damage through mediated reactive oxygen levels". E3S Web of Conferences 131 (2019): 01018. http://dx.doi.org/10.1051/e3sconf/201913101018.

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Many anti-tumor drugs can induce tumor apoptosis by increasing intracellular ROS. In the present study, we build a model which did not directly cause DNA damage, but simulated damage products. The model of this injury was transferred into the cell so that the cell’s damage recognition mechanism mistakenly recognized that its own DNA was damaged, which in turn induced a response. Based on this model, the damaged plasmids (exogenous DNA damage) were transferred into the cells and the amount of reactive oxygen in the cells was improved, and DNA damage of the cells was increased. Therefore, exogenous DNA damage can affect the accumulation of damage in cells by affecting the level of reactive oxygen species, which provides a reference for DNA damage repair research.

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32

Guérillon, Claire, Stine Smedegaard, Ivo A. Hendriks, Michael L. Nielsen i Niels Mailand. "Multisite SUMOylation restrains DNA polymerase η interactions with DNA damage sites". Journal of Biological Chemistry 295, nr 25 (29.04.2020): 8350–62. http://dx.doi.org/10.1074/jbc.ra120.013780.

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Translesion DNA synthesis (TLS) mediated by low-fidelity DNA polymerases is an essential cellular mechanism for bypassing DNA lesions that obstruct DNA replication progression. However, the access of TLS polymerases to the replication machinery must be kept tightly in check to avoid excessive mutagenesis. Recruitment of DNA polymerase η (Pol η) and other Y-family TLS polymerases to damaged DNA relies on proliferating cell nuclear antigen (PCNA) monoubiquitylation and is regulated at several levels. Using a microscopy-based RNAi screen, here we identified an important role of the SUMO modification pathway in limiting Pol η interactions with DNA damage sites in human cells. We found that Pol η undergoes DNA damage- and protein inhibitor of activated STAT 1 (PIAS1)-dependent polySUMOylation upon its association with monoubiquitylated PCNA, rendering it susceptible to extraction from DNA damage sites by SUMO-targeted ubiquitin ligase (STUbL) activity. Using proteomic profiling, we demonstrate that Pol η is targeted for multisite SUMOylation, and that collectively these SUMO modifications are essential for PIAS1- and STUbL-mediated displacement of Pol η from DNA damage sites. These findings suggest that a SUMO-driven feedback inhibition mechanism is an intrinsic feature of TLS-mediated lesion bypass functioning to curtail the interaction of Pol η with PCNA at damaged DNA to prevent harmful mutagenesis.

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33

OCHOA, JUAN G. DIAZ, i MICHAEL WULKOW. "DNA DAMAGES AS A DEPOLYMERIZATION PROCESS". International Journal of Modern Physics C 23, nr 03 (marzec 2012): 1250018. http://dx.doi.org/10.1142/s0129183112500180.

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The damage of DNA chains by environmental factors like radiation or chemical pollutants is a topic that has been frequently explored from an experimental and a theoretical perspective. Such damages, like the damage of the strands of a DNA chain, are toxic for the cell and can induce mutagenesis or apoptosis. Several models make strong assumptions for the distribution of damages; for instance a frequent supposition is that these damages are Poisson distributed. [L. Ma, J. J. Wagner, W. Hu, A. J. Levine and G. A. Stolovitzki, Proc. Natl. Acad. Sci.PNAS 102, 14266 (2005).] Only few models describe in detail the damage and the mechanisms associated to the formation and evolution of this damage distribution [H. Nikjoo, P. O'neill and D. T. Goodhead, Radiat. Res. 156, 577 (2001).] Nevertheless, such models do not include the repair processes which are continuously active inside the cell. In this work we present a novel model, based on a depolymerization process, describing the distribution of damages on DNA chains coupled to the dynamics associated to its repair processes. The central aim is not to give a final and comprehensive model, but a hint to represent in more detail the complex dynamics involved in the damage and repair of DNA. We show that there are critical parameters associated to this repair process, in particular we show how critical doses can be relevant in deciding whether the cell continues its repair process or starts apoptosis. We also find out that the damage concentration is related to the dose via a power law relation.

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34

Yasui, Akira, Shin-ichiro Kanno i Masashi Takao. "DNA damage, repair and aging". Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 40, nr 6 (2003): 593–95. http://dx.doi.org/10.3143/geriatrics.40.593.

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35

Verma, Nagendra, Matteo Franchitto, Azzurra Zonfrilli, Samantha Cialfi, Rocco Palermo i Claudio Talora. "DNA Damage Stress: Cui Prodest?" International Journal of Molecular Sciences 20, nr 5 (1.03.2019): 1073. http://dx.doi.org/10.3390/ijms20051073.

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DNA is an entity shielded by mechanisms that maintain genomic stability and are essential for living cells; however, DNA is constantly subject to assaults from the environment throughout the cellular life span, making the genome susceptible to mutation and irreparable damage. Cells are prepared to mend such events through cell death as an extrema ratio to solve those threats from a multicellular perspective. However, in cells under various stress conditions, checkpoint mechanisms are activated to allow cells to have enough time to repair the damaged DNA. In yeast, entry into the cell cycle when damage is not completely repaired represents an adaptive mechanism to cope with stressful conditions. In multicellular organisms, entry into cell cycle with damaged DNA is strictly forbidden. However, in cancer development, individual cells undergo checkpoint adaptation, in which most cells die, but some survive acquiring advantageous mutations and selfishly evolve a conflictual behavior. In this review, we focus on how, in cancer development, cells rely on checkpoint adaptation to escape DNA stress and ultimately to cell death.

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36

Baumann, Kim. "Brain DNA damage hotspots". Nature Reviews Molecular Cell Biology 22, nr 5 (7.04.2021): 304–5. http://dx.doi.org/10.1038/s41580-021-00367-5.

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Ștefani, Constantin, Alexandra Totan, Daniela Miricescu, Ana Maria Alexandra Stănescu i Maria Greabu. "Obesity induces DNA damage". Romanian Medical Journal 66, nr 4 (31.12.2019): 342–45. http://dx.doi.org/10.37897/rmj.2019.4.9.

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38

Raloff, J. "Chemically Fingerprinting DNA Damage". Science News 135, nr 13 (1.04.1989): 199. http://dx.doi.org/10.2307/3973485.

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39

Lewis, Sian. "DNA damage drives sleep". Nature Reviews Neuroscience 23, nr 2 (14.12.2021): 69. http://dx.doi.org/10.1038/s41583-021-00550-9.

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40

Nepal, Manoj, Raymond Che, Chi Ma, Jun Zhang i Peiwen Fei. "FANCD2 and DNA Damage". International Journal of Molecular Sciences 18, nr 8 (19.08.2017): 1804. http://dx.doi.org/10.3390/ijms18081804.

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41

Collins, Andrew R. "Alcohol and DNA damage". Journal of Laboratory and Clinical Medicine 136, nr 4 (październik 2000): 258–59. http://dx.doi.org/10.1067/mlc.2000.109098.

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42

Schärer, Orlando D., i Arthur J. Campbell. "Wedging out DNA damage". Nature Structural & Molecular Biology 16, nr 2 (luty 2009): 102–4. http://dx.doi.org/10.1038/nsmb0209-102.

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43

White, Eileen, i Carol Prives. "DNA damage enables p73". Nature 399, nr 6738 (czerwiec 1999): 735–37. http://dx.doi.org/10.1038/21539.

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44

Friedberg, Errol C. "DNA damage and repair". Nature 421, nr 6921 (styczeń 2003): 436–40. http://dx.doi.org/10.1038/nature01408.

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45

Ström, Lena, i Camilla Sjögren. "DNA Damage-Induced Cohesion". Cell Cycle 4, nr 4 (28.01.2005): 536–39. http://dx.doi.org/10.4161/cc.4.4.1613.

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LeBrasseur, Nicole. "Deacetylase undoes DNA damage". Journal of Cell Biology 160, nr 7 (31.03.2003): 981. http://dx.doi.org/10.1083/jcb1607iti3.

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47

Wang, JYJ. "DNA damage and apoptosis". Cell Death & Differentiation 8, nr 11 (30.10.2001): 1047–48. http://dx.doi.org/10.1038/sj.cdd.4400938.

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48

Ray, L. B. "Dealing with DNA Damage". Science's STKE 2006, nr 357 (10.10.2006): tw359. http://dx.doi.org/10.1126/stke.3572006tw359.

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Ray, L. B. "DNA Damage-Response Teams". Science's STKE 2007, nr 388 (23.05.2007): tw189. http://dx.doi.org/10.1126/stke.3882007tw189.

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50

Barnes, Jessica L., Maria Zubair, Kaarthik John, Miriam C. Poirier i Francis L. Martin. "Carcinogens and DNA damage". Biochemical Society Transactions 46, nr 5 (4.10.2018): 1213–24. http://dx.doi.org/10.1042/bst20180519.

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Humans are variously and continuously exposed to a wide range of different DNA-damaging agents, some of which are classed as carcinogens. DNA damage can arise from exposure to exogenous agents, but damage from endogenous processes is probably far more prevalent. That said, epidemiological studies of migrant populations from regions of low cancer risk to high cancer risk countries point to a role for environmental and/or lifestyle factors playing a pivotal part in cancer aetiology. One might reasonably surmise from this that carcinogens found in our environment or diet are culpable. Exposure to carcinogens is associated with various forms of DNA damage such as single-stand breaks, double-strand breaks, covalently bound chemical DNA adducts, oxidative-induced lesions and DNA–DNA or DNA–protein cross-links. This review predominantly concentrates on DNA damage induced by the following carcinogens: polycyclic aromatic hydrocarbons, heterocyclic aromatic amines, mycotoxins, ultraviolet light, ionising radiation, aristolochic acid, nitrosamines and particulate matter. Additionally, we allude to some of the cancer types where there is molecular epidemiological evidence that these agents are aetiological risk factors. The complex role that carcinogens play in the pathophysiology of cancer development remains obscure, but DNA damage remains pivotal to this process.

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