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Artykuły w czasopismach na temat „DNA damage”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Chakarov, Stoyan, Rumena Petkova, George Ch Russev, and Nikolai Zhelev. "DNA damage and mutation. Types of DNA damage." BioDiscovery 11 (February 23, 2014): e8957. https://doi.org/10.7750/BioDiscovery.2014.11.1.

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This review outlines the basic types of DNA damage caused by exogenous and endogenous factors, analyses the possible consequences of each type of damage and discusses the need for different types of DNA repair. The mechanisms by which a minor damaging event to DNA may eventually result in the introduction of heritable mutation/s are reviewed. The major features of the role of DNA damage in ageing and carcinogenesis are outlined and the role of iatrogenic DNA damage in human health and disease (with curative intent as well as a long-term adverse effect of genotoxic therapies) are discussed in d

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2

Mitra, Manu. "DNA Repairing and its Mechanism in the Cell." ACTA Scientific Medical Sciences 3, no. 8 (2019): 116–19. https://doi.org/10.5281/zenodo.3338556.

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DNA (Deoxyribonucleic Acid) repair denotes collection of processes by which a cell identifies and corrects the damage to the DNA molecules that encode its genome. Several incisions causes structural damage to the DNA molecule and may alter or eliminate the cell’s ability to transcribe the gene that are affected DNA encodes. There are many techniques and methods to repair DNA, however, in this paper few methods are reviewed. For instance – Mechanism for repairing damaged DNA, Novel technique to repair damaged DNA, Scientist confirm DNA repair, Repairing faulty genes to cure diseases

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3

Chakarov, Stoyan, Rumena Petkova, George Russev, and Nikolai Zhelev. "DNA damage and mutation. Types of DNA damage." BioDiscovery, no. 11 (February 23, 2014): 1. http://dx.doi.org/10.7750/biodiscovery.2014.11.1.

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4

Yeung, ManTek, and Daniel Durocher. "Engineering a DNA damage response without DNA damage." Genome Biology 9, no. 7 (2008): 227. http://dx.doi.org/10.1186/gb-2008-9-7-227.

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Bagchi, Srilata, and Pradip Raychaudhuri. "Damaged-DNA Binding Protein-2 Drives Apoptosis Following DNA Damage." Cell Division 5, no. 1 (2010): 3. http://dx.doi.org/10.1186/1747-1028-5-3.

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Wallace, Bret D., and R. Scott Williams. "Ribonucleotide triggered DNA damage and RNA-DNA damage responses." RNA Biology 11, no. 11 (2014): 1340–46. http://dx.doi.org/10.4161/15476286.2014.992283.

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7

Nawy, Tal. "DNA variants or DNA damage?" Nature Methods 14, no. 4 (2017): 341. http://dx.doi.org/10.1038/nmeth.4254.

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Chakarov, Stoyan, Rumena Petkova, George Ch Russev, and Nikolai Zhelev. "DNA damage and the circadian clock." BioDiscovery 13 (September 14, 2014): e8960. https://doi.org/10.7750/BioDiscovery.2014.13.1.

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The role of the circadian clock has already been demonstrated for virtually all physiological processes, but it was only recently shown that cells were more sensitive to DNA damage at specific times of the day; that the peak of synthesis of mRNA and proteins of genes coding for products involved directly or indirectly in DNA repair was differentially timed in different tissues; and that the growth of some types of cancer followed a circadian pattern. The paper reviews the specificities of the clockwork mechanism in living cells associated with repair of DNA damage with regards to its role in a

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9

Stokes, Matthew P., Ruth Van Hatten, Howard D. Lindsay, and W. Matthew Michael. "DNA replication is required for the checkpoint response to damaged DNA in Xenopus egg extracts." Journal of Cell Biology 158, no. 5 (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

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10

Chakarov, Stoyan, Rumena Petkova, and George Ch Russev. "DNA repair systems." BioDiscovery 13 (September 22, 2014): e8961. https://doi.org/10.7750/BioDiscovery.2014.13.2.

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This paper provides detailed insight into the mechanisms of repair of different types of DNA damage and the direct molecular players (enzymes repairing the damage or tagging the damaged site for further processing; damage sensor molecules; other signalling and effector molecules). The genetic bases of diseases and conditions associated with defective DNA repair are comprehensively reviewed, from the ''classic'' severe diseases such as xeroderma pigmentosum and Cockayne syndrome to the much more subtle UV sensitivity syndromes. The review analyses the basic molecular mechanisms underlying the r

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11

Henkel, Ralf R., and Daniel R. Franken. "Sperm DNA Fragmentation: Origin and Impact on Human Reproduction." Journal of Reproductive and Stem Cell Biotechnology 2, no. 2 (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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12

Bush, Stephen P., Peter E. Hart, and Eric M. Russell. "Investigating DNA Damage." American Biology Teacher 68, no. 5 (2006): 280–84. http://dx.doi.org/10.2307/4451989.

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13

Oksenych, Valentyn, and Denis E. Kainov. "DNA Damage Response." Biomolecules 11, no. 1 (2021): 123. http://dx.doi.org/10.3390/biom11010123.

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14

Bush, Stephen P., Peter E. Hart, and Eric M. Russell. "Investigating DNA Damage." American Biology Teacher 68, no. 5 (2006): 280. http://dx.doi.org/10.1894/0038-4909(2006)68[280:idd]2.0.co;2.

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15

Skrypnyk, N. V., and O. O. Maslova. "Oxidative DNA damage." Biopolymers and Cell 23, no. 3 (2007): 202–14. http://dx.doi.org/10.7124/bc.000766.

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16

Giglia-Mari, G., A. Zotter, and W. Vermeulen. "DNA Damage Response." Cold Spring Harbor Perspectives in Biology 3, no. 1 (2010): a000745. http://dx.doi.org/10.1101/cshperspect.a000745.

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17

Dabney, J., M. Meyer, and S. Paabo. "Ancient DNA Damage." Cold Spring Harbor Perspectives in Biology 5, no. 7 (2013): a012567. http://dx.doi.org/10.1101/cshperspect.a012567.

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18

Lou, Kai-Jye. "DNA damage control." Science-Business eXchange 1, no. 38 (2008): 916. http://dx.doi.org/10.1038/scibx.2008.916.

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19

Rossi, Harald H. "Interactive DNA Damage." Radiation Research 140, no. 2 (1994): 295. http://dx.doi.org/10.2307/3578915.

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20

Cadet, Jean, and Michael Weinfeld. "DETECTING DNA DAMAGE." Analytical Chemistry 65, no. 15 (1993): 675A—682A. http://dx.doi.org/10.1021/ac00063a724.

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21

Alderton, Gemma K. "Secreted DNA damage?" Nature Reviews Cancer 13, no. 2 (2013): 77. http://dx.doi.org/10.1038/nrc3455.

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22

Coon, Elizabeth A., and Eduardo E. Benarroch. "DNA damage response." Neurology 90, no. 8 (2018): 367–76. http://dx.doi.org/10.1212/wnl.0000000000004989.

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23

Beshay, Victor E., and Orhan Bukulmez. "Sperm DNA damage." Current Opinion in Obstetrics and Gynecology 24, no. 3 (2012): 172–79. http://dx.doi.org/10.1097/gco.0b013e32835211b5.

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24

Friedman, Danielle. "DNA Damage Pathways." JAMA 304, no. 15 (2010): 1645. http://dx.doi.org/10.1001/jama.2010.1346.

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25

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

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26

Pereira, Cristiana, Rosa Coelho, Daniela Grácio, et al. "DNA Damage and Oxidative DNA Damage in Inflammatory Bowel Disease." Journal of Crohn's and Colitis 10, no. 11 (2016): 1316–23. http://dx.doi.org/10.1093/ecco-jcc/jjw088.

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27

Babazadeh, Zahra, Shahnaz Razavi, Marziyeh Tavalaee, Mohammad Reza Deemeh, Maryam Shahidi, and Mohammad Hossein Nasr-Esfahani. "Sperm DNA damage and its relation with leukocyte DNA damage." Reproductive Toxicology 29, no. 1 (2010): 120–24. http://dx.doi.org/10.1016/j.reprotox.2009.09.002.

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28

Popp, Kohl, Naumann, et al. "DNA Damage and DNA Damage Response in Chronic Myeloid Leukemia." International Journal of Molecular Sciences 21, no. 4 (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

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29

Bouziane, M., F. Miao, N. Ye, G. Holmquist, G. Chyzak, and T. R. O'Connor. "Repair of DNA alkylation damage." Acta Biochimica Polonica 45, no. 1 (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 comp

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30

BRYANT, P. E. "DNA damage, repair and chromosomal damage." International Journal of Radiation Biology 71, no. 6 (1997): 675–80. http://dx.doi.org/10.1080/095530097143680.

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31

Guo, Peiyan, Ning Ma, Jingbo Shan, et al. "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, exogen

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32

Kemp, Michael G., Laura A. Lindsey-Boltz, and 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, no. 22 (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 pr

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33

Rzeszowska-Wolny, J., and P. Widłak. "Damaged DNA-binding proteins: recognition of N-acetoxy-acetylaminofluorene-induced DNA adducts." Acta Biochimica Polonica 46, no. 1 (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-

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34

Basu, Ashis, Suse Broyde, Shigenori Iwai, and 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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Griffin, Shaun. "DNA damage, DNA repair and disease." Current Biology 6, no. 5 (1996): 497–99. http://dx.doi.org/10.1016/s0960-9822(02)00525-0.

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Guérillon, Claire, Stine Smedegaard, Ivo A. Hendriks, Michael L. Nielsen та Niels Mailand. "Multisite SUMOylation restrains DNA polymerase η interactions with DNA damage sites". Journal of Biological Chemistry 295, № 25 (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 modificat

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37

OCHOA, JUAN G. DIAZ, and MICHAEL WULKOW. "DNA DAMAGES AS A DEPOLYMERIZATION PROCESS." International Journal of Modern Physics C 23, no. 03 (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 describ

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38

Yasui, Akira, Shin-ichiro Kanno, and Masashi Takao. "DNA damage, repair and aging." Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics 40, no. 6 (2003): 593–95. http://dx.doi.org/10.3143/geriatrics.40.593.

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Dmitrieva, Natalia I., Dmitry V. Bulavin, and Maurice B. Burg. "High NaCl causes Mre11 to leave the nucleus, disrupting DNA damage signaling and repair." American Journal of Physiology-Renal Physiology 285, no. 2 (2003): F266—F274. http://dx.doi.org/10.1152/ajprenal.00060.2003.

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High NaCl causes DNA double-strand breaks and cell cycle arrest, but the mechanism of its genotoxicity has been unclear. In this study, we describe a novel mechanism that contributes to this genotoxicity. The Mre11 exonuclease complex is a central component of DNA damage response. This complex assembles at sites of DNA damage, where it processes DNA ends for subsequent activation of repair and initiates cell cycle checkpoints. However, this does not occur with DNA damage caused by high NaCl. Rather, following high NaCl, Mre11 exits from the nucleus, DNA double-strand breaks accumulate in the S

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40

Verma, Nagendra, Matteo Franchitto, Azzurra Zonfrilli, Samantha Cialfi, Rocco Palermo, and Claudio Talora. "DNA Damage Stress: Cui Prodest?" International Journal of Molecular Sciences 20, no. 5 (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 whe

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41

Han, Jun Song, Xin Lu Lv, Ya Li Gao, Xiang Gao, and De Qi Xiong. "Analysis of DNA Damages of Gonadal Cells of Hemicentrotus pulcherrimus in Petroleum Hydrocarbons." Applied Mechanics and Materials 522-524 (February 2014): 251–56. http://dx.doi.org/10.4028/www.scientific.net/amm.522-524.251.

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The single cell gel electrophoresis (SCGE) is a rapid and sensitive procedure for measuring strand breaks in DNA. In the present study, sea urchin (Hemicentrotus pulcherrimus) was chosen as the test organism and SCGE was applied to assess DNA damage of its gonadal cells exposed to petroleum hydrocarbon. The gonadal cells of sea urchin had been seriously damaged above 50 mg/L of Water Accommodated Fractions (WAFs), whileas no damages occurred in the lower concentrations. There were good linear relationships between exposure days and DNA damage rate, percentage of DNA in the comet tail (%TDNA) a

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42

Anuradha, A., Suresh Babu Undavalli, and A. Jagadeesh Kumar. "DNA mutilation: A telltale sign of cancer inception." Journal of Oral and Maxillofacial Pathology 27, no. 2 (2023): 374–81. http://dx.doi.org/10.4103/jomfp.jomfp_513_22.

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DNA damage is a discrepancy in its chemical structure precipitated by a multitude of factors. Most DNA damages can be repaired efficiently through diverse restorative mechanisms subjective to the type of damage. DNA-damaging agents elicit a medley of cellular retorts like cell cycle arrest, followed by DNA repair mechanisms or apoptosis. An unrepaired DNA damage in a nonreplicating cell does not generally engender mutations but a similar scenario in replicating cell routes to permanent modification of genetic material shrugging to carcinogenesis. DNA mutilation can be allied to disarray in bas

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Baumann, Kim. "Brain DNA damage hotspots." Nature Reviews Molecular Cell Biology 22, no. 5 (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, and Maria Greabu. "Obesity induces DNA damage." Romanian Medical Journal 66, no. 4 (2019): 342–45. http://dx.doi.org/10.37897/rmj.2019.4.9.

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Raloff, J. "Chemically Fingerprinting DNA Damage." Science News 135, no. 13 (1989): 199. http://dx.doi.org/10.2307/3973485.

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Lewis, Sian. "DNA damage drives sleep." Nature Reviews Neuroscience 23, no. 2 (2021): 69. http://dx.doi.org/10.1038/s41583-021-00550-9.

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Nepal, Manoj, Raymond Che, Chi Ma, Jun Zhang, and Peiwen Fei. "FANCD2 and DNA Damage." International Journal of Molecular Sciences 18, no. 8 (2017): 1804. http://dx.doi.org/10.3390/ijms18081804.

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Collins, Andrew R. "Alcohol and DNA damage." Journal of Laboratory and Clinical Medicine 136, no. 4 (2000): 258–59. http://dx.doi.org/10.1067/mlc.2000.109098.

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Schärer, Orlando D., and Arthur J. Campbell. "Wedging out DNA damage." Nature Structural & Molecular Biology 16, no. 2 (2009): 102–4. http://dx.doi.org/10.1038/nsmb0209-102.

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White, Eileen, and Carol Prives. "DNA damage enables p73." Nature 399, no. 6738 (1999): 735–37. http://dx.doi.org/10.1038/21539.

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