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Relevant bibliographies by topics / Bulky DNA adduct

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Journal articles

Academic literature on the topic 'Bulky DNA adduct'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Bulky DNA adduct"

1

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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2

Jha, Vikash, та Hong Ling. "Structural basis for error-free bypass of bulky adduct by DNA polymerase Polκ". Acta Crystallographica Section A Foundations and Advances 70, a1 (2014): C1401. http://dx.doi.org/10.1107/s2053273314085982.

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Humans are frequently exposed to the environmentally ubiquitous and potentially carcinigenic polycyclic aromatic hydrocarbon, benzo[a]pyrene (BP). BP is metabolized to highly reactive benzo[a]pyrene diol epoxides (BPDEs) in the cells. BPDEs react with DNA predominantly at the N2 position of guanine and form bulky adducts. The major BP adduct is (+)-trans-anti-[BP]-N2-dG (BP-N2-dG) that is carcinogenic. The bulky adduct block DNA synthesis by replicative or high-fidelity DNA polymerases. Some of the specialized lesion bypass polymerases (mostly belonging to Y-family) can replicate through this

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3

Kasiviswanathan, Rajesh, Irina G. Minko, R. Stephen Lloyd та William C. Copeland. "Translesion Synthesis Past Acrolein-derived DNA Adducts by Human Mitochondrial DNA Polymerase γ". Journal of Biological Chemistry 288, № 20 (2013): 14247–55. http://dx.doi.org/10.1074/jbc.m113.458802.

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Acrolein, a mutagenic aldehyde, is produced endogenously by lipid peroxidation and exogenously by combustion of organic materials, including tobacco products. Acrolein reacts with DNA bases forming exocyclic DNA adducts, such as γ-hydroxy-1,N2-propano-2′-deoxyguanosine (γ-HOPdG) and γ-hydroxy-1,N6-propano-2′-deoxyadenosine (γ-HOPdA). The bulky γ-HOPdG adduct blocks DNA synthesis by replicative polymerases but can be bypassed by translesion synthesis polymerases in the nucleus. Although acrolein-induced adducts are likely to be formed and persist in mitochondrial DNA, animal cell mitochondria l

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4

Hang, Bo. "Formation and Repair of Tobacco Carcinogen-Derived Bulky DNA Adducts." Journal of Nucleic Acids 2010 (2010): 1–29. http://dx.doi.org/10.4061/2010/709521.

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DNA adducts play a central role in chemical carcinogenesis. The analysis of formation and repair of smoking-related DNA adducts remains particularly challenging as both smokers and nonsmokers exposed to smoke are repetitively under attack from complex mixtures of carcinogens such as polycyclic aromatic hydrocarbons andN-nitrosamines. The bulky DNA adducts, which usually have complex structure, are particularly important because of their biological relevance. Several known cellular DNA repair pathways have been known to operate in human cells on specific types of bulky DNA adducts, for example,

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5

Wei, D., V. M. Maher, and J. J. McCormick. "Site-specific excision repair of 1-nitrosopyrene-induced DNA adducts at the nucleotide level in the HPRT gene of human fibroblasts: effect of adduct conformation on the pattern of site-specific repair." Molecular and Cellular Biology 16, no. 7 (1996): 3714–19. http://dx.doi.org/10.1128/mcb.16.7.3714.

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Studies showing that different types of DNA adducts are repaired in human cells at different rates suggest that DNA adduct conformation is the major determinant of the rate of nucleotide excision repair. However, recent studies of repair of cyclobutane pyrimidine dimers or benzo[a]pyrene diol epoxide (BPDE)-induced adducts at the nucleotide level in DNA of normal human fibroblasts indicate that the rate of repair of the same adduct at different nucleotide positions can vary up to 10-fold, suggesting an important role for local DNA conformation. To see if site-specific DNA repair is a common ph

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6

Sahasrabudhe, S. R., X. Luo, and M. Z. Humayun. "Specificity of base substitutions induced by the acridine mutagen ICR-191: mispairing by guanine N7 adducts as a mutagenic mechanism." Genetics 129, no. 4 (1991): 981–89. http://dx.doi.org/10.1093/genetics/129.4.981.

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Abstract As the most nucleophilic site in DNA, the guanine N7 atom is a major site of adduction by a large number of alkylating mutagens and carcinogens. Aflatoxin B1, a powerful mutagen, is believed to act through its reaction with this DNA site. On the basis of the specificity of base substitutions induced by various adduct forms of aflatoxin, we have proposed that bulky guanine N7 adducts elicit base substitutions by two mechanisms. The first mechanism is similar to that observed for a number of bulky noninstructive lesions, whereas the second mechanism invokes mispairing between N7-adducte

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7

Dunn, Bruce P. "Detection of Aromatic DNA Adducts in Human Cells and Fish Liver." Journal of the American College of Toxicology 8, no. 5 (1989): 905–12. http://dx.doi.org/10.3109/10915818909018051.

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Both nuclease PI treatment and reverse-phase high-performance liquid chromatography (HPLC) were used to enrich hydrophobic/bulky DNA adducts in DNA digests. 32P-postlabeling procedures and thin layer chromatography were then used to detect and quantitate aromatic/bulky DNA adducts. For both human and fish DNA from individuals exposed to environmental carcinogens, the nuclease PI and HPLC enrichment procedures generally gave similar results. The bottom sediments of the Buffalo and Detroit rivers are contaminated with polycyclic aromatic hydrocarbon carcinogens, and brown bullheads in these rive

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8

Hambley, Trevor W., Susan J. Berners-Price, Murray S. Davies, et al. "Steric Determinants of Pt/DNA Interactions and Anticancer Activity." Metal-Based Drugs 5, no. 4 (1998): 197–206. http://dx.doi.org/10.1155/mbd.1998.197.

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Studies directed at establishing the structural features that control Pt/DNA interactions and the anticancer activity of Pt drugs are described. [H1,N15]-HSQC 2D NMR spectroscopic studies of the reactions of cisplatin with oligonucleotides containing ApG and GpA binding sites reveal dramatic differences in the rates of formation of monofunctional adducts at the two sites. When the reactant is cis-[Pt(NH3)2(OH2)2]2+ no such differences are observed suggesting that outer-sphere interactions between the reactant and the oligonucleotide may play a substantial role in determining the rates. Rates o

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9

Jung, Hunmin, Naveen Kumar Rayala та Seongmin Lee. "Translesion synthesis of the major nitrogen mustard-induced DNA lesion by human DNA polymerase η". Biochemical Journal 477, № 23 (2020): 4543–58. http://dx.doi.org/10.1042/bcj20200767.

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Nitrogen mustards are among the first modern anticancer chemotherapeutics that are still widely used as non-specific anticancer alkylating agents. While the mechanism of action of mustard drugs involves the generation of DNA interstrand cross-links, the predominant lesions produced by these drugs are nitrogen half-mustard-N7-dG (NHMG) adducts. The bulky major groove lesion NHMG, if left unrepaired, can be bypassed by translesion synthesis (TLS) DNA polymerases. However, studies of the TLS past NHMG have not been reported so far. Here, we present the first synthesis of an oligonucleotide contai

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10

Castaño-Vinyals, Gemma, Glenn Talaska, Nathaniel Rothman, et al. "Bulky DNA Adduct Formation and Risk of Bladder Cancer." Cancer Epidemiology Biomarkers & Prevention 16, no. 10 (2007): 2155–59. http://dx.doi.org/10.1158/1055-9965.epi-07-0184.

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