Relevant bibliographies by topics / Uracil N-glycosylase

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  2. Dissertations / Theses

Academic literature on the topic 'Uracil N-glycosylase'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 September 2023

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Journal articles on the topic "Uracil N-glycosylase"

1

Focher, F., A. Verri, S. Spadari, R. Manservigi, J. Gambino, and G. E. Wright. "Herpes simplex virus type 1 uracil-DNA glycosylase: isolation and selective inhibition by novel uracil derivatives." Biochemical Journal 292, no. 3 (1993): 883–89. http://dx.doi.org/10.1042/bj2920883.

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We have purified Herpes simplex type 1 (HSV1) uracil-DNA glycosylase from the nuclei of HSV1-infected HeLa cells harvested 8 h post-infection, at which time the induction of the enzyme is a maximum. The enzyme has been shown to be distinct from the host enzyme, isolated from HeLa cells, by its lack of sensitivity to a monoclonal antibody to human uracil-DNA glycosylase. Furthermore, several uracil analogues were synthesized and screened for their capacity to discriminate between the viral and human uracil-DNA glycosylases. Both enzymes were inhibited by 6-(p-alkylanilino)uracils, but the viral
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2

SHATILLA, Andrea, and Dindial RAMOTAR. "Embryonic extracts derived from the nematode Caenorhabditis elegans remove uracil from DNA by the sequential action of uracil-DNA glycosylase and AP (apurinic/apyrimidinic) endonuclease." Biochemical Journal 365, no. 2 (2002): 547–53. http://dx.doi.org/10.1042/bj20020375.

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DNA bases continuously undergo modifications in response to endogenous reactions such as oxidation, alkylation or deamination. The modified bases are primarily removed by DNA glycosylases, which cleave the N-glycosylic bond linking the base to the sugar, to generate an apurinic/apyrimidinic (AP) site, and this latter lesion is highly mutagenic. Previously, no study has demonstrated the processing of these lesions in the nematode Caenorhabditis elegans. Herein, we report the existence of uracil-DNA glycosylase and AP endonuclease activities in extracts derived from embryos of C. elegans. These
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3

Di Noia, Javier M., Gareth T. Williams, Denice T. Y. Chan, Jean-Marie Buerstedde, Geoff S. Baldwin, and Michael S. Neuberger. "Dependence of antibody gene diversification on uracil excision." Journal of Experimental Medicine 204, no. 13 (2007): 3209–19. http://dx.doi.org/10.1084/jem.20071768.

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Activation-induced deaminase (AID) catalyses deamination of deoxycytidine to deoxyuridine within immunoglobulin loci, triggering pathways of antibody diversification that are largely dependent on uracil-DNA glycosylase (uracil-N-glycolase [UNG]). Surprisingly efficient class switch recombination is restored to ung−/− B cells through retroviral delivery of active-site mutants of UNG, stimulating discussion about the need for UNG's uracil-excision activity. In this study, however, we find that even with the overexpression achieved through retroviral delivery, switching is only mediated by UNG mu
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4

KROKAN, Hans E., Rune STANDAL, and Geir SLUPPHAUG. "DNA glycosylases in the base excision repair of DNA." Biochemical Journal 325, no. 1 (1997): 1–16. http://dx.doi.org/10.1042/bj3250001.

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A wide range of cytotoxic and mutagenic DNA bases are removed by different DNA glycosylases, which initiate the base excision repair pathway. DNA glycosylases cleave the N-glycosylic bond between the target base and deoxyribose, thus releasing a free base and leaving an apurinic/apyrimidinic (AP) site. In addition, several DNA glycosylases are bifunctional, since they also display a lyase activity that cleaves the phosphodiester backbone 3′ to the AP site generated by the glycosylase activity. Structural data and sequence comparisons have identified common features among many of the DNA glycos
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5

Loewy, Z. G., J. Mecca, and R. Diaco. "Enhancement of Borrelia burgdorferi PCR by uracil N-glycosylase." Journal of Clinical Microbiology 32, no. 1 (1994): 135–38. http://dx.doi.org/10.1128/jcm.32.1.135-138.1994.

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6

Kavli, Bodil, Tobias S. Iveland, Edith Buchinger, et al. "RPA2 winged-helix domain facilitates UNG-mediated removal of uracil from ssDNA; implications for repair of mutagenic uracil at the replication fork." Nucleic Acids Research 49, no. 7 (2021): 3948–66. http://dx.doi.org/10.1093/nar/gkab195.

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Abstract Uracil occurs at replication forks via misincorporation of deoxyuridine monophosphate (dUMP) or via deamination of existing cytosines, which occurs 2–3 orders of magnitude faster in ssDNA than in dsDNA and is 100% miscoding. Tethering of UNG2 to proliferating cell nuclear antigen (PCNA) allows rapid post-replicative removal of misincorporated uracil, but potential ‘pre-replicative’ removal of deaminated cytosines in ssDNA has been questioned since this could mediate mutagenic translesion synthesis and induction of double-strand breaks. Here, we demonstrate that uracil-DNA glycosylase
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7

Prorok, Paulina, Inga R. Grin, Bakhyt T. Matkarimov, et al. "Evolutionary Origins of DNA Repair Pathways: Role of Oxygen Catastrophe in the Emergence of DNA Glycosylases." Cells 10, no. 7 (2021): 1591. http://dx.doi.org/10.3390/cells10071591.

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It was proposed that the last universal common ancestor (LUCA) evolved under high temperatures in an oxygen-free environment, similar to those found in deep-sea vents and on volcanic slopes. Therefore, spontaneous DNA decay, such as base loss and cytosine deamination, was the major factor affecting LUCA’s genome integrity. Cosmic radiation due to Earth’s weak magnetic field and alkylating metabolic radicals added to these threats. Here, we propose that ancient forms of life had only two distinct repair mechanisms: versatile apurinic/apyrimidinic (AP) endonucleases to cope with both AP sites an
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8

Delbos, Frédéric, Said Aoufouchi, Ahmad Faili, Jean-Claude Weill та Claude-Agnès Reynaud. "DNA polymerase η is the sole contributor of A/T modifications during immunoglobulin gene hypermutation in the mouse". Journal of Experimental Medicine 204, № 1 (2006): 17–23. http://dx.doi.org/10.1084/jem.20062131.

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Mutations at A/T bases within immunoglobulin genes have been shown to be generated by a repair pathway involving the DNA-binding moiety of the mismatch repair complex constituted by the MSH2–MSH6 proteins, together with DNA polymerase η (pol η). However, residual A/T mutagenesis is still observed upon inactivation in the mouse of each of these factors, suggesting that the panel of activities involved might be more complex. We reported previously (Delbos, F., A. De Smet, A. Faili, S. Aoufouchi, J.-C. Weill, and C.-A. Reynaud. 2005. J. Exp. Med. 201:1191–1196) that residual A/T mutagenesis in po
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9

Wynn, Emily, Emma Purfeerst, and Alan Christensen. "Mitochondrial DNA Repair in an Arabidopsis thaliana Uracil N-Glycosylase Mutant." Plants 9, no. 2 (2020): 261. http://dx.doi.org/10.3390/plants9020261.

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Substitution rates in plant mitochondrial genes are extremely low, indicating strong selective pressure as well as efficient repair. Plant mitochondria possess base excision repair pathways; however, many repair pathways such as nucleotide excision repair and mismatch repair appear to be absent. In the absence of these pathways, many DNA lesions must be repaired by a different mechanism. To test the hypothesis that double-strand break repair (DSBR) is that mechanism, we maintained independent self-crossing lineages of plants deficient in uracil-N-glycosylase (UNG) for 11 generations to determi
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10

Zeitlin, Samantha G., Brian R. Chapados, Norman M. Baker, Caroline Tai, Geir Slupphaug, and Jean Y. J. Wang. "Uracil DNA N-Glycosylase Promotes Assembly of Human Centromere Protein A." PLoS ONE 6, no. 3 (2011): e17151. http://dx.doi.org/10.1371/journal.pone.0017151.

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Dissertations / Theses on the topic "Uracil N-glycosylase"

1

Mohammed, Arif Sheikh. "Structural and Biochemical Studies on Mycobacterial Uracil- DNA N-glycosylase and Mut T1." Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4283.

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Maintenance of the genomic integrity of the cell is crucial for the survival and successful propagation of an organism. However, this integrity is under continuous threat from DNA-damaging agents. In addition, errors in replication and transcription, resulting in the incorporation of inappropriate bases and hence mutations, disrupt the genomic integrity. Therefore, cells have developed a number of DNA-repair and error avoidance mechanisms to maintain the genomic integrity. The genome of pathogenic mycobacteria, including Mycobacterium tuberculosis, is more prone to damage, as they are constan
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2

Kaushal, Prem Singh. "Structural Studies Of Mycobacterial Uracil-DNA Glycosylase (Ung) And Single-Stranded DNA Binding Protein (SSB)." Thesis, 2010. https://etd.iisc.ac.in/handle/2005/1432.

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For survival and successful propagation, every organism has to maintain the genomic integrity of the cell. The information content, in the form of nucleotide bases, is constantly threatened by endogenous agents and environmental pollutants. In particular, pathogenic mycobacteria are constantly exposed to DNA-damaging assaults such as reactive oxygen species (ROS) and reactive nitrogen intermediate (RNI), in their habitat which is inside host macrophage. In addition, the genome of Mycobacterium tuberculosis makes it more susceptible for guanine oxidation and cytosine deamination as it is G-C ri
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3

Kaushal, Prem Singh. "Structural Studies Of Mycobacterial Uracil-DNA Glycosylase (Ung) And Single-Stranded DNA Binding Protein (SSB)." Thesis, 2010. http://etd.iisc.ernet.in/handle/2005/1432.

Full text
Abstract:
For survival and successful propagation, every organism has to maintain the genomic integrity of the cell. The information content, in the form of nucleotide bases, is constantly threatened by endogenous agents and environmental pollutants. In particular, pathogenic mycobacteria are constantly exposed to DNA-damaging assaults such as reactive oxygen species (ROS) and reactive nitrogen intermediate (RNI), in their habitat which is inside host macrophage. In addition, the genome of Mycobacterium tuberculosis makes it more susceptible for guanine oxidation and cytosine deamination as it is G-C ri
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