Relevant bibliographies by topics / NEIL1

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Academic literature on the topic 'NEIL1'

Author: Grafiati
Published: 31 May 2022
Last updated: 7 July 2024

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Journal articles on the topic "NEIL1"

1

Shinmura, Kazuya, Hisami Kato, Yuichi Kawanishi, Hisaki Igarashi, Masanori Goto, Hong Tao, Yusuke Inoue, et al. "Abnormal Expressions of DNA Glycosylase Genes NEIL1, NEIL2, and NEIL3 Are Associated with Somatic Mutation Loads in Human Cancer." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/1546392.

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The effects of abnormalities in the DNA glycosylases NEIL1, NEIL2, and NEIL3 on human cancer have not been fully elucidated. In this paper, we found that the median somatic total mutation loads and the median somatic single nucleotide mutation loads exhibited significant inverse correlations with the median NEIL1 and NEIL2 expression levels and a significant positive correlation with the median NEIL3 expression level using data for 13 cancer types from the Cancer Genome Atlas (TCGA) database. A subset of the cancer types exhibited reduced NEIL1 and NEIL2 expressions and elevated NEIL3 expression, and such abnormal expressions of NEIL1, NEIL2, and NEIL3 were also significantly associated with the mutation loads in cancer. As a mechanism underlying the reduced expression of NEIL1 in cancer, the epigenetic silencing ofNEIL1through promoter hypermethylation was found. Finally, we investigated the reason why an elevated NEIL3 expression level was associated with an increased number of somatic mutations in cancer and found that NEIL3 expression was positively correlated with the expression of APOBEC3B, a potent inducer of mutations, in diverse cancers. These results suggested that the abnormal expressions of NEIL1, NEIL2, and NEIL3 are involved in cancer through their association with the somatic mutation load.
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2

Albelazi, Martin, Mohammed, Mutti, and Elder. "The Biochemical Role of the Human NEIL1 and NEIL3 DNA Glycosylases on Model DNA Replication Forks." Genes 10, no. 4 (April 23, 2019): 315. http://dx.doi.org/10.3390/genes10040315.

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Endonuclease VIII-like (NEIL) 1 and 3 proteins eliminate oxidative DNA base damage and psoralen DNA interstrand crosslinks through initiation of base excision repair. Current evidence points to a DNA replication associated repair function of NEIL1 and NEIL3, correlating with induced expression of the proteins in S/G2 phases of the cell cycle. However previous attempts to express and purify recombinant human NEIL3 in an active form have been challenging. In this study, both human NEIL1 and NEIL3 have been expressed and purified from E. coli, and the DNA glycosylase activity of these two proteins confirmed using single- and double-stranded DNA oligonucleotide substrates containing the oxidative bases, 5-hydroxyuracil, 8-oxoguanine and thymine glycol. To determine the biochemical role that NEIL1 and NEIL3 play during DNA replication, model replication fork substrates were designed containing the oxidized bases at one of three specific sites relative to the fork. Results indicate that whilst specificity for 5- hydroxyuracil and thymine glycol was observed, NEIL1 acts preferentially on double-stranded DNA, including the damage upstream to the replication fork, whereas NEIL3 preferentially excises oxidized bases from single stranded DNA and within open fork structures. Thus, NEIL1 and NEIL3 act in concert to remove oxidized bases from the replication fork.
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Hanna, Bishoy M. F., Maurice Michel, Thomas Helleday, and Oliver Mortusewicz. "NEIL1 and NEIL2 Are Recruited as Potential Backup for OGG1 upon OGG1 Depletion or Inhibition by TH5487." International Journal of Molecular Sciences 22, no. 9 (April 27, 2021): 4542. http://dx.doi.org/10.3390/ijms22094542.

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DNA damage caused by reactive oxygen species may result in genetic mutations or cell death. Base excision repair (BER) is the major pathway that repairs DNA oxidative damage in order to maintain genomic integrity. In mammals, eleven DNA glycosylases have been reported to initiate BER, where each recognizes a few related DNA substrate lesions with some degree of overlapping specificity. 7,8-dihydro-8-oxoguanine (8-oxoG), one of the most abundant DNA oxidative lesions, is recognized and excised mainly by 8-oxoguanine DNA glycosylase 1 (OGG1). Further oxidation of 8-oxoG generates hydantoin lesions, which are recognized by NEIL glycosylases. Here, we demonstrate that NEIL1, and to a lesser extent NEIL2, can potentially function as backup BER enzymes for OGG1 upon pharmacological inhibition or depletion of OGG1. NEIL1 recruitment kinetics and chromatin binding after DNA damage induction increase in cells treated with OGG1 inhibitor TH5487 in a dose-dependent manner, whereas NEIL2 accumulation at DNA damage sites is prolonged following OGG1 inhibition. Furthermore, depletion of OGG1 results in increased retention of NEIL1 and NEIL2 at damaged chromatin. Importantly, oxidatively stressed NEIL1- or NEIL2-depleted cells show excessive genomic 8-oxoG lesions accumulation upon OGG1 inhibition, suggesting a prospective compensatory role for NEIL1 and NEIL2. Our study thus exemplifies possible backup mechanisms within the base excision repair pathway.
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Makasheva, Kristina A., Anton V. Endutkin, and Dmitry O. Zharkov. "Requirements for DNA bubble structure for efficient cleavage by helix–two-turn–helix DNA glycosylases." Mutagenesis 35, no. 1 (November 30, 2019): 119–28. http://dx.doi.org/10.1093/mutage/gez047.

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Abstract Oxidative DNA lesions, constantly generated by both endogenous and environmentally induced reactive oxygen species, are removed via the base excision repair pathway. In bacteria, Fpg and Nei DNA glycosylases, belonging to the helix–two-turn–helix (H2TH) structural superfamily, remove oxidised purines and pyrimidines, respectively. Interestingly, the human H2TH family glycosylases, NEIL1, NEIL2 and NEIL3, have been reported to prefer oxidative lesions in DNA bubbles or single-stranded DNA. It had been hypothesised that NEIL2 might be involved in the repair of lesions in transcription bubbles; however, bubble-like structures may appear in other cellular contexts such as displacement loops (D-loops) associated with transcription, recombination or telomere maintenance. The activities of bacterial Fpg and Nei on bubble substrates were not addressed. Also, it is not known whether H2TH enzymes process bubbles containing the third DNA or RNA strand, and how the bubble length and position of the lesion within a bubble affect the excision. We have investigated the removal of 8-oxoguanine (8-oxoG) and 5,6-dihydrouracil (DHU) by Escherichia coli Fpg and Nei and human NEIL1 and NEIL2 from single-strand oligonucleotides, perfect duplexes, bubbles with different numbers of unpaired bases (6–30), bubbles containing the lesion in different positions and D-loops with the third strand made of DNA or RNA. Fpg, NEIL1 and NEIL2 efficiently excised lesions located within bubbles, with NEIL1 and NEIL2 being specific for DHU, and Fpg removing both 8-oxoG and DHU. Nei, in contrast, was significantly active only on DHU located in double-stranded DNA. Fpg and NEIL1 also tolerated the presence of the third strand of either DNA or RNA in D-loops if the lesion was in the single-stranded part, and Fpg, Nei and NEIL1 excised lesions from the double-stranded DNA part of D-loops. The presence of an additional unpaired 5′-tail of DNA or RNA did not affect the activity. No significant position preference for lesions in a 12-mer bubble was found. Overall, the activities of Fpg, NEIL1 and NEIL2 on these non-canonical substrates are consistent with the possibility that these enzymes may participate in the repair in structures arising during transcription or homologous recombination.
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Zhou, Jia, Minmin Liu, Aaron M. Fleming, Cynthia J. Burrows, and Susan S. Wallace. "Neil3 and NEIL1 DNA Glycosylases Remove Oxidative Damages from Quadruplex DNA and Exhibit Preferences for Lesions in the Telomeric Sequence Context." Journal of Biological Chemistry 288, no. 38 (August 7, 2013): 27263–72. http://dx.doi.org/10.1074/jbc.m113.479055.

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The telomeric DNA of vertebrates consists of d(TTAGGG)n tandem repeats, which can form quadruplex DNA structures in vitro and likely in vivo. Despite the fact that the G-rich telomeric DNA is susceptible to oxidation, few biochemical studies of base excision repair in telomeric DNA and quadruplex structures have been done. Here, we show that telomeric DNA containing thymine glycol (Tg), 8-oxo-7,8-dihydroguanine (8-oxoG), guanidinohydantoin (Gh), or spiroiminodihydantoin (Sp) can form quadruplex DNA structures in vitro. We have tested the base excision activities of five mammalian DNA glycosylases (NEIL1, NEIL2, mNeil3, NTH1, and OGG1) on these lesion-containing quadruplex substrates and found that only mNeil3 had excision activity on Tg in quadruplex DNA and that the glycosylase exhibited a strong preference for Tg in the telomeric sequence context. Although Sp and Gh in quadruplex DNA were good substrates for mNeil3 and NEIL1, none of the glycosylases had activity on quadruplex DNA containing 8-oxoG. In addition, NEIL1 but not mNeil3 showed enhanced glycosylase activity on Gh in the telomeric sequence context. These data suggest that one role for Neil3 and NEIL1 is to repair DNA base damages in telomeres in vivo and that Neil3 and Neil1 may function in quadruplex-mediated cellular events, such as gene regulation via removal of damaged bases from quadruplex DNA.
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Cherbuin, Nicolas, Hardip Patel, Erin I. Walsh, Ananthan Ambikairajah, Richard Burns, Anne Brüstle, and Lene Juel Rasmussen. "Cognitive Function Is Associated with the Genetically Determined Efficiency of DNA Repair Mechanisms." Genes 15, no. 2 (January 24, 2024): 153. http://dx.doi.org/10.3390/genes15020153.

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Several modifiable risk factors for neurodegeneration and dementia have been identified, although individuals vary in their vulnerability despite a similar risk of exposure. This difference in vulnerability could be explained at least in part by the variability in DNA repair mechanisms’ efficiency between individuals. Therefore, the aim of this study was to test associations between documented, prevalent genetic variation (single nucleotide polymorphism, SNP) in DNA repair genes, cognitive function, and brain structure. Community-living participants (n = 488,159; 56.54 years (8.09); 54.2% female) taking part in the UK Biobank study and for whom cognitive and genetic measures were available were included. SNPs in base excision repair (BER) genes of the bifunctional DNA glycosylases OGG1 (rs1052133, rs104893751), NEIL1 (rs7402844, rs5745906), NEIL2 (rs6601606), NEIL3 (rs10013040, rs13112390, rs13112358, rs1395479), MUTYH (rs34612342, rs200165598), NTHL1 (rs150766139, rs2516739) were considered. Cognitive measures included fluid intelligence, the symbol–digit matching task, visual matching, and trail-making. Hierarchical regression and latent class analyses were used to test the associations between SNPs and cognitive measures. Associations between SNPs and brain measures were also tested in a subset of 39,060 participants. Statistically significant associations with cognition were detected for 12 out of the 13 SNPs analyzed. The strongest effects amounted to a 1–6% difference in cognitive function detected for NEIL1 (rs7402844), NEIL2 (rs6601606), and NTHL1 (rs2516739). Associations varied by age and sex, with stronger effects detected in middle-aged women. Weaker associations with brain measures were also detected. Variability in some BER genes is associated with cognitive function and brain structure and may explain variability in the risk for neurodegeneration and dementia.
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Konis, Sifaddin M. R., Jonathan R. Hughes, and Jason L. Parsons. "TRIM26 Maintains Cell Survival in Response to Oxidative Stress through Regulating DNA Glycosylase Stability." International Journal of Molecular Sciences 23, no. 19 (October 1, 2022): 11613. http://dx.doi.org/10.3390/ijms231911613.

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Oxidative DNA base lesions in DNA are repaired through the base excision repair (BER) pathway, which consequently plays a vital role in the maintenance of genome integrity and in suppressing mutagenesis. 8-oxoguanine DNA glycosylase (OGG1), endonuclease III-like protein 1 (NTH1), and the endonuclease VIII-like proteins 1–3 (NEIL1–3) are the key enzymes that initiate repair through the excision of the oxidized base. We have previously identified that the E3 ubiquitin ligase tripartite motif 26 (TRIM26) controls the cellular response to oxidative stress through regulating both NEIL1 and NTH1, although its potential, broader role in BER is unclear. We now show that TRIM26 is a central player in determining the response to different forms of oxidative stress. Using siRNA-mediated knockdowns, we demonstrate that the resistance of cells to X-ray radiation and hydrogen peroxide generated as a consequence of trim26 depletion can be reversed through suppression of selective DNA glycosylases. In particular, a knockdown of neil1 or ogg1 can enhance sensitivity and DNA repair rates in response to X-rays, whereas a knockdown of neil1 or neil3 can produce the same effect in response to hydrogen peroxide. Our study, therefore, highlights the importance of TRIM26 in balancing cellular DNA glycosylase levels required for an efficient BER response.
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Kabziński, Jacek, Anna Walczak, Michał Mik, and Ireneusz Majsterek. "Sirt3 regulates the level of mitochondrial DNA repair activity through deacetylation of NEIL1, NEIL2, OGG1, MUTYH, APE1 and LIG3 in colorectal cancer." Polish Journal of Surgery 92, no. 1 (November 4, 2019): 1–5. http://dx.doi.org/10.5604/01.3001.0013.5539.

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Colorectal cancer (CRC) is one of the most common malignant tumors. One of the factors increasing the risk of its occurrence may be the reduced efficiency of repairing DNA damage, both nuclear and mitochondrial. The main mechanism for repairing oxidative damage is the BER system (in mitochondria mtBER), whose key proteins NEIL1, NEIL2, OGG1, MUTYH, APE1 and LIG3 obtain full efficiency only at the appropriate level of acetylation. Sirtuin 3 is a key protein for mitochondrial homeostasis, regulating a number of metabolic processes related mainly to the control of the level of reactive oxygen species. Because Sirt3 possesses acetylase activity, it can modulate the level of activity of mtBER proteins by their deacetylation. The conducted study showed that the tested proteins NEIL1, NEIL2, OGG1, MUTYH, APE1 and LIG3 are the substrate for the enzymatic deacetylation activity of Sirt3, which may lead to modulation of the risk of CRC, and in cancer cells may be a potential therapeutic target enhancing the action of cytostatic drugs.
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Kabzinski, J., A. Walczak, and I. Majsterek. "Sirt3 Regulates Response to Oxidative Stress by Interacting with BER Proteins in Colorectal Cancer." Genetics Research 2022 (April 7, 2022): 1–10. http://dx.doi.org/10.1155/2022/7299555.

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The oxidative damages are well-recognized factors in the pathogenesis of colorectal cancer (CRC). Increased levels of reactive oxygen species (ROS) can lead to oxidative DNA damage, which, if unrepaired, can be an underlying cause of cancerogenic transformation. To defend against these threats, cells have developed a range of defense mechanisms. One of the most important protection mechanisms is DNA repair systems, both nuclear and mitochondrial. Sirt3 is a mitochondrial protein involved in regulating NEIL1, NEIL2, MUTYH, APE1, and LIG3 proteins, which are involved in DNA repair, including mitochondrial repair through mtBER (mitochondrial Base Excision Repair). In this work, we show that NEIL1, NEIL2, MUTYH, APE1, and LIG3 are regulated by Sirt3 through deacetylation, and moreover, Sirt3 is directly involved in physical interaction with MUTYH, NEIL1, and APE1, which indicates the controlling role of Sirt3 over the mtBER mechanism. Also, if the cells deprived of Sirt3 are exposed to oxidative stress, altered levels of those proteins can be observed, which supports the theory of the regulatory role of Sirt3. Finally, to fully confirm the role of Sirt3 in DNA repair, we examined its role in apoptosis and found the impact of this protein on cell survival rate. Using the knowledge obtained in the course of conducted experiments, we postulate consideration of Sirt3 as a target in the rising vulnerability of cancer cells during therapy and therefore increasing the effectiveness of cancer treatment.
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Xue, Wanjuan, Yongcheng Liu, Ningning Xin, Jiyu Miao, Juan Du, Yu Wang, Haiyan Shi, et al. "Nei Endonuclease VIII-Like1 (NEIL1) Inhibits Apoptosis of Human Colorectal Cancer Cells." BioMed Research International 2020 (June 27, 2020): 1–11. http://dx.doi.org/10.1155/2020/5053975.

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The study is aimed at investigating the role of Nei endonuclease VIII-like1 (NEIL1) in the pathogenesis of colorectal cancer (CRC). The human CRC (HCT116 and SW480) cells were subjected to the siRNA silencing and recombinant plasmid overexpression of NEIL1. Transfection of siNEIL1 significantly inhibited the cell growth. It also increased the Bax expression levels, while it decreased the Bcl-2 expression levels in human CRC cells, leading the Bax/Bcl-2 balance toward apoptosis. Moreover, the apoptosis was promoted through the caspase-9 signaling pathway. One the other hand, high expression of NEIL1 promoted the cell viability and reduced the apoptosis, inducing the balance of Bax/Bcl-2 in the human colon cancer cells to be antiapoptotic. In addition, the caspase-9 signaling pathway inhibited apoptosis, contrary to the results obtained by downregulating NEIL1 expression. Furthermore, NEIL1 was negatively regulated by miR-7-5p, indicating that miR-7-5p inhibited the NEIL1 expression after transcription. Overexpression of miR-7-5p reversed the effects of NEIL1 on these CRC cells. In conclusion, NEIL1 promotes the proliferation of CRC cells, which is regulated negatively by miR-7-5p. These findings suggest that NEIL1 is a potential therapeutic target for CRC.
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Dissertations / Theses on the topic "NEIL1"

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Little, Laura Grace. "Response of a NEIL1 deficient murine epithelial cell line to chromate." CONNECT TO THIS TITLE ONLINE, 2008. http://etd.lib.umt.edu/theses/available/etd-04172008-090537/.

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Wanschoor, Paul. "Impact de la déficience de NEIL1 sur l'inflammation médiée par la voie des senseurs des ADNs cytosoliques." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL032.

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Des recherches récentes ont établi des liens essentiels entre les dommages à l'ADN, le stress réplicatif et l'inflammation, révélant ainsi un mécanisme complexe dans lequel les fragments d'acides nucléiques résultants sont exportés dans le cytosol. Une fois dans le cytosol, ces fragments peuvent être détecté par des senseurs cellulaires tels que cGAS et RIG1, qui, avec l'aide respective de STING ou MAVS, déclenche la production de cytokines inflammatoires et l'activation des réponses immunitaires innées ou des voies de la mort cellulaire. Cette découverte souligne l'importance cruciale des voies de signalisation des senseurs pour la compréhension des interactions entre dommages à l'ADN, inflammation et réponse immunitaire. La capacité à cibler spécifiquement ces voies de signalisation dans la thérapie anticancéreuse, offre des possibilités d'élimination ciblée des cellules cancéreuses et contribue aux effets abscopaux observés après irradiation grâce à l'activation du système immunitaire. La compréhension approfondie des mécanismes sous-jacents à la production de ces fragments d'acides nucléiques pourrait permettre d'identifier de nouvelles cibles thérapeutiques pour moduler l'inflammation et renforcer les réponses thérapeutiques.Le stress oxydatif induit par des traitements anticancéreux tels que la radiothérapie, peut entraîner des dommages à l'ADN et provoquer un stress réplicatif. Cette thèse se concentre sur le rôle du mécanisme de réparation par excision de base (BER). Au sein du BER, j'ai porté une attention particulière au rôle d'une glycosylase, protéine clef qui initie la voie du BER en reconnaissant les bases endommagées et en les excisant notamment lors de la réplication de l'ADN. En étudiant l'interaction entre le BER et les voies de signalisation des senseurs de l'ADN cytosolique, cette recherche vise à approfondir notre compréhension de l'impact de la gestion des dommages oxydatifs et de l'inflammation dans le contexte du cancer.Une meilleure compréhension de ces interactions pourrait non seulement permettre d'améliorer les réponses thérapeutiques anticancéreuses, mais également contribuer à prédire les résultats des traitements chez les patients. En conclusion, l'étude de ces mécanismes complexes ouvre la voie à de nouvelles perspectives thérapeutiques dans la lutte contre le cancer, en exploitant les liens intimes entre dommages à l'ADN, inflammation et réponse immunitaire pour développer des thérapies plus ciblées et efficaces
Recent studies have established essential links between DNA damage, replicative stress, and inflammation, revealing a complex mechanism in which the resulting nucleic acid fragments are exported into the cytosol. Once in the cytosol, these fragments can be detected by cellular sensors such as cGAS and RIG1, which, with the help of STING or MAVS repectively, trigger the production of inflammatory cytokines and activation of innate immune responses or cell death pathways. This discovery underlines the crucial importance of sensor signaling pathways for understanding the interactions between DNA damage, inflammation and immune response. The ability to specifically target these signaling pathways in cancer therapy, offers possibilities for targeted elimination of cancer cells and contributes to the abscopal effects observed after irradiation through activation of the immune system. A deeper understanding of the mechanisms underlying the production of these nucleic acid fragments could lead to the identification of new therapeutic targets to modulate inflammation and enhance therapeutic responses.Oxidative stress induced by anticancer treatments such as radiotherapy, can lead to DNA damage and cause replicative stress. This thesis focuses on the role of the base excision repair (BER) mechanism. Within BER, special attention has been paid to the role of a glycosylase, a key protein that initiates the BER pathway by recognizing damaged bases and excising them, notably during DNA replication. By elucidating the interaction between BER and cytosolic DNA sensor signaling pathways, this research aims to deepen our understanding of the impact of oxidative damage management and inflammation in the context of cancer.A better understanding of these interactions could not only lead to improve anticancer therapeutic responses, but also help predict treatment outcomes in patients. In conclusion, the study of these complex mechanisms opens the way to new therapeutic perspectives in the fight against cancer, by exploiting the intimate links between DNA damage, inflammation, and immune response to develop more targeted and effective therapies
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Cros, Julien. "OGG1 et NEIL1, de nouvelles cibles pour la lutte contre le cancer : recherche et caractérisation fonctionnelle et structurale d’inhibiteurs." Thesis, Orléans, 2021. https://theses.univ-orleans.fr/prive/accesESR/2021ORLE3145_va.pdf.

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L’ADN de tout organisme est continuellement endommagé par des agents physiques ou chimiques d’origines endogène ou exogène. Les dommages de l’ADN qui en résultent peuvent être à l’origine de l’apparition de mutations ou de mort cellulaire. Pour pallier à ces effets délétères, les organismes ont développé des systèmes de réparation de l’ADN. Le système de réparation par excision de base (BER) est la voie majeure de réparation des bases endommagées et est initié par des ADN glycosylases telles que hOGG1 et hNEIL1. Ces enzymes reconnaissent spécifiquement les bases lésées et les éliminent. Paradoxalement, les réparations initiées par ces protéines peuvent diminuer l’effet thérapeutique de certains traitements, notamment anti-cancéreux. En exploitant le principe de létalité synthétique, le ciblage thérapeutique de hOGG1 et hNEIL1 pourrait être pertinent pour lutter contre certains cancers, mais aussi contre des maladies neurodégénératives (Huntington) ou des processus inflammatoires pathologiques. Au travers du criblage « moyen débit » de banques de petites molécules naturelles ou synthétiques, mon travail de thèse a consisté en l’identification de nouveaux inhibiteurs sélectifs de hNEIL1 et hOGG1 et en la caractérisation de leur mode d’action par des études biochimiques et structurales. Si nous avons pu mettre en lumière des fonctions chimiques essentielles et quelques déterminants structuraux et fonctionnels relatifs à leurs modes d’action, de nombreuses zones d’ombre demeurent et mériterons d’être explorés dans le futur. En revanche, l’utilisation d’un homologue archéen de hOGG1, l’enzyme PabAGOG, a permis de proposer un modèle tridimensionnel cohérent d’un complexe hOGG1/inhibiteur pour l’un des meilleurs inhibiteurs que nous avons identifiés. Finalement, ces nouveaux composés comptent parmi les meilleurs inhibiteurs de hOGG1 et hNEIL1 identifiés à ce jour et certains d’entre eux devraient bénéficier d’une évaluation in cellulo
DNA is continuously damaged by physical or chemical agents from endogenous or exogenous sources. These damages can induce mutation or cell death. To counteract these deleterious effects, organisms have developed DNA repair systems. The Base Excision Repair System (BER) is the major pathway to repair damaged bases. It is initiated by DNA Glycosylases such as hNEIL1 and hOGG1 which specifically recognize and remove oxidized bases. However, in some situation like conventional cancer treatment, the repairs initiated by these enzymes can lead to therapeutic resistance. Therefore, based on the synthetic lethality concept, selective inhibition of hNEIL1 and hOGG1 could be relevant in some pathologic contexts like cancer, but also against neurodegenerative diseases (Huntington) or pathological inflammatory processes. This thesis work aimed to identify new selective inhibitors of hNEIL1 and hOGG1 with a "medium throughput" screening of natural or synthetic small molecule libraries, and to characterize their mode of action through biochemical and structural studies. Although we identified some essentials chemicals functions and some leads to understand the action mode of our inhibitors, many areas remains unveiled and deserve to be explored in the future. However, the use of an archaeal homologue of hOGG1, the enzyme PabAGOG, has allowed us to propose a coherent three-dimensional model of an hOGG1/inhibitor complex for one of the best inhibitors we have identified. Finally, these new inhibitors are among the best inhibitors of hOGG1 and hNEIL1 identified to date and some of them will undergo in cellulo evaluation
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Curtis, Jenefer. "Neil Postman on television." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ57764.pdf.

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5

Pernot-Deschamps, Marguerite. "L'oeuvre de Neil Jordan." Paris 3, 1991. http://www.theses.fr/1993PA030034.

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Neil jordan, crivain et realisateur irlandais contemporain, reflete par son oeuvre la transition culturelle que, d'apres richard kearney, l'irlande connait depuis quelque temps. Ses nouvelles, ses romans et ses cinq films presentent un melange de tradition et d'innovation qui caracterise aussi son pays. De l'ensemble de ses oeuvres se degagent trois themes principaux: l'autre; le temps; le reel et l'apparence. Les etres de l'univers de neil jordan, adolescents ou adultes, souffrent de solitude et d'incomprehension dans une vie faite d'ennui ou de routine. Dans les oeuvres, le temps se brise: la linearite traditionnelle eclate en plusieurs modes d'apprehension du temps. Le theme du reel et de l'apparence resume la forme de pensee de l'ecrivain-realisateur qui aime partir de bases realistes pour entrainer lecteurs et spectateurs dans des zones d'ombres etranges et inconnues
Neil jordan, an irish writer-director in his forties, seems to epitomize in his work the cultural transition that, according to richard kearney, ireland has experienced for some time. His short stories, novels and five films all partake of a mexiture of tradition and innovation which is also characteristic of his own country. Three main themes can be studied in his works: other people; time; reality and appearance. People in neil jordan's world, whether teenagers or grown-ups, suffer from solitude and lack of communication in a life of boredom or routine. In his work, time is broken: the traditional linear narrative is replaced by various ways of representing time. The theme of reality and appearance encapsulates the writer-director's creative attitude: starting from realistic beginnings and rradually leading readers and spectators to an unknown, shadowy world
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Curtis, Jenefer (Jenefer Ann) Carleton University Dissertation Journalism and Communication. "Neil postman on television." Ottawa, 2000.

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7

Eiden, Nicole. "Neil and the nun." ScholarWorks@UNO, 2004. http://louisdl.louislibraries.org/u?/NOD,89.

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Thesis (M.A.)--University of New Orleans, 2004.
Title from electronic submission form. "A thesis ... in partial fulfillment of the requirements for the degree of Master of Fine Arts in the Department of Drama and Communication."--Thesis t.p. Vita. Includes bibliographical references.
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Kühn, Axel D. "A.S. Neill und Summerhill eine Rezeptions- und Wirkungsanalyse /." [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965433013.

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9

Roedl, T. "Investigating the biological role of human NEIL3." Thesis, University of Salford, 2013. http://usir.salford.ac.uk/29368/.

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Oxidised bases in DNA are removed by a number of DNA glycosylases in the first step of base excision repair. These include 8-oxoguanine DNA glycosylase (OGG1), endonuclease III-like 1 (NTH1) and the Nei-like proteins, NEIL1, NEIL2 and NEIL3. While NEIL1 and NEIL2 are relatively well characterized, the function of NEIL3 is still not fully understood. Although all three proteins show homology to the Escherichia coli Fpg/Nei family, NEIL3 is the largest member with an extended C-terminal domain and contains a valine instead of the highly conserved proline residue at amino acid position two. While it has been reported that recombinant murine NEIL3 shows DNA glycosylase and AP lyase activities in vitro, its biological role remains unclear. Therefore, to gain an insight into the function of NEIL3 in vivo, the full-length human NEIL3 cDNA has been expressed in Saccharomyces cerevisae as a prelude to undertake a yeast 2-hybrid screen to determine specific protein-protein interactions. To date, cDNA library screenings for potential hNEIL3 interactors have been completed and clones expressing potential interactors have been isolated, sequenced and analysed. This data, along with the results of other confirmatory experiments are presented in this thesis. Furthermore, clones of Pichia pastoris harbouring an expression cassette with full-length human NEIL3 or mouse NEIL1 or truncated versions of hNEIL3 with amino acid length 1-394 and 1-502 cDNA have been generated in preparation for its overexpression in a eukaryotic system. It is envisaged that the expression of 6XHis tagged hNEIL3 in P. pastoris will enable the purification of hNEIL3 protein that can be used in enzyme assays and for further in vitro investigations of putative protein interactions discovered by yeast two-hybrid (Y2H) screen.
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Laplace, Philippe. "Les Hautes-Terres, l'histoire et la mémoire dans les romans de Neil M. Gunn." Besançon : Presses universitaires de Franche-Comté, 2006. http://catalogue.bnf.fr/ark:/12148/cb40170360s.

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Books on the topic "NEIL1"

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Jones, Iris Carter. Neal notes: Neal/Neale/Neel/Neele/Neil/Neile, all spellings of the surname. Sacramento, Calif: Links Genealogy Publications, 1988.

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Harvey, Lois Gerstenberger. The Neal name book: Nail, Naille, Nale, Nall, Nalle, Neal, Neel, Neele, Neil, Neill, Niel, Null. Decatur, IL (3766 Colin Ct., Decatur 62526): L.G. Harvey, 1985.

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William, Neill, Neill Uilleam, and Morrison David 1941-, eds. Scotia review: William Neill Uilleam Neill issue. Wick): Scotia Review (18, MacArthur Street, Wick, Caithness KW1 5AX, Scotland, 2001.

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Christie, Agatha. Egklema sto Neilo. Athens: Minoas, 2000.

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O'Neill =: Ó Neill. Dublin: Gill & Macmillan, 2003.

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Neil Kinnock. London: R. Hale, 1994.

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Hickson, Kevin. Neil Kinnock. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003254393.

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Petridis, Alexis. Neil Young. London: Unanimous, 2000.

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Pramaggiore, Maria. Neil Jordan. Urbana: University of Illinois Press, 2007.

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Nina, Volkova. Neil: Roman. Sankt-Peterburg: Inapress, 2005.

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Book chapters on the topic "NEIL1"

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McDonald, Drew T., Pam S. Wang, Jennifer Moitoza Johnson, and Miaw-Sheue Tsai. "Using Affinity Pulldown Assays to Study Protein–Protein Interactions of Human NEIL1 Glycosylase and the Checkpoint Protein RAD9–RAD1–HUS1 (9-1-1) Complex." In Base Excision Repair Pathway, 199–207. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3373-1_13.

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McDonald, Drew T., Pam S. Wang, Jennifer Moitoza Johnson, and Miaw-Sheue Tsai. "Using Affinity Pulldown Assays to Study Protein–Protein Interactions of Human NEIL1 Glycosylase and the Checkpoint Protein RAD9–RAD1–HUS1 (9-1-1) Complex." In Base Excision Repair Pathway, 199–207. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3373-1_13.

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Hickson, Kevin. "Kinnock's Socialism." In Neil Kinnock, 19–28. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003254393-4.

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Turner, Alwyn. "'A Lot of Fun with the Kids'." In Neil Kinnock, 53–62. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003254393-7.

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Clarke, Charles. "Working in the Kinnock Team." In Neil Kinnock, 205–9. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003254393-21.

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Williams, Ben. "Social Policy." In Neil Kinnock, 124–38. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003254393-14.

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Seldon, Anthony. "Neil Kinnock Reflects." In Neil Kinnock, 7–18. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003254393-3.

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Taylor, Harry. "Tackling the Trots." In Neil Kinnock, 74–82. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003254393-9.

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Lee, Simon. "One Nation Socialism." In Neil Kinnock, 42–52. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003254393-6.

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Wainwright, Hilary. "A Tale of Two Parties Revisited." In Neil Kinnock, 244–51. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003254393-29.

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Conference papers on the topic "NEIL1"

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Sweasy, Joann B., Heather Galick, Scott Kathe, and Susan Wallace. "Abstract 3590: A Neil1 DNA glycosylase germline variant induces genomic instability and cellular transformation." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3590.

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Rathi, Radhika, Surabhi Suchanti, Prashant Povel Dwivedi, Gyanendra Singh, Abhijeet Singh, and Rajeev Mishra. "Hyper-methylation of DNA damage repair genes in KIRP: NEIL1/LIG4 is almost exclusively methylated in KIRP." In PROCEEDINGS OF THE 11TH INTERNATIONAL ADVANCES IN APPLIED PHYSICS AND MATERIALS SCIENCE CONGRESS & EXHIBITION. AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0139217.

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Paul, Titan C., A. K. M. M. Morshed, Elise B. Fox, Ann E. Visser, Nicholas J. Bridges, and Jamil A. Khan. "Natural Convection in Rectangular Cavity With Nanoparticle Enhanced Ionic Liquids (NEILs)." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-88297.

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A systematic natural convection heat transfer experiment has been carried out of nanoparticle enhanced ionic liquids (NEILs) in rectangular enclosures (lengthxwidthxheight, 50×50×50mm and 50×50×75mm) heated from below condition. In the present experiment NEIL was made of N-butyl-N-methylpyrrolidinium bis{(trifluoromethyl)sulfonyl} imide, ([C4mpyrr][NTf2]) ionic liquid with 0.5% (weight%) Al2O3 nanoparticles. In addition to characterize the natural convection behavior of NEIL, thermophysical properties such as thermal conductivity, heat capacity, and viscosity were also measured. The result shows that the thermal conductivity of NEIL enhanced ∼3% from the base ionic liquid (IL), heat capacity enhanced ∼12% over the measured temperature range. The natural convection experimental result shows consistent for two different enclosures based on the degrading natural convection heat transfer rate over the measured Rayleigh number range. Possible reasons of the degradation of natural convection heat transfer may be the relative change of the thermophysical properties of NEIL compare to the base ionic liquid.
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Dizdaroglu, Miral. "Abstract 618: Identification and quantification of human DNA repair protein NEIL1 by liquid chromatography/isotope-dilution tandem mass spectrometry as a potential cancer biomarker." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-618.

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Neill, Ben, and Bill Jones. "Ben Neill and Bill Jones." In the 28th of the international conference extended abstracts. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1753846.1753927.

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Bing, Wang. "Exploring Neil Simon’s Humor Art." In Annual International Conference on Language, Literature and Linguistics. Global Science & Technology Forum (GSTF), 2015. http://dx.doi.org/10.5176/2251-3566_l315.98.

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Henglein, Fritz. "In memoriam Neil Deaton Jones." In PEPM '24: 2024 ACM SIGPLAN International Workshop on Partial Evaluation and Program Manipulation. New York, NY, USA: ACM, 2024. http://dx.doi.org/10.1145/3635800.3639464.

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Paul, Titan C., A. K. M. M. Morshed, Elise B. Fox, Ann E. Visser, Nicholas J. Bridges, and Jamil A. Khan. "Enhanced Thermal Performance of Ionic Liquid-Al2O3 Nanofluid as Heat Transfer Fluid for Solar Collector." In ASME 2013 7th International Conference on Energy Sustainability collocated with the ASME 2013 Heat Transfer Summer Conference and the ASME 2013 11th International Conference on Fuel Cell Science, Engineering and Technology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/es2013-18145.

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Next generation Concentrating Solar Power (CSP) system requires high operating temperature and high heat storage capacity heat transfer fluid (HTF), which can significantly increase the overall system efficiency for power generation. In the last decade several research going on the efficacy of ionic liquids (ILs) as a HTF in CSP system. ILs possesses superior thermophysical properties compare to currently using HTF such as Therminol VP-1 (mixture of biphenyl and diphenyl oxide) and thermal oil. However, advanced thermophysical properties of ILs can be achieved by dispersing small volume percentage of nanoparticles forming nanofluids, which is called Nanoparticle Enhanced Ionic Liquids (NEILs). In the present study NEILs were prepared by dispersing 0.5% Al2O3 nanoparticles (spherical and whiskers) in N-butyl-N, N, N-trimetylammonium bis(trifluormethylsulfonyl)imide ([N4111][NTf2]) IL. Viscosity, heat capacity and thermal conductivity of NEILs were measured experimentally and compared with the existing theoretical models for liquid–solid suspensions. Additional, the convective heat transfer experiment was performed to investigate thermal performance. The thermal conductivity of NEILs enhanced by ∼5%, heat capacity enhanced by ∼20% compared to the base IL, which also gives 15% enhancement in heat transfer performance.
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Chen, Xinlei, Abhinav Shrivastava, and Abhinav Gupta. "NEIL: Extracting Visual Knowledge from Web Data." In 2013 IEEE International Conference on Computer Vision (ICCV). IEEE, 2013. http://dx.doi.org/10.1109/iccv.2013.178.

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Hussaini, Bushra, Melanie J. Hopkins, Anastasia Rashkova, and Matthew Garb. "HONORING THE LEGACY OF NEIL H. LANDMAN." In GSA Connects 2023 Meeting in Pittsburgh, Pennsylvania. Geological Society of America, 2023. http://dx.doi.org/10.1130/abs/2023am-391154.

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Reports on the topic "NEIL1"

1

Dunne, Neil, Greta Cattabriga, and Nathan O’Néill. Narrating Homeownership: Media Discourse and Lived Experiences of Mortgaged Homeownership in Sweden. Malmö University, 2023. http://dx.doi.org/10.24834/isbn.9789178773497.

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In the housing literature, Sweden is often portrayed as a so-called “cost-rental” society associated with tenure neutrality, where rental housing should be an attractive alternative – and not just a step in the way – to homeownership. A large and well-developed rental sector has traditionally made it possible for young adults to leave their family home at a relatively young age. However, this logic has been clearly disrupted as rental housing has become harder to access and homeownership has been favoured by incremental ideological political shifts and fiscal policy encouraging homeownership. As more households – also young ones – are steered into homeownership, Sweden has become one of the most mortgage-indebted nations in the OECD. This working paper on homeownership and mortgagization takes on the question of mortgaged indebtedness in discourse and practice. The working paper is the joint product of two different studies written as part of the research internship in the project “Financialisation of everyday life. Intersectional perspectives on housing and labor precarity” at Malmö university, led by Chiara Valli. In the first section, Neil Dunne presents a discourse analysis on how homeownership has been discussed in the largest newspapers in Sweden over the last decades, while Greta Cattabriga and Nathan O’Néill in the second section discuss perceptions and lived experiences of mortgaged homeownership on the basis of interviews with young adults. Put together, the two studies contribute with significant additions to the discussion about whether Sweden is moving towards a homeownership society and what the potential consequences are for young adults.
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