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Добірка наукової літератури з теми "HNEIL1"

Автор: Grafiati
Опубліковано: 31 травня 2022

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Статті в журналах з теми "HNEIL1"

1

Rieux, Charlotte, Stéphane Goffinont, Franck Coste, Zahira Tber, Julien Cros, Vincent Roy, Martine Guérin, et al. "Thiopurine Derivative-Induced Fpg/Nei DNA Glycosylase Inhibition: Structural, Dynamic and Functional Insights." International Journal of Molecular Sciences 21, no. 6 (March 17, 2020): 2058. http://dx.doi.org/10.3390/ijms21062058.

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DNA glycosylases are emerging as relevant pharmacological targets in inflammation, cancer and neurodegenerative diseases. Consequently, the search for inhibitors of these enzymes has become a very active research field. As a continuation of previous work that showed that 2-thioxanthine (2TX) is an irreversible inhibitor of zinc finger (ZnF)-containing Fpg/Nei DNA glycosylases, we designed and synthesized a mini-library of 2TX-derivatives (TXn) and evaluated their ability to inhibit Fpg/Nei enzymes. Among forty compounds, four TXn were better inhibitors than 2TX for Fpg. Unexpectedly, but very interestingly, two dithiolated derivatives more selectively and efficiently inhibit the zincless finger (ZnLF)-containing enzymes (human and mimivirus Neil1 DNA glycosylases hNeil1 and MvNei1, respectively). By combining chemistry, biochemistry, mass spectrometry, blind and flexible docking and X-ray structure analysis, we localized new TXn binding sites on Fpg/Nei enzymes. This endeavor allowed us to decipher at the atomic level the mode of action for the best TXn inhibitors on the ZnF-containing enzymes. We discovered an original inhibition mechanism for the ZnLF-containing Fpg/Nei DNA glycosylases by disulfide cyclic trimeric forms of dithiopurines. This work paves the way for the design and synthesis of a new structural class of inhibitors for selective pharmacological targeting of hNeil1 in cancer and neurodegenerative diseases.
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2

Jia, Lei, Vladimir Shafirovich, Nicholas E. Geacintov, and Suse Broyde. "Lesion Specificity in the Base Excision Repair Enzyme hNeil1: Modeling and Dynamics Studies†." Biochemistry 46, no. 18 (May 2007): 5305–14. http://dx.doi.org/10.1021/bi062269m.

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3

Krishnamurthy, Nirmala, Xiaobei Zhao, Cynthia J. Burrows, and Sheila S. David. "Superior Removal of Hydantoin Lesions Relative to Other Oxidized Bases by the Human DNA Glycosylase hNEIL1†." Biochemistry 47, no. 27 (July 2008): 7137–46. http://dx.doi.org/10.1021/bi800160s.

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4

Ocampo-Hafalla, Maria T., Alvin Altamirano, Ashis K. Basu, Michael K. Chan, Jose Eliseo A. Ocampo, Archie Cummings, Robert J. Boorstein, Richard P. Cunningham, and George W. Teebor. "Repair of thymine glycol by hNth1 and hNeil1 is modulated by base pairing and cis–trans epimerization." DNA Repair 5, no. 4 (April 2006): 444–54. http://dx.doi.org/10.1016/j.dnarep.2005.12.004.

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5

Zhang, Qiu-Mei, Shin-Ichiro Yonekura, Masashi Takao, Akira Yasui, Hiroshi Sugiyama, and Shuji Yonei. "DNA glycosylase activities for thymine residues oxidized in the methyl group are functions of the hNEIL1 and hNTH1 enzymes in human cells." DNA Repair 4, no. 1 (January 2005): 71–79. http://dx.doi.org/10.1016/j.dnarep.2004.08.002.

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6

Kakhkharova, Zarina I., Dmitry O. Zharkov, and Inga R. Grin. "A Low-Activity Polymorphic Variant of Human NEIL2 DNA Glycosylase." International Journal of Molecular Sciences 23, no. 4 (February 17, 2022): 2212. http://dx.doi.org/10.3390/ijms23042212.

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Human NEIL2 DNA glycosylase (hNEIL2) is a base excision repair protein that removes oxidative lesions from DNA. A distinctive feature of hNEIL2 is its preference for the lesions in bubbles and other non-canonical DNA structures. Although a number of associations of polymorphisms in the hNEIL2 gene were reported, there is little data on the functionality of the encoded protein variants, as follows: only hNEIL2 R103Q was described as unaffected, and R257L, as less proficient in supporting the repair in a reconstituted system. Here, we report the biochemical characterization of two hNEIL2 variants found as polymorphisms in the general population, R103W and P304T. Arg103 is located in a long disordered segment within the N-terminal domain of hNEIL2, while Pro304 occupies a position in the β-turn of the DNA-binding zinc finger motif. Similar to the wild-type protein, both of the variants could catalyze base excision and nick DNA by β-elimination but demonstrated a lower affinity for DNA. Steady-state kinetics indicates that the P304T variant has its catalytic efficiency (in terms of kcat/KM) reduced ~5-fold compared with the wild-type hNEIL2, whereas the R103W enzyme is much less affected. The P304T variant was also less proficient than the wild-type, or R103W hNEIL2, in the removal of damaged bases from single-stranded and bubble-containing DNA. Overall, hNEIL2 P304T could be worthy of a detailed epidemiological analysis as a possible cancer risk modifier.
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7

Kaplan. "Jón Hnefill Aðalsteinsson (1927-2010)." Journal of American Folklore 124, no. 494 (2011): 318. http://dx.doi.org/10.5406/jamerfolk.124.494.0318.

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8

Fleming, Aaron M., and Cynthia J. Burrows. "Formation and processing of DNA damage substrates for the hNEIL enzymes." Free Radical Biology and Medicine 107 (June 2017): 35–52. http://dx.doi.org/10.1016/j.freeradbiomed.2016.11.030.

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9

Schaller, F. "In memoriam Wilhelm K�hnelt 1905?1988." Biology and Fertility of Soils 9, no. 2 (April 1990): 91–92. http://dx.doi.org/10.1007/bf00335788.

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10

Sogawa, Chiharu, Kei Kumagai, Norio Sogawa, Katsuya Morita, Toshihiro Dohi, and Shigeo Kitayama. "C-terminal region regulates the functional expression of human noradrenaline transporter splice variants." Biochemical Journal 401, no. 1 (December 11, 2006): 185–95. http://dx.doi.org/10.1042/bj20060495.

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The NET [noradrenaline (norepinephrine) transporter], an Na+/Cl−-dependent neurotransmitter transporter, has several isoforms produced by alternative splicing in the C-terminal region, each differing in expression and function. We characterized the two major isoforms of human NET, hNET1, which has seven C-terminal amino acids encoded by exon 15, and hNET2, which has 18 amino acids encoded by exon 16, by site-directed mutagenesis in combination with NE (noradrenaline) uptake assays and cell surface biotinylation. Mutants lacking one third or more of the 24 amino acids encoded by exon 14 exhibited neither cell surface expression nor NE uptake activity, with the exception of the mutant lacking the last eight amino acids of hNET2, whose expression and uptake resembled that of the WT (wild-type). A triple alanine replacement of a candidate motif (ENE) in this region mimicked the influences of the truncation. Deletion of either the last three or another four amino acids of the C-terminus encoded by exon 15 in hNET1 reduced the cell surface expression and NE uptake, whereas deletion of all seven residues reduced the transport activity but did not affect the cell surface expression. Replacement of RRR, an endoplasmic reticulum retention motif, by alanine residues in the C-terminus of hNET2 resulted in a similar expression and function compared with the WT, while partly recovering the effects of the mutation of ENE. These findings suggest that in addition to the function of the C-terminus, the common proximal region encoded by exon 14 regulates the functional expression of splice variants, such as hNET1 and hNET2.
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Більше джерел

Дисертації з теми "HNEIL1"

1

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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Книги з теми "HNEIL1"

1

Institute, Hawaii Natural Energy, and University of Hawaii at Manoa. School of Ocean and Earth Science and Technology., eds. HNEI at 20. [Manoa]: School of Ocean and Earth Science and Technology, University of Hawaii at Manoa, 1994.

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2

j̈Ø lŁf og j̇Ø trĐ: Ritger ir helga ar JØni Hnefli A alsteinssyni. [ReykjavŁk]: j̈Ø saga, 2003.

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Частини книг з теми "HNEIL1"

1

Neill, D., B. Hoist, C. Yu, N. Huang, and J. Wei. "HNEI WIND-HYDROGEN PROGRAM." In Hydrogen Energy Progress VIII, 71–77. Elsevier, 1990. http://dx.doi.org/10.1016/b978-0-08-040408-0.50014-6.

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Тези доповідей конференцій з теми "HNEIL1"

1

"Single-nucleotide polymorphisms of hNEIL2 gene: from protein structure to functions in base excision DNA repair." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-350.

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Звіти організацій з теми "HNEIL1"

1

UHM/HNEI EV test and evaluation program. Office of Scientific and Technical Information (OSTI), March 1992. http://dx.doi.org/10.2172/5407882.

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2

UHM/HNEI EV test and evaluation program. Final report. Office of Scientific and Technical Information (OSTI), March 1992. http://dx.doi.org/10.2172/10137687.

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