Добірка наукової літератури з теми "Zinc; genomic stability; DNA damage"
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Статті в журналах з теми "Zinc; genomic stability; DNA damage"
Hosseinpour, Arash, Kamil Haliloglu, Kagan Tolga Cinisli, Guller Ozkan, Halil Ibrahim Ozturk, Alireza Pour-Aboughadareh, and Peter Poczai. "Application of Zinc Oxide Nanoparticles and Plant Growth Promoting Bacteria Reduces Genetic Impairment under Salt Stress in Tomato (Solanum lycopersicum L. ‘Linda’)." Agriculture 10, no. 11 (November 3, 2020): 521. http://dx.doi.org/10.3390/agriculture10110521.
Повний текст джерелаAbdel-Halim, Khaled Yassin, Safaa Ramadan Osman, Atef Mohamed Khedr Nassar, Alaa Khozimy, and Heba Mohamed El-Danasoury. "Use of DNA adduct and histopathological defects as indications for bio-persistence potency of zinc oxide nanoparticles in gastropod, Monacha cartusiana (Mǜller) after short-term exposure." Environmental Analysis Health and Toxicology 37, no. 3 (September 8, 2022): e2022025. http://dx.doi.org/10.5620/eaht.2022025.
Повний текст джерелаJohnson, R. E., S. T. Henderson, T. D. Petes, S. Prakash, M. Bankmann, and L. Prakash. "Saccharomyces cerevisiae RAD5-encoded DNA repair protein contains DNA helicase and zinc-binding sequence motifs and affects the stability of simple repetitive sequences in the genome." Molecular and Cellular Biology 12, no. 9 (September 1992): 3807–18. http://dx.doi.org/10.1128/mcb.12.9.3807-3818.1992.
Повний текст джерелаJohnson, R. E., S. T. Henderson, T. D. Petes, S. Prakash, M. Bankmann, and L. Prakash. "Saccharomyces cerevisiae RAD5-encoded DNA repair protein contains DNA helicase and zinc-binding sequence motifs and affects the stability of simple repetitive sequences in the genome." Molecular and Cellular Biology 12, no. 9 (September 1992): 3807–18. http://dx.doi.org/10.1128/mcb.12.9.3807.
Повний текст джерелаSrivastav, Anurag Kumar, Akhilesh Kumar, Jyoti Prakash, Dhirendra Singh, Pankaj Jagdale, Jai Shankar, and Mahadeo Kumar. "Genotoxicity evaluation of zinc oxide nanoparticles in Swiss mice after oral administration using chromosomal aberration, micronuclei, semen analysis, and RAPD profile." Toxicology and Industrial Health 33, no. 11 (September 26, 2017): 821–34. http://dx.doi.org/10.1177/0748233717717842.
Повний текст джерелаLee, Su-jin, Han Byeol Oh, and Sung-il Yoon. "Crystal Structure of the Recombination Mediator Protein RecO from Campylobacter jejuni and Its Interaction with DNA and a Zinc Ion." International Journal of Molecular Sciences 23, no. 17 (August 26, 2022): 9667. http://dx.doi.org/10.3390/ijms23179667.
Повний текст джерелаVoisset, Edwige, Eva Moravcsik, Eva W. Stratford, Amie Jaye, Christopher J. Palgrave, Robert K. Hills, Paolo Salomoni, Scott C. Kogan, Ellen Solomon, and David Grimwade. "Pml Nuclear Body Disruption Cooperates in APL Pathogenesis, Impacting DNA Damage Repair Pathways." Blood 128, no. 22 (December 2, 2016): 742. http://dx.doi.org/10.1182/blood.v128.22.742.742.
Повний текст джерелаIshikawa, Kazuhiro, Hideshi Ishii, and Toshiyuki Saito. "DNA Damage-Dependent Cell Cycle Checkpoints and Genomic Stability." DNA and Cell Biology 25, no. 7 (July 2006): 406–11. http://dx.doi.org/10.1089/dna.2006.25.406.
Повний текст джерелаZong, Chunyan, Tianyu Zhu, Jie He, Rui Huang, Renbing Jia, and Jianfeng Shen. "PARP mediated DNA damage response, genomic stability and immune responses." International Journal of Cancer 150, no. 11 (January 12, 2022): 1745–59. http://dx.doi.org/10.1002/ijc.33918.
Повний текст джерелаLavin, Martin F., Geoff Birrell, Philip Chen, Sergei Kozlov, Shaun Scott, and Nuri Gueven. "ATM signaling and genomic stability in response to DNA damage." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 569, no. 1-2 (January 2005): 123–32. http://dx.doi.org/10.1016/j.mrfmmm.2004.04.020.
Повний текст джерелаДисертації з теми "Zinc; genomic stability; DNA damage"
Li, Han. "Impact of KU80 in genomic stability, cancer and aging: a dissertation /." San Antonio : UTHSC, 2007. http://proquest.umi.com/pqdweb?did=1324370271&sid=2&Fmt=2&clientId=70986&RQT=309&VName=PQD.
Повний текст джерелаSilva, Gisele Espinha Teixeira da. "Sinalização da GTPase RhoA nas respostas celulares após estresse genotóxico promovido por radiação ultravioleta." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-19102016-165552/.
Повний текст джерелаThe RhoA GTPase signaling pathway acts on many cellular processes. To evaluate this possible RhoA function after stress caused by ultraviolet radiation, mutant clones expressing RhoA in its constitutively active or dominant negative forms were generated. After exposure of the cells to ultraviolet radiation, cell lines showed a higher sensitivity and a delayed recovery capacity when the RhoA activity is reduced. The impaired repair reduced the cells proliferation and survival under RhoA deficiency. In cell lines deficient in NER pathway, we notice that these cell lines, have a further reduced ability to repair damaged DNA under RhoA inhibition.
Osaki, Juliana Harumi. "O papel de RhoA e Rac1 GTPases nas respostas celulares após danos no DNA induzidos por radiação ionizante gama." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-22092015-075415/.
Повний текст джерелаThe mechanism by which a cell responds to DNA damage is extremely important. This occurs by a quick activation of the DNA damage repair machinery, which consists of an intricate protein signaling network culminating in DNA repair. But if the damages are irreparable occurs there is activation of cell death mechanisms. RhoA and Rac1 belong to family of small Rho GTPases, signaling proteins that act as molecular switches cycling between the active state (GTP-bound) and inactive state (GDP-bound). Members of this family are implicated in the control of diverse cellular process such as cytoskeletal remodeling, migration, adhesion, endocytosis, cell cycle progression, and oncogenesis. However, despite Rho proteins are involved in a broad spectrum of biological activities, there is just a few information about their roles in the maintenance of genomic integrity, that is, when the cells are subjected to some kinf of genotoxic agent. To investigate the involvement of the GTPases RhoA and Rac1 in cellular responses to gamma radiation, we generated from human cervix carcinoma cells - HeLa, clonal sublines of RhoA and Rac1 mutants, exogenous and stably expressing the constitutively active RhoA (HeLa-RhoA V14), the dominant negative RhoA (HeLa-RhoA N19), the constitutively active Rac1 (HeLa-Rac1 V12) and the dominant negative Rac1 (HeLa-Rac1 N17). After all these cell lines have been exposed to different doses of gamma radiation, we found that both GTPases, RhoA and Rac1, are activated in response to the radiation effects. Furthermore, the modulation of two enzymes activity, by using the mutant clones, led to a change in cellular responses to the DNA damage, as the reduction in the capacity of repairing DNA single and double strand breaksr. On the other hand, the deficiency of RhoA or Rac1 GTPase led to a reduction of Chk1 and Chk2 activation, or on the phosphorylation of histone H2AX, respectively, hindering the mechanisms of DNA damage detection and arresting cells in the G1/S and/or G2/M checkpoints of cell cycle. These factors significantly contributed to the reduction of cell proliferation and survival, leading cells to death. Finally, cellular assays of DNA damage repair of exogenous DNA by Homologous Recombination (HR) and Non-Homologous End Joining (NHEJ), demonstrated that RhoA inhibition significantly reduced the repair efficiency of both pathways. Thus, this work demonstrates and reinforces the existence of other biological functions of small GTPases RhoA and Rac1 in HeLa cells, by regulating cellular responses to DNA damage induced by exposure to gamma radiation, modulating the survival, proliferation and indirectly modulating the response to DNA damage repair pathway through the Homologous Recombination and Non-Homologous Recombination
Sharif, Razinah. "Zinc and genomic stability." Thesis, 2012. http://hdl.handle.net/2440/85982.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Medicine, 2012
Costa, Maria Inês Couceiro. "The role of micronutrients in the DNA damage response - The case of zinc in acute myeloid leukemia." Master's thesis, 2020. http://hdl.handle.net/10316/94332.
Повний текст джерелаA integridade genómica é assegurada por várias moléculas que trabalham conjuntamente para erradicar ou minimizar a lesão do DNA. Estas constituem a resposta à lesão do DNA (DDR). Vários micronutrientes atuam em reações essenciais da DDR, sendo a adequada biodisponibilidade destes fatores dietéticos crucial para o seu ótimo funcionamento. O zinco (Zn) é particularmente relevante por estar envolvido em várias funções fundamentais à célula desde a resposta ao stress oxidativo, apoptose, regulação do ciclo celular, do metabolismo, síntese e reparação do DNA. Notavelmente, vários mecanismos de reparação do DNA envolvem o Zn. Apesar do papel do Zn na prevenção da doença ser bem definido, as suas funções na carcinogénese são menos conhecidas. No contexto do sistema hematopoiético, uma adequada DDR é essencial à manutenção das células estaminais hematopoiéticas, evitando a acumulação de lesões nestes precursores. Alterações da DDR têm sido reportadas na leucemia mielóide aguda (LMA) e relacionadas com a origem da doença. Outra observação comum nos doentes com leucemia é o decréscimo sérico de Zn. Apesar da frequência deste achado, o significado biológico do Zn na LMA e a relação com a DDR nas células leucémicas não são bem compreendidos. Este trabalho pretendeu estudar o papel do Zn na modulação da DDR na LMA e explorar o seu potencial como coadjuvante da terapia anticancerígena. Para tal, um modelo celular de LMA (HEL) foi incubado em condições normais de cultura (standard) com o teor basal de zinco presente no soro fetal bovino, bem como em depleção de Zn e em suplementação com ZnSO4 por 2, 7 e 15 dias. As respostas basais e induzidas por exposição de 30 minutos a 10µM de H2O2 e a 60 segundos de radiação ultravioleta (Ee=2.9841 W.cm-2) foram avaliadas a cada momento temporal. Para compreender se os papéis do Zn variam no contexto fisiológico e patológico, uma linha celular de linfócitos humanos normais (IMC) foi submetida às mesmas experiências. A lesão cromossómica, morte celular e níveis de divisão celular foram avaliados pelo teste do micronúcleo com bloqueio da citocinese. A monitorização da yH2AX, biomarcador da lesão e da cinética de reparação, foi feita a cada momento temporal antes da exposição genotóxica, após indução da lesão e 1 hora e 24 horas após exposição. A expressão de genes da DDR (PARP1, XRCC1, MSH2, MSH6, MLH1, XPA, ERCC1, RAD23B, RAD51, PRKDC, XRCC6, PALB2, FANCD2 e MGMT) foi avaliada por qRT-PCR. Para compreender o papel do Zn na modulação de inibidores da DDR e de compostos quimioterapêuticos utilizados na LMA, as células HEL foram incubadas com olaparib e citarabina em monoterapia e combinação com Zn. Os resultados foram analisados estatisticamente considerando um nível de significância de 95% (p <0,05). Comparativamente a standard, a suplementação com Zn diminuiu a lesão basal e a morte celular nos linfócitos normais e aumentou ligeiramente a proliferação. Pelo contrário, nas células de LMA verificou-se aumento da lesão basal ao longo do tempo de suplementação, ligeiro aumento da morte celular e redução dos níveis de divisão celular. Após estímulo genotóxico, os linfócitos suplementados apresentaram uma resposta mais eficiente à lesão do que os da condição standard, manifestado pelo decréscimo da lesão cromossómica, particularmente ao 7º e 15º dia de suplementação, aumento da morte celular e diminuição dos níveis de divisão celular. Por oposição, os linfócitos em depleção de Zn revelaram uma resposta menos eficiente e maior lesão cromossómica. Nas células de LMA suplementadas houve aumento da lesão cromossómica comparativamente às da condição standard, enquanto que os menores níveis de lesão se verificaram na ausência de Zn. A monitorização da yH2AX pareceu corroborar que nos linfócitos suplementados poderá haver reparação, que não é atingida na ausência de Zn, e que na linha de LMA a lesão persiste após exposição genotóxica. A análise da expressão génica não revelou diferenças significativas entre condições, com exceção da diminuição significativa (1.02 vezes inferior, p=0.0315) da expressão basal de XRCC6 nas células HEL suplementadas. Os resultados da monoterapia e da terapia combinada revelaram redução da proliferação e viabilidade celular de forma dependente da dose e do tempo, tendo a terapia combinada apresentado efeitos mais eficazes. Estes foram claramente demonstrados pelo efeito sinérgico do Zn com o olaparib e citarabina na maioria das doses testadas e pelo marcado decréscimo do IC50 do olaparib e da citarabina em combinação com o Zn comparativamente à monoterapia (doses 2,8 vezes e 5,4 vezes inferiores, respetivamente). Em suma, os dados corroboram a importância do Zn na manutenção de respostas adequadas à lesão do DNA no contexto preventivo da doença e a sua possível aplicabilidade como coadjuvante potenciador de terapias genotóxicas ou das que têm como alvo a DDR, revelando um duplo papel do zinco no contexto preventivo e terapêutico do cancro, em particular da LMA.
Genome integrity is assured by a plethora of molecules that work together to eradicate or minimize repair DNA damage. These constitute the DNA damage response (DDR). Many micronutrients are crucial for key DDR reactions, meaning that adequate bioavailability of these dietary factors is critical for optimal DDR functioning. Zinc (Zn) is particularly important for playing pivotal roles in the cell, from oxidative stress responses, to apoptosis, cell cycle regulation, metabolism, DNA synthesis and repair. Notably, many DNA repair mechanisms involve Zn. Despite the role of Zn in disease prevention is well defined, its functions in carcinogenesis are far less explored. In the context of the hematopoietic system, an appropriate DDR is essential for the maintenance of the hematopoietic stem cells’ pool homeostasis, by avoiding the accumulation of DNA damage in these precursors. DDR alterations have been found in acute myeloid leukemia (AML) and related to the leukemogenesis process. Moreover, a common observation in leukemia patients is the decrease in serological Zn. Despite the frequency of this finding, the biological significance of Zn for the leukemogenesis process and relation with the DDR in AML cells is not understood. This work aimed to study the role of Zn in the modulation of the DDR in AML and explore its potential as co-adjuvant in leukemia therapy. To do so, cellular model of AML (HEL) was incubated in standard (Std) culture conditions containing the basal Zn levels presented in fetal bovine serum, in Zn depletion and in supplementation with ZnSO4 for 2, 7 and 15 days. Basal and induced cellular responses to exposure to 10µM of H2O2 for 30 minutes and 60 seconds of UV radiation (Ee=2.9841 W.cm-2) were evaluated at each time point. To understand whether Zn’s roles differ in health and disease, a cell line of normal human lymphocytes (IMC) was submitted to the same experiments. Chromosomal damage, cell death and cell division rates were assessed by the cytokinesis-block micronucleus assay. The monitorization of yH2AX, biomarker of DNA damage and repair kinetics, was performed at all evaluation times before genotoxic exposure, after initial damage induction, and 1 hour and 24 hours following exposure. The expression of DDR genes (PARP1, XRCC1, MSH2, MSH6, MLH1, XPA, ERCC1, RAD23B, RAD51, PRKDC, XRCC6, PALB2, FANCD2 and MGMT) was evaluated by two-step qRT-PCR. To acknowledge the role of Zn in the modulation of DDR inhibitors and chemotherapeutic compounds used in AML, HEL cells were submitted to treatment with olaparib and cytarabine in monotherapy and in combination with Zn. Results were statistically analyzed considering a confidence level of 95% (p<0.05). Comparatively to Std Zn conditions, supplementation reduced basal chromosomal damage and cell death in normal lymphocytes and led to slight increases in proliferation. Oppositely, in AML cells it was observed an increase of basal chromosomal damage through time of supplementation, a slight increase in basal cell death and a decrease in cell division rates. Upon genotoxic exposure, Zn-supplemented lymphocytes demonstrated a more efficient response than those from Std conditions, manifested by the decrease in chromosomal damage, particularly at the 7th and 15th days of supplementation, increase in cell death and decrease of cell division rates. Contrastingly, Zn-depleted lymphocytes shown a less efficient damage response, presenting increased chromosomal damage levels. Supplemented AML cells shown an increase in DNA damage comparatively to those from Std conditions, while the lowest chromosomal damage scores were found in Zn-depletion. The monitorization of yH2AX seemed to corroborate that in supplemented lymphocytes there may be a repair response that is not achieved in Zn absence, and that in the AML cell line damage persists following initial genotoxic exposure. Gene expression analyses did not reveal significant differences between conditions, except for a significant decrease (1.0 fold, p=0.0315) in XRCC6 basal expression in HEL supplemented cells. The results from monotherapy as well as combination therapy revealed a reduction in cellular proliferation and viability in a dose and time dependent manner, with combination therapy displaying more efficient effects. This was clearly demonstrated by the synergistical effect of Zn with olaparib and cytarabine in most of the tested concentrations and the marked decrease in olaparib and cytarabine IC50 when in combination with Zn comparatively to monotherapy (2.8-fold and 5.4-fold decreases, respectively). In sum, the results corroborate the importance of Zn in the maintenance of adequate responses to DNA damage in the context of disease prevention and a possible application of Zn as a co-adjuvant potentiator of the effects of genotoxic or DDR-targeting therapies, revealing a dual role of Zn both in cancer prevention and therapy, particularly in AML.
Laubenthal, Julian, O. Zlobinskaya, Krzysztof Poterlowicz, Adolf Baumgartner, Michal R. Gdula, E. Fthenou, M. Keramarou, et al. "Cigarette smoke-induced transgenerational alterations in genome stability in cord blood of human F1 offspring." 2012. http://hdl.handle.net/10454/6063.
Повний текст джерелаCondé, Lionel. "Implication de la protéine Staufen 2 dans les voies de réponse aux dommages à l’ADN." Thesis, 2020. http://hdl.handle.net/1866/24468.
Повний текст джерелаMany complex cellular pathways are induced in response to DNA damages. This cellular response is indispensable to prevent the accumulation of mutations and to avoid malignant transformation. These different pathways are highly coordinated and are organized in a global mechanism called DNA damage response (DDR). Proteins involved in the DDR are regulated at different levels of the gene expression process. Notably, several RNA binding proteins are involved in the regulation of DDR gene expression through the post-transcriptional control of their mRNA. The RBP STAU2 is known to bind various mRNAs coding for proteins involved in the DDR or cell cycle control. STAU2 is regulated at the transcriptional levels by the major transcription factor E2F1. Recent observations suggest that CHK1 could be implicated in the control of the steady-state level of STAU2. Otherwise, the cellular consequences of STAU2 downregulation remain elusive. The purpose of this research was first to elucidate the implication of CHK1 pathway in STAU2 regulation. CHK1 is a major protein involved in the DDR regulation as well as in the control of cell cycle progression in the absence of DNA damage. Our data show that the downregulation of CHK1 rapidly leads to a caspase-dependent degradation of STAU2 independently of apoptosis. The link between STAU2 and mechanisms of DNA repair was reinforced by our BioID2 experiment that identified several proteins of the DDR in close proximity with STAU2. On the other hand, the aim of this study was to determine the consequences of STAU2 downregulation in different cell lines. Given that STAU2 is an RBP, its dysregulation will inevitably change the fate of several mRNA. In order to increase our understanding of theses consequences, we generated an hTert-RPE1 STAU2-KO cell line using the CRISPR/Cas9 technique. Our data show that these cells accumulate DNA damage and have an increased proliferation rate. Moreover, several genes involved in the DNA repair pathway are downregulated. We also downregulated STAU2 in IMR90 to determine if the previous observations are cell-type specifics. In the latter case, STAU2 diminution triggers cell cycle arrest and cellular senescence. Altogether, these results contribute to improve our knowledge of STAU2 function, especially in DNA damage response pathway and in cell cycle regulation.
Частини книг з теми "Zinc; genomic stability; DNA damage"
Richard, Marie-Jeanne, Nathalie Emonet-Piccardi, Christine Didier, Eric Jourdan, Marie-Thérèse Leccia, Marie-Odile Parat, Jean Cadet, Jean Claude Béani, and Alain Favier. "Cooperative Effects of Zinc / Selenium and Thiols in the Protection Against UV-Induced Genomic DNA Damage." In Trace Elements in Man and Animals 10, 77–82. New York, NY: Springer US, 2002. http://dx.doi.org/10.1007/0-306-47466-2_16.
Повний текст джерелаAnh, Tuan, Chul-Hwan Lee, and Yeon-Soo Seo. "Lagging Strand Synthesis and Genomic Stability." In DNA Repair - On the Pathways to Fixing DNA Damage and Errors. InTech, 2011. http://dx.doi.org/10.5772/22007.
Повний текст джерелаLucchesi, John C. "DNA repair and genomic stability." In Epigenetics, Nuclear Organization & Gene Function, 173–83. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.003.0015.
Повний текст джерелаHetman, M. "Nucleolar Contributions to DNA-Damage Response and Genomic (In)Stability in the Nervous System." In Genome Stability, 527–39. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-803309-8.00030-6.
Повний текст джерелаBenarroch, Eduardo E. "DNA." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 46–61. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0004.
Повний текст джерела