Academic literature on the topic 'Uracilo'

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Journal articles on the topic "Uracilo"

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Lindo-Samanamud, Saúl, Mario Cornejo-Olivas, Olimpio Ortega, Victoria Marca, Keren Espinoza-Huertas, and Pilar Mazzetti. "Estrategia de genotipado del gen FMR1: Método de diagnóstico alternativo para el Síndrome X Frágil y otras enfermedades por expansión de trinucleotidos." Revista Medica Herediana 24, no. 4 (2013): 269. http://dx.doi.org/10.20453/rmh.v24i4.269.

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Objetivos: Diseñar una estrategia alternativa por PCR para el genotipado de secuencias ricas en citosinas, basada en modificación nucleotídica. Material y métodos: Se modificó el gen FMR1 nativo de ocho individuos clínicamente no afectados por el Síndrome X frágil, cambiando las citosinas por uracilos, empleando bisulfito de sodio. El ADN modificado fue purificado y cuantificado por espectrofotometría. Las estructuras alternativas y potenciales islas CpG que adopta el microsatélite inestable fueron simuladas con los programas MFOLD y CpGplot. Se generaron cebadores específicos que hibriden tanto con el microsatélite modificado (Primer T) y con una secuencia modificada de las islas CpG (Primer M), utilizando el programa MethPrimer. Finalmente, ambas secuencias fueron amplificadas por PCR y los amplicones fueron separados por electroforesis en gel de poliacrilamida (PAGE por sus siglas en inglés) al 6% y visualizados con tinción de nitrato de plata. Resultados: La modificación del ADN fue evidenciada por espectrofotometría al uracilo. Las estructuras observadas en la simulación fueron las horquillas encontrándose dos potenciales islas CpG. La amplificación con los cebadores T, confirmó el diseño in silico desarrollado para abordar la estructura en horquillas. La amplificación con los cebadores M permitió detectar metilación de la primera isla CpG del gen FMR1.Conclusión: Se propone un diseño alternativo para amplificación de secuencias de microsatélite que contengan citosinas metiladas y no metiladas. Se requieren estudios posteriores con muestras de ADN que contengan microsatélites muy expandidos para validar su aplicación para diagnóstico molecular.
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Trilleras, Jorge, Omar Rodríguez, and Edwin Javier González López. "5-Deazaflavinas: síntesis química." Revista de Ciencias 21, no. 1 (2018): 133. http://dx.doi.org/10.25100/rc.v21i1.6346.

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Las 5-Deazaflavinas, están involucradas en reacciones enzimáticas redox de una variedad de sistemas biológicos y guardan similitud estructural con la riboflavina. Las propiedades electroquímicas y fotoquímicas son resultado de la sustitución del N-5 del anillo de la isoaloxazina por un átomo de carbono. En esta revisión, se describen los avances en la obtención de 5-deazaflavinas y análogos a partir de ácido barbitúrico, análogos de uracilo, triamino-tricloropirimidinas y quinolincarbonitrilos. El grado y tipo de sustitución de las 5-deazaflavinas, se obtiene a través de los aldehídos y aminas utilizadas, vía reacciones clásicas, simples y convergentes. Comparando las diferentes estrategias sintéticas reportadas, para la construcción de 5-deazaflavinas y análogos, estas se clasifican en dos estrategias generales: i) la construcción del anillo de quinolina sobre el anillo pirimidínico o ii) la construcción del anillo pirimidínico sobre el anillo quinolínico.
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Bojarska, Elżbieta, Jarosław Kamiński, Ryszard Stolarski, and Zygmunt Kazimierczuk. "Novel Electrochemically Derived Dimers of Methylated Uracils." Zeitschrift für Naturforschung B 52, no. 6 (1997): 742–48. http://dx.doi.org/10.1515/znb-1997-0612.

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Abstract Electrolysis of acetic acid/sodium acetate solutions of N-methylated uracils results in the formation of 5-substituted methyl and acethoxy derivatives. Electrolysis of trifluoroacetic acid/potassium trifluoroacetate solutions of N-1-and N-3-methylated uracils provided, be­ sides 5-trifluoromethyl derivatives, novel N-C uracil dimers. In the case of 1,3-dimethyluracil in trifluoroacetic acid. N-l demethylathion was also observed.
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Maruyama, Tokumi, Shigetada Kozai, Tetsuo Yamasaki, et al. "Synthesis and Antiviral Activity of 1,3-Disubstituted Uracils against HIV-1 and HCMV." Antiviral Chemistry and Chemotherapy 14, no. 5 (2003): 271–79. http://dx.doi.org/10.1177/095632020301400506.

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The development of new non-nucleoside reverse transcriptase inhibitors (NNRTIs) is an efficient strategy for finding new therapeutic agents against human immunodeficiency virus (HIV). A large number of 6-substituted uracil derivatives have been prepared in order to explore new NNRTIs. However, there are few approaches to anti-HIV agents from 1,3-disubstituted uracil derivatives. Therefore, we tried to prepare several 1,3-disubstituted uracils, which were easily obtainable from uracil by preparation under alkali and Mitsunobu conditions, and examined their antiviral activity against HIV-1 and human cytomegalovirus (HCMV). We found that 1-benzyl-3-(3,5-dimethylbenzyl)uracil and 1-cyanomethyl-3-(3,5-dimethylbenzyl)-4-thiouracil showed powerful inhibition against HCMV and HIV-1, respectively.
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Girelli Zubani, Giulia, Marija Zivojnovic, Annie De Smet, et al. "Pms2 and uracil-DNA glycosylases act jointly in the mismatch repair pathway to generate Ig gene mutations at A-T base pairs." Journal of Experimental Medicine 214, no. 4 (2017): 1169–80. http://dx.doi.org/10.1084/jem.20161576.

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During somatic hypermutation (SHM) of immunoglobulin genes, uracils introduced by activation-induced cytidine deaminase are processed by uracil-DNA glycosylase (UNG) and mismatch repair (MMR) pathways to generate mutations at G-C and A-T base pairs, respectively. Paradoxically, the MMR-nicking complex Pms2/Mlh1 is apparently dispensable for A-T mutagenesis. Thus, how detection of U:G mismatches is translated into the single-strand nick required for error-prone synthesis is an open question. One model proposed that UNG could cooperate with MMR by excising a second uracil in the vicinity of the U:G mismatch, but it failed to explain the low impact of UNG inactivation on A-T mutagenesis. In this study, we show that uracils generated in the G1 phase in B cells can generate equal proportions of A-T and G-C mutations, which suggests that UNG and MMR can operate within the same time frame during SHM. Furthermore, we show that Ung−/−Pms2−/− mice display a 50% reduction in mutations at A-T base pairs and that most remaining mutations at A-T bases depend on two additional uracil glycosylases, thymine-DNA glycosylase and SMUG1. These results demonstrate that Pms2/Mlh1 and multiple uracil glycosylases act jointly, each one with a distinct strand bias, to enlarge the immunoglobulin gene mutation spectrum from G-C to A-T bases.
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Isono, Yohei, Norikazu Sakakibara, Paula Ordonez, et al. "Synthesis of 1-benzyl-3-(3,5-dimethylbenzyl)Uracil Derivatives with Potential Anti-HIV Activity." Antiviral Chemistry and Chemotherapy 22, no. 2 (2011): 57–65. http://dx.doi.org/10.3851/imp1844.

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Background: Nine novel uracil analogues were synthesized and evaluated as inhibitors of HIV-1. Methods: Key structural modifications included replacement of the 6-chloro group of 1-benzyl-6-chloro-3-(3,5-dimethylbenzyl)uracil by other functional groups or N1-alkylation of 3-(3,5-dimethylbenzyl)-5-fluorouracil. Results: These compounds showed only micromolar potency against HIV-1 in MT-4, though two of them; 6-azido-1-benzyl-3-(3,5-dimethylbenzyl) uracil and 6-amino-1-benzyl-3-(3,5-dimethylbenzyl) uracil were highly potent (half maximal effective concentration =0.067 and 0.069 μM) and selective (selectivity index =685 and 661), respectively. Structure–activity relationships among the newly synthesized uracil analogues suggest the importance of the H-bond formed between 6-amino group of 6-amino-1-benzyl-3-(3,5-dimethylbenzyl) uracil and amide group of HIV-1 reverse transcriptase. Conclusions: We discovered two 6-substituted 1-benzyl-3-(3,5-dimethylbenzyl) uracils, (6-azido-1-benzyl-3-(3,5-dimethylbenzyl) uracil and 6-amino-1-benzyl-3-(3,5-dimethylbenzyl) uracil) as novel anti-HIV agents. These compounds should be further pursued for their toxicity and pharmacokinetics in vivo as well as antiviral activity against non-nucleoside reverse transcriptase inhibitor-resistant strains.
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Heidari, Ali, Arash Ghorbani-Choghamarani, Maryam Hajjami, and Robert H. E. Hudson. "Fluorescent Biaryl Uracils with C5-Dihydro- and Quinazolinone Heterocyclic Appendages in PNA." Molecules 25, no. 8 (2020): 1995. http://dx.doi.org/10.3390/molecules25081995.

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There has been much effort to exploit fluorescence techniques in the detection of nucleic acids. Canonical nucleic acids are essentially nonfluorescent; however, the modification of the nucleobase has proved to be a fruitful way to engender fluorescence. Much of the chemistry used to prepare modified nucleobases relies on expensive transition metal catalysts. In this work, we describe the synthesis of biaryl quinazolinone-uracil nucleobase analogs prepared by the condensation of anthranilamide derivatives and 5-formyluracil using inexpensive copper salts. A selection of modified nucleobases were prepared, and the effect of methoxy- or nitro- group substitution on the photophysical properties was examined. Both the dihydroquinazolinone and quinazolinone modified uracils have much larger molar absorptivity (~4–8×) than natural uracil and produce modest blue fluorescence. The quinazolinone-modified uracils display higher quantum yields than the corresponding dihydroquinazolinones and also show temperature and viscosity dependent emission consistent with molecular rotor behavior. Peptide nucleic acid (PNA) monomers possessing quinazolinone modified uracils were prepared and incorporated into oligomers. In the sequence context examined, the nitro-substituted, methoxy-substituted and unmodified quinazolinone inserts resulted in a stabilization (∆Tm = +4.0/insert; +2.0/insert; +1.0/insert, respectively) relative to control PNA sequence upon hybridization to complementary DNA. All three derivatives responded to hybridization by the “turn-on” of fluorescence intensity by ca. 3-to-4 fold and may find use as probes for complementary DNA sequences.
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Colasurdo, Diego D., Matías N. Pila, Dacio A. Iglesias, Sergio L. Laurella, and Danila L. Ruiz. "Tautomerism of uracil and related compounds: A mass spectrometry study." European Journal of Mass Spectrometry 24, no. 2 (2017): 214–24. http://dx.doi.org/10.1177/1469066717712461.

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It has been demonstrated that uracil has a preponderant tautomeric form, but it is also known that different tautomers co-exist in this equilibrium. In this work, mass spectrometry is used as a helpful tool to analyse the equilibria, using derivative compounds to forbid the presence of some tautomers and ion trap mass spectrometry to follow relevant fragmentation pathways. Theoretical calculations were performed to confirm tautomers abundance by energy minimization in gas phase. Analysis of mass spectra of uracil, three methyl-substituted uracils, 2-thiouracil and three benzouracils suggest that uracil exists mainly as three tautomers in gas phase: one major structure that corresponds to the classical structure of uracil (pyrimidine-2,4(1H,3H)-dione) bearing two carbonyls and two NH moieties, and two minor enolic forms (4-hydroxypyrimidin-2(1H)-one and 2-hydroxypyrimidin-4(1H)-one). Such tautomeric distribution is supported by theoretical calculations, which show that they are the three most stable tautomers.
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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 enzyme was significantly more sensitive than the HeLa enzyme to most analogues. Substituents providing the best inhibitors of HSV1 uracil-DNA glycosylase were found to be in the order: p-n-butyl < p-n-pentl = p-n-hexyl < p-n-heptyl < p-n-octyl. The most potent HSV1 enzyme inhibitor, 6-(p-n-octylanilino)uracil (OctAU), with an IC50 of 8 microM, was highly selective for the viral enzyme. Short-term [3H]thymidine incorporation into the DNA of HeLa cells in culture was partially inhibited by OctAU, whereas it was unchanged when 6-(p-n-hexylanilino)uracil was present at concentrations that completely inhibited HSV1 uracil-DNA glycosylase activity. These compounds represent the first class of inhibitors that inhibit HSV1 uracil-DNA glycosylase at concentrations in the micromolar range. The results suggest their possible use to evaluate the functional role of HSV1 uracil-DNA glycosylase in viral infections and re-activation in nerve cells.
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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 mutants that retain detectable excision activity, with this switching being especially dependent on MSH2. In contrast to their potentiation of switching, low-activity UNGs are relatively ineffective in restoring transversion mutations at C:G pairs during hypermutation, or in restoring gene conversion in stably transfected DT40 cells. The results indicate that UNG does, indeed, act through uracil excision, but suggest that, in the presence of MSH2, efficient switch recombination requires base excision at only a small proportion of the AID-generated uracils in the S region. Interestingly, enforced expression of thymine-DNA glycosylase (which can excise U from U:G mispairs) does not (unlike enforced UNG or SMUG1 expression) potentiate efficient switching, which is consistent with a need either for specific recruitment of the uracil-excision enzyme or for it to be active on single-stranded DNA.
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Dissertations / Theses on the topic "Uracilo"

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Matias, Carolina Raquel Guedes. "Decomposição do uracilo por colisões átomo-molécula: formação do anião NCO." Master's thesis, Faculdade de Ciências e Tecnologia, 2011. http://hdl.handle.net/10362/6152.

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Dissertação para obtenção do Grau de Mestre em Engenharia Física<br>A interacção da radiação de alta energia (p.ex. raios-X, raios , partículas ) com o meio fisiológico, produz ao longo do percurso de ionização diversas espécies secundárias (p.ex. iões, radicais, electrões) que podem produzir efeito genotóxico mais relevante do que a radiação primária. Dessas espécies formadas, os electrões secundários são as mais abundantes e podem assim interagir com o ADN celular. Encontra-se bem documentado na literatura que por cada MeV de radiação incidente, produzem-se cerca de 5×104 electrões secundários com uma distribuição de energias cinéticas abaixo de 20 eV. Estes electrões podem provocar a quebra simples e dupla das cadeias no ADN. Desta forma é de extrema importância proceder ao estudo de processos de interacção de electrões de baixa energia com moléculas constituintes do ADN, visto que tais quebras podem causar lesões mutagénicas e genotóxicas potenciando em última instância o aparecimento e desenvolvimento de patologias oncológicas. Dada a semelhança estrutural entre as moléculas de timina (base de ADN) e uracilo (base de ARN), preferiu-se nesta dissertação estudar por colisões átomo-molécula a fragmentação da molécula de uracilo. O mecanismo de dissociação destas moléculas resulta da interacção de um feixe neutro de átomos de potássio (K) de energia variável com um alvo molecular gasoso. O primeiro é obtido à custa do processo de troca de carga ressonante, e o último é produzido por evaporação num forno. No processo de colisão átomo-molécula há uma transferência do electrão de valência do projéctil para o alvo, produzindo-se aniões moleculares que são detectados por espectrometria de massa do tipo tempo de voo (TOF). Os padrões de fragmentação são fortemente ditados pela presença do ião de potássio (K+) no complexo de colisão. A resolução do aparelho de feixes moleculares utilizada permitiu a identificação de vários fragmentos, dando-se particular atenção ao estudo da dinâmica da colisão na formação do ião NCO–. Neste trabalho é apresentado o rendimento relativo de NCO– em função da energia de centro de massa disponível, assim como em função da velocidade relativa. Por comparação com estudos de captura electrónica dissociativa, o perfil de formação do ião NCO– em função de energia, apresenta um limiar de aparecimento similar.
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Zamora, F., P. Amo-Ochoa, and B. Lippert. "Nuevos complejos biorganometálicos con iones metálicos pesado por enlace a la posición C(5) del uracilo y la citosina." Revista de Química, 2013. http://repositorio.pucp.edu.pe/index/handle/123456789/100135.

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Dias, Cristina Jesus. "Derivados porfirínicos conjugados com uracilalditóis: sínteses e avaliação das suas propriedades antibacterianas e antitumorais." Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22680.

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Mestrado em Bioquímica - Métodos Biomoleculares<br>A unidade estrutural uracilo é uma estrutura promissora para a descoberta de novos agentes terapêuticos, uma vez que apresenta uma diversificada atividade biológica. Os derivados de uracilo substituídos na posição C-5, entre os quais se destaca o 5-fluorouracilo, apresentam atividade antitumoral significativa. De igual modo os derivados porfirínicos têm sido amplamente estudados como fotossensibilizadores em terapia fotodinâmica (PDT), destacando-se entre os naturais a clorofila a, precursora de alguns agentes como é o caso da clorina e6 e da feoforbida a. A conjugação de unidades de hidratos de carbono a outras moléculas tem demonstrado conferir-lhes solubilidade e seletividade para com determinadas células alvo, tornando estes conjugados adequados para administração intravenosa. Atualmente, já se encontram descritos alguns estudos envolvendo derivados de uracilo conjugados e ou fundidos a derivados porfirínicos e a hidratos de carbono. A conjugação destas moléculas poderá ser um meio para potenciar as propriedades fotossensibilizadoras dos derivados porfirínicos, tornando-os potenciais agentes terapêuticos para PDT antitumoral e antimicrobiana. A PDT tem-se destacado no tratamento de diversas doenças, particularmente no tratamento de tumores e infeções bacterianas. A ação fotodinâmica envolve a combinação da luz visível, oxigénio molecular e um fotossensibilizador, levando à formação de espécies reativas de oxigénio que induzem danos nos tecidos e consequentemente pode conduzir à morte celular. Neste trabalho, é descrita uma estratégia sintética para preparar novos derivados de clorofila a extraída da Spirulina maxima conjugada a diferentes unidades de uracil-alditóis, bem como a avaliação da atividade biológica destes conjugados, nomeadamente atividade antibacteriana e antitumoral. Os compostos preparados, 3 e 9a-c, foram caracterizados estruturalmente por espetrometria de massa e por RMN de 1H, tendo em alguns casos sido necessário recorrer a técnicas bidimensionais (COSY de 1H/1H), bem como por outras técnicas espetroscópicas. Para avaliação da atividade antibacteriana, selecionaram-se duas estirpes bacterianas: Staphylococcus aureus (Gram-positivo) e Escherichia coli (Gram-negativo). Os resultados obtidos mostraram que os compostos 3 e 9a, a uma concentração de 5,0 μM, inativaram eficientemente a bactéria S. aureus ( 7 log) após 180 min de irradiação com luz branca a uma irradiância de 2,7 mW.cm-2. Os compostos 9b e 9c, nas mesmas condições experimentais de irradiação, foram menos eficazes mostrando uma redução da abundância bacteriana de apenas cerca de 2 log. No ensaio com E. coli verificou-se que nenhum dos compostos estudados, 3 e 9a, foram capazes de inativar a bactéria de Gram-negativo. Nos estudos da avaliação da atividade antitumoral foram selecionadas duas linhas celulares da próstata humana, PNT-2 e PC-3. Os compostos 9a e 9b foram testados a uma concentração de 0,1; 1,0 e 10 μM, tendo sido incubados durante 4 h no escuro e irradiados durante 20 min com luz vermelha a uma irradiância de 1,28 mW.cm-2. Ambos os compostos, na concentração de 10 μM, foram capazes de reduzir a viabilidade das células cancerígenas PC-3, mas também das células pré-neoplásicas (PNT-2). O composto 9a consegue ainda reduzir as células PC-3 de forma significativa na concentração de 1,0 μM. No estudo preliminar de uptake intracelular do composto 9a observou-se não existir uma diferença significativa na concentração intracelular entre as linhas PNT-2 e PC-3 ao fim de 4 h de incubação. Os estudos biológicos realizados permitem concluir que a eficiência dos compostos para inativar S. aureus é dependente da unidade de açúcar utilizado (o derivado conjugado com a xilose é melhor PS do que os derivados de galactose e glucose), mas não parece ser determinante para reduzir a viabilidade das células do cancro da próstata (PC-3) na concentração de 10 μM.<br>Uracil is considered a lead compound, since it has been used as an important platform for chemical modifications in order to improve and to diversify its biological activity. C-5 substituted uracil derivatives, among which the 5-fluorouracil outstands, exhibits relevant antitumoral activity. Among the natural porphyrin derivatives, chlorophyll a is the precursor of some photosensitizing agents in photodynamic therapy (PDT), such as chlorin e6 and pheophorbide a. The conjugation of carbohydrates moieties to other molecules has been shown to confer solubility and selectivity to the new entities to target cells, making these conjugates suitable for intravenous administration. Currently, some studies involving uracil derivatives conjugated to and/or fused to porphyrin derivatives and carbohydrates are described in literature. The conjugation of these molecules may be used to potentiate the photosensitizing properties of the porphyrin derivatives, making them potential therapeutic agents for antitumor and antimicrobial PDT. PDT has been used with success in the treatment of various diseases, particularly in the treatment of tumors and bacterial diseases. Photodynamic action involves the combination of visible light; molecular oxygen and a photosensitizer, leading to the formation of reactive oxygen species, which will induce tissue damage and consequently leads to cell death. In this study, we report an efficient access to new derivatives of chlorophyll a, extracted from Spirulina maxima, bearing different uracil-alditols moieties, as well as the evaluation of their antibacterial and antitumoral activity. The prepared compounds, 3 and 9a-c, were structurally characterized by mass spectrometry and by 1H NMR recurring to mono- and bidimensional techniques (COSY 1H/1H ), and other spectroscopic techniques. To evaluate the antibacterial activity, two bacteria strains, Staphylococcus aureus (Gram-positive strain) and Escherichia coli (Gram-negative strain) were selected. The results showed that compounds 3 and 9a, at a concentration of 5.0 μM, were able to inactivate efficiently the S. aureus bacterium ( 7 log) after 180 min of irradiation with white light at an irradiance of 2.7 mW.cm-2. Compounds 9b and 9c, under the same experimental conditions, were much less efficient showing a reduction of only 2 log. In the E. coli assay it was found that none of the studied compounds 3 and 9a, were able to photoinactivate Gram-negative bacterium. In the antitumoral activity evaluation studies, two human prostate cell lines, PNT-2 e PC-3, were selected. Compounds 9a and 9b were tested at a concentration of 0.1, 1.0 and 10 μM, and incubated for 4 h in the dark and irradiated for 20 min with red light at an irradiance of 1.28 mW.cm-2. Both compounds, at a concentration of 10 μM, were able to reduce the viability of PC-3 cancer cells and pre-malignant cells (PNT-2). Compound 9a was further able to significantly reduce PC-3 cells at a concentration of 1.0 μM. In the preliminary intracellular uptake study of compound 9a, there was no significant difference in intracellular concentration between the PNT-2 and PC-3 cell lines after 4 h of incubation. These conducted studies allow us to conclude that the efficiency of the compounds to photoinactivate S. aureus is dependent on the sugar moiety (the xylose derivative is better PS than the galactose and glucose derivatives), but does not seem be determinant to reduce the viability of prostate cancer cells (PC-3) at a concentration of 10 μM.
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Galarza, Andrés Fernando Andrade. "Avaliação genotípica e fenotípica da enzima diidropirimidina desidrogenase (DPD) e risco de toxicidade com o uso de fluoropirimidinas." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/143351.

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Base teórica: As fluoropirimidinas possuem significativa variabilidade na resposta terapêutica e na ocorrência de toxicidade, o que tem sido relacionado à deficiência na depuração metabólica mediada pela enzima diidropirimidina desidrogenase (DPD). Mutações nos genes codificadores da enzima, bem como fatores ambientais podem levar à baixa ou nula expressão enzimática, provocando efeitos adversos graves devido ao acúmulo destes fármacos. Até o presente, nenhum teste reconhecidamente valido para a identificação de indivíduos em risco de toxicidade severa está estabelecido na prática oncológica. A genotipagem para o gene DPYD apresenta poder preditivo limitado, pois é capaz de rastrear somente as mutações já conhecidas, que apresentam baixa frequência populacional. Por esta razão, ensaios funcionais baseados na avaliação da redução fisiológica do uracil (U) para diidrouracil (UH2), igualmente medidada pela DPD, têm sido propostos na identificação de pacientes predispostos à toxicidade. Nesta abordagem são estimadas as razões plasmáticas [UH2]/[U] em níveis basais ou após uma dose oral do U. Recentemente, foi sugerida a realização do teste funcional em saliva como amostra alternativa ao plasma, com maior estabilidade dos analitos. Entretanto, a associação entre as razões metabólicas nesta matriz e a toxicidade não foi validada em amostras clínicas. Objetivos: Avaliar a efetividade dos métodos de determinação da razão metabólica [UH2]/[U] em plasma e saliva e a genotipagem para o gene DPYD como preditores de toxicidade por fluoropirimidinas em pacientes com neoplasias gastrointestinais. Adicionalmente, o trabalho propôs o desenvolvimento de um método bioanalítico para a determinação de U e UH2 por cromatografia líquida de alta eficiência. Métodos: Foram obtidas amostras pareadas de plasma e saliva de 60 pacientes diagnosticados com neoplasia gastrointestinal e com indicação de tratamento com fluoropirimidinas. As concentrações de U e UH2 foram determinadas nas duas matrizes através de LC-MS/MS. Os efeitos adversos do primeiro ciclo de quimioterapia foram classificados de acordo com o NCI-CTCAE versão 4. A genotipagem da DYDP foi realizada por PCR tempo real e incluiu os alelos *2A; *13, Y186C; I560S, *7 Y186C. Resultados: 35% dos pacientes apresentaram toxicidade severa (graus 3/4), sendo a neutropenia a mais frequente (n=11). A genotipagem da DYDP não foi capaz de identificar pacientes em risco de toxicidade, uma vez que não foram encontrados portadores de alelos variáveis. As razões [UH2]/[U] variaram amplamente entre os pacientes, de 0,09 a 26,73 no plasma e de 0,08 a 24 na saliva. As razões [UH2]/[U] no plasma e na saliva demonstraram correlação elevada (rs=-0,575; P<0,01), porém, a saliva demonstrou maior correlação com o grau de toxicidade quando comparada ao plasma (rs=-0,515; P<0,01 vs rs=-0,282 P<0,05). Pacientes com grau de toxicidade 3/4 (n=21) apresentaram menor razão metabólica em comparação a pacientes com grau 1/2 (n=26) ou com ausência de toxicidade (n=13) (média 0.59 vs 2.22 e 2.83 no plasma e 1.62 vs 6.88 e 6.75 na saliva, P<0.01). A partir de curva ROC foi determinado o valor de corte de 1,16 para a razão em saliva com 86% de sensibilidade e 77% de especificidade para a identificação de pacientes com toxicidade severa. Nas amostras de plasma o valor de corte foi 4.0 com 71% de sensibilidade e 76% de especificidade. Adicionalmente, foi desenvolvido e validado um método bioanalítico para a dosagem de U e UH2 com exatidão (98.4–105.3%) e precisão precisão intra-ensaio (5.1–12.1%) e inter-ensaios (5.3–10.1%) satisfatórios. Conclusão: Neste grupo de pacientes a genotipagem dos alelos *2A; Y186C; I560S, Y186C e *7 da DPYD não mostrou-se útil na identificação de indivíduos com deficiência severa da DPD. Entretanto, as razões metabólicas [UH2]/[U] demonstraram ser um promissor teste para avaliar a funcionalidade da enzima e identificar a maioria dos casos de pacientes com sujeitos a toxicidade grave à fluoropirimidinas, com sensibilidade superior da saliva.<br>Background: Variation on therapeutic response to fluoropirimidines and toxicity have been related to impaired dihydropyrimidine dehydrogenase (DPD) mediated metabolism. Mutations in genes encoding the enzyme as well as environmental factors can lead to reduced or absent enzyme expression, causing serious adverse effects due to the accumulation of these drugs. To date, there is no clinically recognized valid assay, for the identification of individuals at risk of severe toxicity in oncological practice. DPYD genotyping has a limited prediction power, since it is able to identify only the already known mutations, which have low frequency in population. Therefore, functional DPD assays based on the assessment of uracil (U) to dihydrouracil (UH2) metabolism, which is also dependent on DPD, have been proposed to identify patients prone to toxicity. Thus, endogenous metabolic ratios of [UH2]/[U] or after an oral dose of U are determined in plasma. Recently, the use of saliva has been suggested as alternative matrix to plasma, with higher stability of analytes. However, the association between salivary metabolic ratios and toxicity has not been validated in clinical samples. Objective: To evaluate the use of plasma and saliva uracil (U) to dihydrouracil (UH2) metabolic ratios and DPYD genotyping, as a means to identify patients with dihydropyrimidine dehydrogenase (DPD) deficiency and fluoropyrimidine toxicity. Additionally, the work proposed the development of a bioanalytical method for the determination of U and UH2 by high-performance liquid chromatography. Methods: Paired plasma and saliva samples were obtained from 60 patients with gastrointestinal cancer before fluoropyrimidine treatment. U and UH2 concentrations were measured by LC-MS/MS. DPYD was genotyped for alleles *2A; Y186C; I560S, Y186C and *7. Results: 35% of the patients had severe toxicity. There was no variant allele carrier for DPYD. The [UH2]/[U] metabolic ratios were 0.09-26.73 in plasma and 0.08-24.0 in saliva, with higher correlation with toxicity grade in saliva compared to plasma (rs=-0.515 vs rs=-0.282). Median metabolic ratios were lower in patients with severe toxicity as compared to those with absence of toxicity (0.59 vs 2.83 plasma; 1.62 vs 6.75 saliva, P<0.01). A cut-off of 1.16 for salivary ratio was set with 86% sensitivity and 77% specificity for the identification of patients with severe toxicity. Similarly, a plasma cut-off of 4.0 revealed a 71% sensitivity and 76% specificity. Additionally, a bioanalytical method for the quantification of U and UH2, with adequate accuracy (98.4–105.3%) and precision (intra-assay CV 5.1–12.1% and inter-assay CV 5.3–10.1%) was develop and validated. Conclusions: DPYD genotyping for alleles *2A; Y186C; I560S, Y186C and *7 was not helpful in the identification of patients with severe DPD deficiency in this series of patients. The [UH2]/[U] metabolic ratios, however, proved to be a promising functional test to identify the majority of cases of severe DPD activity, with saliva performing better than plasma.
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Guillet, Marie. "Les sites abasiques, leur origine et les systèmes de répération chez Saccharomyces cerevisiae." Paris 11, 2003. http://www.theses.fr/2003PA112149.

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Les cellules sont constamment soumises à des stress endogène et exogène qui provoquent la formation de lésions de l'ADN. Il a été estimé que les lésions les plus abondantes dans l'ADN sont les sites abasiques (sites AP) provenant du clivage du lien glycosidique entre la base et le désoxyribose. Ce clivage peut être spontané ou médié par une ADN glycosylase au cours la réparation par excision de bases (BER) endommagées ou anormales de l'ADN. Le clivage des sites AP en 5' ou en 3' provoquent la formation de cassures simple brin avec une extrémité 5' ou 3' bloquée, respectivement. Au début de ma thèse, seul le BER était connu comme intervenant dans la réparation des sites AP via les deux AP endonucléases Apn1 et Apn2 chez Saccharomyces cerevisiae. Cependant, alors que les sites AP sont mutagènes et potentiellement létaux, le double mutant apn1 apn2 est viable, ce qui suggère la présence d'autres voies de réparation des sites AP. J'ai pu montré que le système de réparation par excision de nucléotides (NER) intervient dans la réparation des sites AP. L'hétérodimère Rad1-Rad10 (flap-endonucléase) possède également un rôle dans la réparation des sites AP, en effet, le triple mutant apn1 apn2 rad1 est létal et forme une microcolonie composée d'environ 300 cellules 4 jours après dissection. Ce phénotype nous a permis de montrer que l'hétérodimère Mus81-Mms4 permet une réparation partielle des cassures simple brin avec une extrémité 3' bloquée responsables de la létalité du triple mutant apn1 apn2 rad1. La suppression de la létalité du triple mutant apn1 apn2 rad1 est possible par la délétion d'UNG1 codant pour l'uracile glycosylase ou par la surexpression de DUT1 codant pour la désoxyuridine triphosphate pyrophosphatase. Ces derniers résultats montrent qu'une source majoritaire spontanée de sites AP est la réparation de l'uracile dans l'ADN provenant de l'incorporation de dUTP du stock de dNTP par les ADN polymérases au cours de la réplication ou de la réparation<br>Cellular DNA is continuously damaged by exogenous and endogenous reactive species. One of the most frequent lesion in DNA is abasic sites (AP sites) that come from the cleavage of the glycosidic bond between the base and the deoxyribose. This cleavage could be spontaneous or due to the action of a DNA glycosylase during the base excision repair (BER) of damaged or abnormal bases. The cleavage of AP sites on the 5' or the 3' side leads to the formation of single strand breaks with a 5' or a 3' blocked end, respectively. At the beginning of my thesis, only the BER pathway was known to repair AP sites via the action of the two AP endonucleases Apn1 and Apn2 in Saccharomyces cerevisiae. However, while AP sites are known to be mutagenic and potentially lethal, the double mutant apn1 apn2 is viable that suggests the presence of other pathway(s) for AP site repair. I showed that the nucleotide excision repair (NER) pathway occurs a role in the repair of AP sites. The Rad1-Rad10 heterodimer is also implicated in the repair of AP sites since the apn1 apn2 rad1 triple mutant is lethal. This triple mutant forms a micro-colony of an average of 300 cells 4 days after dissection. This phenotype helps us to show that the Mus81-Mms4 can partially repair single strand break with 3' blocked end that are damages that cause the death of the apn1 apn2 rad1 triple mutant. The lethality of the apn1 apn2 rad1 triple mutant is suppressed by the deletion of UNG1 coding for the uracil DNA glycosylase or the overexpression of DUT1 coding for the deoxyuridine triphosphate pyrophosphatase. These results show that a critical spontaneous source of AP sites is the repair of uracil in DNA that come from the incorporation of dUTP from the dNTP pool by DNA polymerases during replication or repair
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Studebaker, Adam W. "Targeting uracil exclusion mechanisms for development of anti-viral and anti-cancer therapies." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1056034774.

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Thesis (Ph. D.)--Ohio State University, 2003.<br>Title from first page of PDF file. Document formatted into pages; contains xiii, 210 p.; also includes graphics (some col.). Includes bibliographical references (p. 174-210). Available online via OhioLINK's ETD Center
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Kandasamy, Dineshkumar. "Study on yeast enzymes Urc1p and Urc4p in a novel uracil catabolism pathway (URC)." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-185013.

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Purine and pyrimidine bases are the central precursors of DNA and RNA and theirintracellular concentration is balanced by three pathways- de novo, salvage and catabolicpathways. Uracil catabolism pathway has been found in several bacteria and in some fungi(including yeast). Seven genes, URC1-7 have been found to be involved in this novelpathway. There are two “unknown genes” in the yeast Lachancea (Saccharomyces) kluyveri,namelyURC1 and URC4, which play a central role in this pathway and their exact functionremains a mystery.In this project, two S. kluyveri genes, URC1&amp;URC4, were over-expressed in the bacterialsystem and successfully purified. Our preliminary functional assay showed that uridinemonophosphate (UMP) is a likely substrate for Urc1p at pH7, 25ºC. It was shown clearly thatboth uracil and uridine were not the substrate for Urc1p. We tried to phosphorylatechemically synthesized ribosylurea using Drosophila melanogaster deoxyribonucleosidekinase and compared the activity between phosphorylated and non- phosphorylated RU atdifferent conditions. Phosphorylated ribosylurea seemed to be a likely substrate for Urc4p atpH7, 37ºC. Keywords: Uridine monophosphate (UMP), ribosylurea (RU), uracil catabolism.
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Kemmerich, Kristin. "Studies of genomic uracil and its excision." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610133.

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Brom, Jacques. "Squelettes pyrimidohétérocycliques dérivés d'amino- et d'hydrazino- uraciles." Mulhouse, 1991. http://www.theses.fr/1991MULH0205.

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Les 6-amino-, 6-hydrazino- et 6-(azavinyl) pyrimidinediones riches en électrons réagissent par leur carbone 5 avec différents électrophiles (l’O-tosylisonitrosomalodinitrile (OTMD), le tétracyanoéthylène (TCNE), l'acétylènedicarboxylate de diméthyle (DMAD), et le diméthylacétal du diméthylformamide (DMFDMA) pour conduire après cyclisation à toute une série d'hétérocycles polycycliques. La 6-amino-1,3-diméthylpyrimidine-2,4(1H, 3H)-dione fournit ainsi, avec l'OTMD, une lumazine précurseur de pyrimido [5,4-g] ptéridines, et avec le TCNE, une pyrido [2,3-d] pyrimidine. Une isomérisation du squelette carboné est mise en évidence dans le cas de la réaction entre la 6-hydrazino-1,3-diméthylpyrimidine-2,4(1H, 3H) dione et le TCNE. Des réactions analogues sur carbone sont également observées dans les séries naphtaléniques et anthracéniques
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HANNIER, REGIS. "Les cardiomyopathies au 5 fluoro-uracile (5 fu)." Lille 2, 1990. http://www.theses.fr/1990LIL2M281.

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Books on the topic "Uracilo"

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Pavittiran̲. Uracal ōcaikaḷ. Tēciya Kalai Ilakkiyap Pēravai, 2002.

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McKinnell, Denise. Phototransformation of 5-[inferior t]-butyl uracil derivatives. University of Birmingham, 1997.

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Bouzid, Bachir. Electrochemical behaviour and flow injection determination of uracil derivatives. University of Birmingham, 1987.

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Mutikainen, Ilpo. X-ray structural studies on metal complexes of uracil and orotic acid: A survey of coordination induced changes in the uracil fragment. Suomalainen Tiedeakatemia, 1988.

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National Institute for Clinical Excellence. Guidance on the use of capecitabine and tegafur with uracil for metastatic colorectal cancer. National Institute for Clinical Excellence, 2003.

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Paramacivam, Mu. Ti. Ka. Ci. en̲n̲umoru tir̲an̲āyvut ten̲r̲al: 1950-90kaḷil Tamil̲ilakkiya varalāṛṛōṭu tōḷ uraci naṭanta oru man̲itarin̲ carittiram. Narmatā Patippakam, 1999.

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Slupphaug, Geir, and Hans Einar Krokan. Genomic Uracil. WORLD SCIENTIFIC, 2018. http://dx.doi.org/10.1142/10803.

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Krokan, Hans Einar, and Geir Slupphaug. Genomic Uracil: Evolution, Biology, Immunology and Disease. World Scientific Publishing Co Pte Ltd, 2018.

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Sanderson, Russell J. Uracil-DNA glycosylase inhibitor protein: Role of carboxylic acid residues and use for measuring the fidelity of uracil-excision DNA repair synthesis in human cell extracts. 1998.

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Sanderson, Russell J. Uracil-DNA glycosylase inhibitor protein: Role of carboxylic acid residues and use for measuring the fidelity of uracil-excision DNA repair synthesis in human cell extracts. 1998.

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Book chapters on the topic "Uracilo"

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Miyakawa, Shin. "Uracil (Ura)." In Encyclopedia of Astrobiology. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27833-4_1631-3.

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Miyakawa, Shin. "Uracil (Ura)." In Encyclopedia of Astrobiology. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-11274-4_1631.

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Schomburg, Dietmar, and Dörte Stephan. "Uracil phosphoribosyltransferase." In Enzyme Handbook 12. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_215.

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Miyakawa, Shin. "Uracil (Ura)." In Encyclopedia of Astrobiology. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-44185-5_1631.

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Schomburg, Dietmar, and Dörte Stephan. "Uracil dehydrogenase." In Enzyme Handbook 10. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-57756-7_148.

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Schomburg, Dietmar, and Ida Schomburg. "uracil-DNA glycosylase 3.2.2.27." In Class 2–3.2 Transferases, Hydrolases. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36240-8_123.

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Krokan, Hans E., Frank Skorpen, Marit Otterlei, et al. "Human Uracil-DNA Glycosylase." In Advances in DNA Damage and Repair. Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4865-2_18.

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Arnemann, J. "UNG (Uracil-DNA-Glycosidase)." In Lexikon der Medizinischen Laboratoriumsdiagnostik. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_3628-1.

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Schomburg, Dietmar, and Dörte Stephan. "tRNA (uracil-5-)-methyltransferase." In Enzyme Handbook 11. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61030-1_33.

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Arnemann, J. "UNG (Uracil-DNA-Glycosidase)." In Springer Reference Medizin. Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_3628.

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Conference papers on the topic "Uracilo"

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Stewart, Jessica, Shanqiao Wei, Madhurima Datta, Umesh Varshney, and Ashok Bhagwat. "Abstract 3802: A novel uracil-DNA glycosylase, UdgX, as a new biochemical tool to directly detect uracils in DNA." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3802.

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Kowalski, Konrad, Joanna Skiba, Ingo Ott, Jolanta Solecka, and Bruno Therrien. "Ferrocenylated uracils: synthesis and biology." In XVIth Symposium on Chemistry of Nucleic Acid Components. Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2014. http://dx.doi.org/10.1135/css201414310.

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Shih, Yu-Chiao, Ying-Shun Liao, Chun-Chi Lin, et al. "Synthesis of 6-substituted uracil and uridine derivatives." In XVIth Symposium on Chemistry of Nucleic Acid Components. Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2014. http://dx.doi.org/10.1135/css201414129.

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Fritz, Hans-Joachim. "Mechanistic and evolutionary aspects of DNA-uracil glycosylases." In XIIth Symposium on Chemistry of Nucleic Acid Components. Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2002. http://dx.doi.org/10.1135/css200205230.

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Lin, Xiumei, Tanja Deckert-Gaudig, Regina Treffer, Volker Deckert, P. M. Champion, and L. D. Ziegler. "Tip-Enhanced Raman Scattering (TERS) Of Uracil Strands." In XXII INTERNATIONAL CONFERENCE ON RAMAN SPECTROSCOPY. AIP, 2010. http://dx.doi.org/10.1063/1.3482412.

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Elkin, P. M., M. A. Erman, and O. V. Pulin. "Anharmonic analysis of vibrational spectra of substituted uracil." In SPIE Proceedings, edited by Vladimir L. Derbov, Leonid A. Melnikov, and Lev M. Babkov. SPIE, 2006. http://dx.doi.org/10.1117/12.696923.

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Grof, P., S. Gaspar, and A. Berces. "Uracil thin layers in dosimetry of UV-radiation." In Europto Biomedical Optics '93, edited by Kazuhiko Atsumi, Cornelius Borst, Frank W. Cross, et al. SPIE, 1994. http://dx.doi.org/10.1117/12.169152.

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Bulgar, Alina, Lachelle D. Weeks, Yanling Miao, et al. "Abstract A104: Removal of uracil by uracil DNA glycosylase limits pemetrexed cytotoxicity: Overriding the limit with methoxyamine (TRC102) to inhibit base excision repair." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a104.

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Villar, Vincent, Carlos Casanova, Mari Luz Moreno Sancho, et al. "Antioxidant activity of 5-FU and new fluorinated uracil derivates." In MOL2NET 2017, International Conference on Multidisciplinary Sciences, 3rd edition. MDPI, 2017. http://dx.doi.org/10.3390/mol2net-03-04968.

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Fujita, Marta Akemi, Carla Marisa Brito Carvalho, Timothy John Brocksom та Kleber Thiago de Oliveira. "Synthesis and photophysical evaluations of β-fused Uracil- Porphyrin derivatives". У 15th Brazilian Meeting on Organic Synthesis. Editora Edgard Blücher, 2013. http://dx.doi.org/10.5151/chempro-15bmos-bmos2013_2013912183035.

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Reports on the topic "Uracilo"

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González-Pacanowska, Dolores. La dUTPasa, una NTP-pirofosfatasa todo-α que controla el nivel de uracilo en el ADN. Sociedad Española de Bioquímica y Biología Molecular (SEBBM), 2014. http://dx.doi.org/10.18567/sebbmdiv_anc.2014.09.1.

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Niedenzu, K., and L. Komorowski. New Boron-Nitrogen Analogues of Uracil Derivatives. Defense Technical Information Center, 1989. http://dx.doi.org/10.21236/ada210164.

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Su, Ning, Jerald S. Bradshaw, Xian X. Zhang, Paul B. Savage, and Krzystof E. Krakowiak. Syntheses of Diaza-18-Crown-6 Ligands Containing Two Units Each of 4-Hydroxyazobenzene, Benzimidazole, Uracil, Anthraquinone, or Ferrocene Groups. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada361715.

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