Dissertations / Theses on the topic 'Dihydrofolate reductase'
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Shrimpton, Paul James. "A computational investigation of dihydrofolate reductase." Thesis, University of Birmingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403014.
Full textHaddow, J. "Potential suicide inhibitors of dihydrofolate reductase." Thesis, University of Strathclyde, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381497.
Full textFan, Yongjia. "Bistability in Human Dihydrofolate Reductase Catalysis." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1280243471.
Full textChui, Wai K. "Non-classical inhibitors of dihydrofolate reductase." Thesis, Aston University, 1990. http://publications.aston.ac.uk/12623/.
Full textEl-Hamamsy, Mervat Hamed Rabu Ibrahem. "Potential antimycobacterial agents targeting dihydrofolate reductase." Thesis, University of Bath, 2005. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418600.
Full textGuo, Jian Nan. "Thermophilicity and catalytic efficiency in dihydrofolate reductase." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/56290/.
Full textBevan, A. W. "Specificity of inhibitor binding to dihydrofolate reductase." Thesis, University College London (University of London), 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.352532.
Full textSingh, Priyanka. "Enzyme catalysis and dynamics in dihydrofolate reductase." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/5635.
Full textAl-Batayneh, Khalid Mubarak. "Mutations in Drosophila dihydrofolate reductase and methotrexate resistance." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63399.pdf.
Full textKhaw, Lake Ee. "Isotopic labelling of dihydrofolate reductase for NMR studies." Thesis, Georgia Institute of Technology, 1991. http://hdl.handle.net/1853/25179.
Full textTey, Lai-Hock. "Studies of site-selective glycosylation of dihydrofolate reductase." Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/55798/.
Full textGibson, Marc William. "Characterisation of Trypanosoma brucei dihydrofolate reductase-thymidylate synthase." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521705.
Full textPang, Jiayun. "Computational studies of dihydrofolate reductase from Thermotoga maritima." Thesis, University of Birmingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433745.
Full textSen, Arundhuti. "Explorations in enzymology: investigating dynamics in dihydrofolate reductase." Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/2768.
Full textRIMET, ODILE. "Etude de l'activite dihydrofolate reductase par spectrofluorimetrie : influence du cofacteur." Aix-Marseille 2, 1990. http://www.theses.fr/1990AIX22981.
Full textBehiry, Enas Mamdouh. "Dihydrofolate reductase and the physical basis of enzyme catalysis." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/56687/.
Full textYap, Chee H. "Potential inhibitors of dihydrofolate reductase: synthesis and NMR spectroscopy." Thesis, Aston University, 1985. http://publications.aston.ac.uk/14508/.
Full textSICA, LUCAS. "Application de la microcalorimetrie aux mesures d'activte enzymatique : exemple de la dihydrofolate reductase." Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX22953.
Full textBasran, Jaswir. "The role of conserved residues in Lactobacillus casei dihydrofolate reductase." Thesis, University of Leicester, 1994. http://hdl.handle.net/2381/35262.
Full textSasso-Bitran, Sophie. "Etude thermodynamique de la selectivite des inhibiteurs de la dihydrofolate reductase." Aix-Marseille 2, 1995. http://www.theses.fr/1995AIX22954.
Full textThomas, Janette Ann. "Structure and activity studies on mutants of the enzyme dihydrofolate reductase." Thesis, University of Leicester, 1990. http://hdl.handle.net/2381/35171.
Full textAlfaraj, Rihaf. "Development of selective inhibitors of dihydrofolate reductase (DHFR) of Mycobacterium tuberculosis." Thesis, University of Bath, 2013. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669020.
Full textLi, Jiayue. "The preservation of protein dynamics from bacteria to human dihydrofolate reductase." Diss., University of Iowa, 2019. https://ir.uiowa.edu/etd/6984.
Full textKolmodin, Karin. "Computer Simulation of Protein Tyrosine Phosphatase Reaction Mechanisms and Dihydrofolate Reductase Inhibition." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : [Univ.-bibl. [distributör]], 2001. http://publications.uu.se/theses/91-554-5148-9/.
Full textGraffner, Nordberg Malin. "Approaches to soft drug analogues of dihydrofolate reductase inhibitors : Design and synthesis." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5017-2/.
Full textWooden, Jason. "Analysis of resistance to inhibitors of Plasmodium falciparum dihydrofolate reductase in yeast /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/10261.
Full textPovinelli, Christine Marie. "Genetic analysis of the dihydrofolate reductase and thymidylate synthase genes of bacteriophage T4." Diss., Georgia Institute of Technology, 1987. http://hdl.handle.net/1853/25347.
Full textRooke, Stuart. "Some reactions of vinyl sulfimides and synthesis of novel inhibitors of dihydrofolate reductase." Thesis, University of Warwick, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263814.
Full textTang, Lei. "The determination and structural analysis of site-directed dihydrofolate reductase and insulin mutants." Thesis, Open University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338337.
Full textMaurer, Barry James. "Dihydrofolate reductase gene amplification in human cell lines VA2-B and hela BU25." Diss., Pasadena, Calif. : California Institute of Technology, 1995. http://resolver.caltech.edu/CaltechETD:etd-10232007-082738.
Full textHastings, Michele Dawn. "Analysis of dihydrofolate reductase variations in relation to antifolate resistance in Plasmodium vivax /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/10269.
Full textYang, Qing X. "Nuclear magnetic resonance studies on the structure and dynamics of dihydrofolate reductase and its ligands." Diss., Georgia Institute of Technology, 1991. http://hdl.handle.net/1853/30856.
Full textDAM, JULIE. "Etudes experimentales et theoriques des interactions proteine-proteine au sein de la dihydrofolate reductase r67." Paris 7, 2000. http://www.theses.fr/2000PA077055.
Full textAdrian, Peter V. "Trimethoprim-resistant dihydrofolate reductase genes in South African isolates of aerobic Gram-negative commensal faecal flora." Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/26335.
Full textMariam, Nakintu. "Detection of mutations in dihydropteroate synthase (dhps) and dihydrofolate reductase (dhfr) in Plasmodium falciparum in eastern Sudan." Thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-155295.
Full textStojkovic, Vanja. "Contribution of active site dynamics to enzyme catalysis: study on a series of mutants of dihydrofolate reductase." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/5062.
Full textDuboué-Dijon, Elise. "Interactions entre une biomolécule et son environnement : de la dynamique d'hydratation à la catalyse enzymatique." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066314/document.
Full textBiomolecules are immersed in an aqueous solvent, which plays a key role in a wide range of biochemical processes. In addition, the properties of water molecules in the hydration shell are perturbed by the presence of the biomolecule. In this thesis, we combine theoretical models and numerical simulations to provide a molecular description of the interplay between a biomolecule and its environment. The manuscript is structured in two parts, addressing two complementary aspects of this complex interaction. In the first part we focus on the perturbation induced by a biomolecule on water molecules. We determine how much the hydration shell differs from bulk water and we identify the molecular factors at play. We then compare the hydration shells of an antifreeze protein and of a typical protein and investigate whether the shell structure and dynamics can explain the antifreeze properties. We finally study the hydration dynamics of a DNA dodecamer where slow water dynamics was suggested. We obtain a spatially resolved picture of DNA hydration and investigate the sources of heterogeneity. In the second part we examine the role of the environment in the chemical step of enzyme catalysis. We focus on two distinct systems with different questions, but relying on a common simulation methodology. We first examine the role of specific active site residues in catalysis by dihydrofolate reductase and we provide a molecular interpretation of recent experimental results. We finally study the role of water in enzyme catalysis in organic solvents, where addition of small amounts of water was shown to accelerate the chemical step. We seek a molecular scale description of this effect
Solé, Ferré Anna. "Correction of point mutations at the endogenous locus of the mammalian dihydrofolate reductase gene using polypurine reverse hoogsteen hairpins." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/379822.
Full textAquest treball es centra en l'estudi de pinces de polipurines "polypurine reverse Hoogsteen (PPRH)", i la seva capacitat com eina en la correcció de gens. La reparació d'una mutació puntual en el seu locus endogen ha sigut el principal tema de molts investigadors en les últimes dècades, utilitzant diverses estratègies com per exemple la teràpia de substitució de gens (GAT) i diferents oligonucleòtids de reparació. La fibrosi quística, anèmia de cèl.lules falciformes i la malaltia de Tay-Sachs son alguns exemples de la gran quantitat de trastorns causats per una mutació puntual. En aquest treball, presentem una metodologia de reparació alternativa que utilitza molècules PPRH, desenvolupades en el nostre laboratori inicialment com a eina de silenciament gènic, amb la hipòtesi que també es podrien aplicar com a eina de correcció de gens. Els PPRH son unes molècules d'ADN de doble cadena, formades per dos dominis de homopurines antiparal•eles, connectades per un bucle de 5 timidines, que formen enllaços de Hoogsteen reversos i intramoleculars. Els PPRHs s'han descrit per unir-se eficaçment a la doble cadena d'ADN formant una estructura de tríplex, i han sigut dissenyats tant contra la cadena motlle com contra la cadena codificant de l'ADN. Tenint en compte la capacitat dels PPRHs per formar una estructura de tríplex amb la cadena de pirimidines de l'ADN, en l'estudi presentat aquí volíem explorar la capacitat dels PPRHs per corregir mutacions puntuals. En primer lloc, es van estudiar les condicions in vitro en les que els PPRHs s'unien a la doble cadena de l'ADN i la mantenien oberta, mitjançant assajos d'unió. Tot seguit, hem dissenyat diferents PPRHs reparadors, tot afegint, al nucli del PPRH, una cua reparadora, complementaria a la regió mutada de l'ADN excepte pel nucleòtid que ha de ser corregit. Aquests PPRHs reparadors s'han utilitzat en cèl.lules de mamífer per reparar una mutació puntual en un plàsmid de la dihydrofolate reductasa (dhfr). Per últim, els resultats positius ens van portar a estudiar la capacitat dels PPRHs reparadors per reparar diferents línies cel.lulars que contenien diferents tipus de mutacions puntuals en el gen endogen de la dhfr. A més, també hem desenvolupat un PPRH millorat, anomenat LDR-PPRH, per "Long-Distance-Repair-PPRH", per reparar mutacions puntuals molt distants respecte la seqüència diana del nucli del PPRH. Tenint en compte la possible alta proporció de guanines en una seqüència de PPRH, es va dur a terme una caracterització in vitro d'aquestes molècules per estudiar l'efecte de les guanines en la formació d'estructures secundàries, com per exemple els G-quàdruplex. També es va estudiar la conformació de triple hèlix formada pels PPRH reparadors amb les seves seqüències diana de pirimidines, fins i tot quan el PPRH reparador es plega en una estructura de G-quàdruplex enlloc de en forma de pinça. Com a segona part de la tesi, hem desenvolupat una nova aplicació de la tècnica d'assaig de canvi de mobilitat electroforètica (EMSA), per demostrar la unció entre els miRNAs i les seves seqüències diana. Durant més de dues dècades, la investigació en el nostre laboratori s'ha centrat en l'estudi farmacogenòmic de la resistència al metotrexat (MTX) en la quimioteràpia contra el càncer, per la inhibició del gen de la dhfr. A més de l'amplificació gènica, el nostre grup ha demostrat que molts gens estan involucrats en el mecanisme, així com també hi estan involucrats els micro-RNAs. El miR-224 i els seus gens diana, SLC4A4, CDS2 i HSPC159 van ser identificats per jugar un paper important en la resistència al MTX en cèl.lules de càncer de colon. Per aquesta raó, el miR-224 va ser l'escollit per mostrar d'una manera directa i específica, la seva habilitat per unir-se al gen diana SLC4A4, establint així la tècnica d'EMSA com un mètode senzill i útil per validar la interacció entre un miRNA i la seva diana específica de mRNA.
Groom, Colin Roger. "Crystallographic studies on the binding of inhibitors to wild-type and site-directed mutants of a mouse dihydrofolate reductase." Thesis, University of Leeds, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397792.
Full textTahar, Rachida. "Etude de la dihydrofolate reductase de plasmodium falciparum et plasmodium vivax, bases moleculaires et biochimiques de la resistance aux antifoliniques." Paris 12, 1999. http://www.theses.fr/1999PA120054.
Full textHankins, Eleanor Gray. "Drug resistance in Plasmodium falciparum : the role of point mutations in dihydropteroate synthase and dihydrofolate reductase analyzed in a yeast model /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/10290.
Full textEldin, de Pecoulas Philippe. ""Plasmodium falciparum" et "Plasmodium vivax" : Etude comparée de la dihydrofolate réductase-thymidylate synthétase, polymorphisme moléculaire et relations avec la chimiosensibilité aux antifoliniques." Paris 5, 1996. http://www.theses.fr/1996PA05P621.
Full textCorrêa, Denis da Silva. "Docking de compostos da família das ariloxazinas em enzimas relacionadas com a malária." Universidade Federal de São Carlos, 2010. https://repositorio.ufscar.br/handle/ufscar/6964.
Full textUniversidade Federal de Minas Gerais
Malaria disease, caused mainly by Plasmodium falciparum parasite, afflicts about 500 million people and causes nearly one million deaths every year. For the development of new drugs against this disease, one possible approach is to identify an enzyme that plays a key role in P. falciparum development and presents significantly different properties from the corresponding human one. These differences can be exploited in the design of specific inhibitors of the parasite s protein, thus, three different enzymes were selected as possible targets. As there are evidences suggesting that increasing oxidative stress can effectively inhibit the growth of the malarial parasite the enzyme Glutathione Reductase of P. falciparum (PfGR), responsible for the parasite s antioxidant defense, has become a potential target for the design and development of inhibitors. The second target was the P. falciparum Dihydrofolate Reductase-Thymidylate Synthase (PfDHFR-TS), and in this case blocking its action stops the dTMP production and DNA synthesis in the parasite. The third chosen target was the P. falciparum Lactate Dehydrogenase (PfLDH), whose inhibition interrupts the ATP formation and thus causing the death of the parasite. So that a family of arilloxazines compounds, together with chloroquine and methylene blue, were studied by means of docking simulations in the binding sites of these enzymes and also in the corresponding human enzymes for comparison. The three-dimensional structures of the enzymes and of chloroquine and methylene blue were obtained from the Protein Data Bank (PDB). The structures of the arilloxazines compounds, in turn, were obtained by molecular modeling with HyperChem 6.01 and MOPAC2009 programs, using as starting models similar crystallographic structures deposited in the Cambridge Structural Database. Docking simulations were performed using GOLD 4.0.1. The docking results showed that the enzymes PfGR and PfDHFR-TS are not the preferential targets of chloroquine. For the methylene blue it was possible to elucidate its binding mode in hGR and PfGR. Regarding the arilloxazines it was possible to show that they present their higher affinity for hGR, followed by PfGR, hDHFR, PfDHFR-TS, PfLDH and hLDH. In the case of GRs, the interface site was the preferred binding site. The results suggest that if arilloxazines compounds with higher affinity for PfGR are desirable then a pentafluorophenyl should be attached at the N10 position, as in the 2e compound. When searching for arilloxazines with higher affinity for PfLDH, it seems to be desirable a carboxymethyl group at the N3 position (as in 5b) and a pentafluorophenyl group at N10 (as in 2e). Finally, the results suggest that in general the studied arilloxazines probably will present a higher affinity for hDHFR than PfDHFR-TS. All these results are an important starting point for the design of new arilloxazines ligands so that they can be used as lead compounds in the search for new drugs against malaria.
A malária, causada principalmente pelo Plasmodium falciparum, atinge cerca de 500 milhões de pessoas e causa aproximadamente um milhão de mortes todos os anos. Para o desenvolvimento de novos fármacos contra esta doença, uma das abordagens possível é identificar uma enzima que desempenhe papel vital no desenvolvimento do P. falciparum e apresente propriedades significantemente diferentes das enzimas humanas correspondentes, de modo que tais diferenças possam ser exploradas no design de inibidores específicos à proteína do parasita. Existem evidências sugerindo que aumentar o estresse oxidativo pode inibir eficientemente o crescimento do parasita causador da malária e, portanto, a enzima Glutationa Redutase do P. falciparum (GRPf), responsável por sua defesa antioxidante, tornou-se um alvo em potencial para o desenvolvimento de inibidores. Também, o bloqueio da ação da Diidrofolato Redutase-Timidilato Sintase do P. falciparum (DHFR-TSPf) interrompe a produção de dTMP e a síntese de DNA no parasita. Ainda, espera-se que a inibição da Lactato Desidrogenase do P. falciparum (LDHPf) interrompa a produção de ATP no parasita e, consequentemente, cause sua morte. Portanto, estudou-se o comportamento de compostos da família das ariloxazinas, da cloroquina e do azul de metileno nos sítios de ligação destas enzimas, além das enzimas humanas correspondentes para fins de comparação, por meio de cálculos de docking. As estruturas tridimensionais das enzimas foram obtidas no Protein Data Bank (PDB). As estruturas dos inibidores da família das ariloxazinas, por sua vez, foram obtidas por meio de modelagem molecular, utilizando os programas HyperChem 6.01 e MOPAC2009, a partir de estruturas cristalográficas semelhantes obtidas no Cambridge Structural Database; já as estruturas da cloroquina e do azul de metileno foram obtidas também no PDB. Os cálculos de docking destes compostos nos sítios de ligação das enzimas estudadas foram realizados utilizando o programa GOLD 4.0.1. Com base nos resultados de docking, sugere-se que as enzimas GRPf e DHFR-TSPf não são alvos preferenciais da cloroquina. Também, pôde-se elucidar o possível modo de ligação do azul de metileno nas enzimas GRh e GRPf. No geral, foi possível sugerir ainda que as ariloxazinas devam apresentar maior afinidade pela GRh, seguida por GRPf, DHFRh, DHFR-TSPf, LDHPf e LDHh, nesta ordem. Nas GRs, o sítio da interface foi o sítio preferencial de ligação. Para se buscar inibidores da família das ariloxazinas com maior afinidade pela GRPf, sugere-se considerar um pentafluorfenil como substituinte na posição N10, como no composto 2e. Ainda, na busca por ariloxazinas com maior afinidade pela LDHPf, sugere-se considerar um carboximetil na posição N3 (como o de 5b) e um pentafluorfenil na posição N10 (como em 2e). Por fim, foi obtido que as ariloxazinas estudadas possivelmente apresentarão, em geral, uma maior afinidade pela DHFRh do que pela DHFR-TSPf. Estes dados podem ser tomados como ponto de partida para o design de novos compostos da família das ariloxazinas, a fim de que possam atuar como compostos líderes na busca por novos fármacos contra a malária.
Karatzas, Antonios. "Evaluation of chemoprotection conferred against alkylating drugs by a bicistronic retroviral vector expressing the A3 isoform of glutathione S-transferase and a variant of human dihydrofolate reductase." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80298.
Full textAlonso, Hernan, and hernan alonso@anu edu au. "Computer Modelling and Simulations of Enzymes and their Mechanisms." The Australian National University. The John Curtin School of Medical Research, 2006. http://thesis.anu.edu.au./public/adt-ANU20061212.161155.
Full textLegrand, Baptiste. "Analyse d'interactions moléculaires par RMN : Étude de la DHFR en présence d'osmolytes et structures de pseudopeptides antimicrobiens en environnement." Phd thesis, Rennes 1, 2009. https://tel.archives-ouvertes.fr/tel-00453405.
Full textThe osmolytes are small molecules accumulated by cells of a wide variety of organisms in response to hyperosmotic stress to maintain the cellular volume. Nervetheless, enzyme activity is inhibited by these cosolutes and the molecular basis of their effects on the proteins properties is of great interest. We studied the DHFR in presence of the osmolytes. We demonstrate that its overall structure is maintained. While the osmolytes stabilize the DHFR structure, they inhibit its activity at the same time. The k[index :]off, of substrate analogues decreases with increasing the osmolyte concentrations and reflects the variation of DHFR catalytic rate. The study of the DHFR dynamic on several timescales gives answer of the origins of the DHFR inhibition in presence of osmolytes. The second chapter concerns the study of the structure-activity relationship of antimicrobial peptides. The main objective of this project is to develop new drugs. We solved NMR solution structure of in various model membranes
Yahashiri, Atsushi. "Comparative investigations of H-transfer in dihydrofolate reductases from different families." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/763.
Full textMartins, João Paulo Machado. "Triagem virtual de inibidores da enzima di-hidrofolato redutase de Schistosoma mansoni (SmDHFR)." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/9/9138/tde-18102017-152832/.
Full textSchistosomiasis is one of morbidity\'s main causes in tropical and subtropical countries, which leads to serious socioeconomic consequences. Praziquantel and oxamniquina are the drugs currently available for treating this disease, but reports points that the parasite has been resistant to both drugs, which suggests the need for new therapeutic strategies for the treatment of this disease. However, there is little interest in the pharmaceutical industry in developing drugs against neglected tropical diseases, including schistosomiasis. Due to these factors, the present work has the general objective to use computational tools to identify SmDHFR inhibitors which could be good candidates for developing new drugs. Evaluation of the exclusive characteristics of the S. mansoni protein were performed by FASTA sequence analyses in comparison to DHFR from other organisms. In order to guarantee the selective action of these molecules against the parasite enzyme, the molecular interaction fields selective for SmDHFR were calculated and used in the construction of the pharmacophoric model, which was further used in the virtual screening of SmDHFR inhibitors. Computational studies were performed and those led us to 20 molecules with a good complementarity with the pharmacophoric model that was previously generated and with potential to be SmDHFR inhibitors.
Tu, Yongxue. "Etude physicochimique et biochimique des dihydrofolates reductases et de l'effet antifolate des thiosemicarbazones." Paris 7, 1988. http://www.theses.fr/1988PA077164.
Full textThomson, Christopher J. "Biochemical analysis of the recent plasmid-encoded trimethoprim-resistant dihydrofolate reductases in gram-negative bacteria." Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/19351.
Full text