Дисертації з теми "DsbD"
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Mavridou, Despoina A. I. "Elucidation of the structure-function relationships in the bacterial transmembrane disulfide oxidoreductase DsbD." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497048.
Повний текст джерелаQuinternet, Marc. "Analyse structurale et dynamique par RMN des domaines N-terminaux des protéines DsbD et PilB de Neisseria meningitidis et de leur interaction." Thesis, Vandoeuvre-les-Nancy, INPL, 2008. http://www.theses.fr/2008INPL102N/document.
Повний текст джерелаWe show, on one hand, that the NMR solution structure of DsbD N-terminal domain from Neisseria meningitidis (nDsbD) displays, in its reduced state, an immunoglobulin fold with a closed conformation of its active site. Nonetheless, our backbone dynamics study shows that the cap-loop region of the protein, which covers active residues in both oxidized and reduced forms, displays internal motions. This illustrates the inner structural adjustment capacities of nDsbD. On the other hand, we show that NMR solution structures of the oxidized and reduced forms of N. meningitidis NterPilB display a thioredoxin-like fold. These two structures appear to be very similar and globally rigid. Consequently, the NterPilB characteristic FLHE loop, which covers one edge of the active site, does not reveal new structural and/or dynamics properties for its involvement in the substrate specificity. Finally, we point out, from the structural and dynamics study of a complex between nDsbD and NterPilB from N. meningitidis, that nDsbD exhibits a powerful adaptability in its complex state. Its cap-loop region opens and comes over the a helix containing the NterPilB active cysteines. In contrast, the NterPilB FLHE loop does not seem to play a role in the complex stabilization. We propose that internal dynamics should facilitate, on one hand, the relative adaptability between the two partners of the complex and, on the other hand, their subsequent dissociation
Quinternet, Marc Cung Manh Thông. "Analyse structurale et dynamique par RMN des domaines N-terminaux des protéines DsbD et PilB de Neisseria meningitidis et de leur interaction." S. l. : S. n, 2008. http://www.scd.inpl-nancy.fr/theses/2008_QUINTERNET_M.pdf.
Повний текст джерелаUrban, Andreas. "Die Rolle der Thiol-Disulfid-Oxidoreduktasen DsbA und DsbC bei der Proteinsekretion in Pseudomonas aeruginosa." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=959986855.
Повний текст джерелаFrank, Lisa Lucie [Verfasser]. "Die Bedeutung der Proteine BamC, HlpA, DsbB, DsbH und DsbA1 für die Integrität der Außenmembran von Pseudomonas aeruginosa / Lisa Lucie Frank." Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/122345116X/34.
Повний текст джерелаBhandari, Murari. "Investigating the role of DsbA enzymes in growth and virulence of uropathogenic Escherichia coli." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/120696/2/Murari_Bhandari_Thesis.pdf.
Повний текст джерелаHittel, Dustin S. "Overexpression of the dsvD gene of Desulfovibrio vulgaris Hildenborough and characterization of the DsvD protein." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ38590.pdf.
Повний текст джерелаMitta, Ever. "Consulting report – DSB Mobile." Master's thesis, Pontificia Universidad Católica del Perú, 2017. http://tesis.pucp.edu.pe/repositorio/handle/123456789/9409.
Повний текст джерелаDSB Mobile es una pequeña empresa peruana de desarrollo de software con sede en Lima. DSB Mobile se especializa en el desarrollo de aplicaciones móviles y web y ha trabajado con grandes empresas como Samsung, Claro y Entel. La compañía está compuesta por el Gerente General, Zico Herrera, un gerente de ventas, un gerente de operaciones y desarrolladores de software a tiempo completo y algunos que se contratan en base a la demanda actual de servicio. DSB Mobile ha establecido una fuerte reputación y marca en Perú y ahora está buscando expandirse fuera de Perú donde puedan introducir sus productos de software en los mercados internacionales. En su aspiración de internacionalización, DSB Mobile está tratando de descubrir no sólo los mercados más rentables para su empresa, sino también los mercados que mejor se alinean con la misión DSB Mobile. La solución a su problema de expansión fue determinar los mejores mercados utilizando una variedad de factores tanto cuantitativos como cualitativos. Al utilizar un informe de competitividad de TI que fue realizado por la British Software Alliance, se utilizó como punto de referencia para determinar los países mejor clasificados para la competitividad de TI y los mejores países para llevar a cabo negocios en base de importantes indicadores asociados a estos. Combinado con estadísticas de datos de software en términos de gastos por proyecto y coste de consultores en TI, esto permitió reducir aún más el alcance para obtener un mercado más atractivo, rentable y mutuamente beneficioso. El plan de implementación propuesto involucró dos líneas de mercado, a saber, la línea del mercado norteamericano y la línea del mercado europeo. La solución propuesta posee diferentes escenarios; por ejemplo, el escenario con trabajo moderado consta de 1 proyecto por mes y tiene un costo total de $391,065 por año obteniendo así una rentabilidad de $180,736. El gráfico de Gantt esbozado pretende guiar a la compañía con la implementación paso a paso de esta expansión internacional y prepararlos para ejecutar este plan de la manera más eficiente y efectiva
Tesis
Mota, Lúcia Santiago. "DSD: interfaces e interacções." Master's thesis, Universidade de Aveiro, 2009. http://hdl.handle.net/10773/4531.
Повний текст джерелаAs ferramentas de Front e Back Office baseadas em serviços Web são actualmente uma realidade comum. Estas fornecem ao utilizador, independentemente do local ou mesmo do terminal, dentro de certos contextos, uma interface única e diferenciada consoante o perfil do utilizador. Para cada perfil, estas interfaces fornecem unicamente o conjunto de comandos e informações necessárias. A plataforma de DSD, onde já se gerem muitas das informações que se relacionam com o processo de manutenção do DETI, tem múltiplos utilizadores com perfis e objectivos muito diferentes. Este documento começa com um estudo do estado inicial da plataforma existente de forma a identificar toda a sua funcionalidade. Posteriormente, é realizada uma análise das novas tarefas a implementar, utilizadores e respectivo modelo de domínio de forma a conhecer toda a nova base estrutural da plataforma. Finalmente é analisada a interface da plataforma a nível de usabilidade para garantir a satisfação dos utilizadores. Toda a plataforma está desenvolvida a pensar em futuras evoluções para continuar a evoluir e trazer valor à organização interna dos departamentos universitários.
The tools of Front and Back Office based on Web Services are nowadays a common reality. These give the user, regardless of location or terminal, within a certain context, a single interface that varies depending of the user profile. For each profile, these interfaces provide only the necessary set of commands and information. The DSD platform, which is already generating a lot of information, related with the managing process of DETI, has multiple users with very different profiles and objectives. The work begins with a study of the initial state of the existing platform with the objective of identifying the available functionality. Furthermore, all the new tasks, users and domain model are analyzed in order to define the new structural basis of the platform. Finally, an usability study of the user interface of the platform is performed in order to obtain an acceptable usability level and ensure user satisfaction. The entire platform is developed considering future developments, in order to continue evolving and bringing value to the internal organization of university departments.
Mizuno, Nobuhiro. "Structure-based functional analysis of DsrD protein." 京都大学 (Kyoto University), 2004. http://hdl.handle.net/2433/147845.
Повний текст джерелаSinha, Sunita. "Functional characterisation of three DsbA proteins of Neisseria meningitidis." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417906.
Повний текст джерелаAnderson, Taylah. "Investigating the repertoire of DsbA enzymes in Klebsiella pneumoniae." Thesis, Queensland University of Technology, 2022. https://eprints.qut.edu.au/235382/1/Taylah%2BAnderson%2BThesis%2BIF80%281%29.pdf.
Повний текст джерелаPonnampalam, Thilaka Vadhanaa. "Phenotypic characterization of a Salmonella typhimurium dsbA null mutant and identification of factors that regulate the expression of the disulfide oxidoreductase DsbA (Salmonella typhimurium)." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0005/MQ42679.pdf.
Повний текст джерелаTeixeira, Vera Marisa Martins. "DSD-mobile: interface móvel para portal departamental." Master's thesis, Universidade de Aveiro, 2010. http://hdl.handle.net/10773/5599.
Повний текст джерелаOs dispositivos móveis permitem aceder à informação em qualquer lugar e em qualquer momento pois, fica imediatamente disponível a quem necessita dela. Os estudantes e docentes de uma Universidade são um grupo de utilizadores que fica potencialmente beneficiado com a evolução das tecnologias móveis. O acesso facilitado a toda a informação torna-se real através do acesso por dispositivos móveis. Criar uma aplicação Web constitui um desafio, pois não basta conhecer os processos realizados pelos potenciais utilizadores, sendo igualmente necessário assegurar que funcionam do mesmo modo quando são executados através de um equipamento com características muito próprias, como é o caso dos telemóveis. O trabalho realizado no contexto desta dissertação, teve como principal finalidade a criação de uma interface móvel do portal departamental dsd.av.it.pt capaz de fornecer aos alunos do Departamento de Electrónica, Telecomunicações e Informática, a possibilidade de acesso a informações necessárias no momento. A dissertação em causa passou, numa primeira fase, por uma investigação do estado da arte no contexto dos dispositivos móveis. Foi realizada a análise de requisitos dos utilizadores de forma a perceber as suas necessidades pois a capacidade e mentalidade dos utilizadores são por vezes um obstáculo à implementação das tecnologias móveis. A criação de uma aplicação enfrenta não só o desafio na concepção e na implementação mas também na aceitação por parte dos seus utilizadores. Seguidamente foi implementada a dita aplicação tendo em consideração os constrangimentos existentes nos dispositivos móveis que pudessem afectar a consistência e coerência da mesma. Por fim, foram realizados testes, através de um protótipo funcional, com utilizadores reais de forma a avaliar a validade da solução proposta.
The mobile devices enable the access to information at any place and at any time since this is immediately available to those who need it. The students and lecturers of a university are a group of users which is potentially benefited with the development of mobile technologies. The easy access to all information becomes real through the access through mobile devices. Creating a Web application is a challenge since it is not enough to know the processes carried out by potential users, being also necessary to guarantee they work the same way when they are executed through equipment with own characteristics, as the case of mobile phones. The work done in the scope of this dissertation had as main aim the creation of a mobile interface of the departmental portal dsd.av.it.pt able to provide the students of the Department of Electronics, Telecommunications and Informatics, with the possibility of access to needed information. This dissertation went in a first phase through an investigation of the state of art in the scope of mobile devices. The analysis of the requirements of users was carried out in order to understand their necessities since the ability and mentality of the users are many times an obstacle to the implementation of mobile technologies. The creation of an application faces not only the challenge in the conception and implementation but also on the acceptance by its users. Then this application was implemented taking into account the existing constraints in the mobile devices that could affect its consistency and coherence. At last, tests were carried out through a functional prototype, with real users in order to assess the validity of the proposed solution.
Ma, Yue. "Double-strand breaks (DSBs) and structure transition on genome-sized DNA." Thesis, https://doors.doshisha.ac.jp/opac/opac_link/bibid/BB13097333/?lang=0, 2018. https://doors.doshisha.ac.jp/opac/opac_link/bibid/BB13097333/?lang=0.
Повний текст джерелаThe protective effect of ascorbic acid (AA) and DMSO against double-strand breaks (DSBs) in DNA was evaluated by single-molecule observation of giant DNA (T4 DNA; 166kbp) through fluorescence microscopy. Samples were exposed to three different forms of radiation: visible light, γ-ray, and ultrasound or freeze/thawing. The change of the higher-order structure of genomic DNA molecules in the presence of alcohols by use of single DNA observation with fluorescence microscopy, by focusing our attention to unveil the different effect between 1-propanol and 2-propanol.
博士(工学)
Doctor of Philosophy in Engineering
同志社大学
Doshisha University
Turcot, Isabelle. "Identification and characterization of the Salmonella enterica serovar Typhimurium disulfide oxidoreductase DsbA." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22410.pdf.
Повний текст джерелаCOUPRIE, JOEL. "Etude structurale et dynamique de l'oxydoreductase de dithiol-disulfure dsba d'escherichia coli." Paris 11, 2001. http://www.theses.fr/2001PA112051.
Повний текст джерелаLiuski, T. (Teemu). "AM- ja DSB modulaatioiden toteuttaminen Simulink-ohjelmistolla USRP-ohjelmistoradioalustalle." Bachelor's thesis, University of Oulu, 2019. http://jultika.oulu.fi/Record/nbnfioulu-201902271248.
Повний текст джерелаChen, Liang M. Eng Massachusetts Institute of Technology. "Product & customer profiling for Direct Store Delivery (DSD)." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/45255.
Повний текст джерелаIncludes bibliographical references (leaves 69-70).
This thesis is to analyze the suitability of different products, suppliers and customers for Direct Store Delivery (DSD) model with respect to the qualitative profile and the quantitative benefits. During the research, interviews with retailers, suppliers and industrial experts provide the basis and insight for the qualitative analysis of factors that make certain products, suppliers and customers best suitable for a DSD model. In order to quantify the benefits that DSD can bring to the entire supply chain, a generic model of the DSD system is built. Based on the quantitative analysis, the stock-out at store shelf is simulated in order to understand the effects of DSD operations to the minimization of stock-out costs at the store shelf, a major benefit that DSD is assumed to generate. With the conceptual framework and the quantitative model, this thesis is aimed at providing supply chain managers a comprehensive perspective to adopt DSD for their products and customers.
by Liang Chen.
M.Eng.in Logistics
Begovic, Michael [Verfasser]. "Häufigkeit der HLA-Null-Allele in der Deutschen Stammzellspenderdatei (DSSD) Ulm / Michael Begovic." Ulm : Universität Ulm, 2018. http://d-nb.info/1162540052/34.
Повний текст джерелаGirardi, Cristina. "Human cell response to ionizing radiation in ground gravity and microgravity condition." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3427434.
Повний текст джерелаLe radiazioni ionizzanti (IR), colpendo le cellule degli organismi eucarioti è in grado di provocare danni a proteine, lipidi e molecole di DNA, in modo diretto o indiretto come risultato della formazione di radicali liberi. Tra i numerosi tipi di danno al DNA, le rotture a doppio filamento o double-strand breaks (DSBs) rappresentano il tipo di lesione più grave, dal momento che una riparazione inefficiente o non accurata può portare a morte cellulare o instabilità genomica. La presenza di DSBs induce una complessa risposta al danno al DNA che vede coinvolti una serie di eventi cellulari quali: la rilevazione del danno, la trasduzione del segnale agli effettori della riparazione, l’arresto del ciclo cellulare e l’induzione di apoptosi. Nei mammiferi, una delle risposte cellulari più precoci dopo l’induzione di una doppia rottura è la fosforilazione dell’istone H2AX (γ-H2AX) in corrispondenza del sito di danno, che avviene per opera delle fosfatidilinositolol-3-OH-chinasi (ATM, DNA-PK and ATR). Questo evento sembra essere importante nel reclutamento di fattori di segnalazione del danno e di proteine coinvolte nella riparazione delle DSBs nei siti danneggiati (i.e 53BP1, Mre11, Rad50, Nbs1), dando origine a ionizing radiation-induced foci (IRIF), che possono essere costituiti da migliaia di queste molecole proteiche. Monitorando la cinetica di formazione e scomparsa degli IRIF, che si accumulano nei siti danneggiati, è possibile analizzare il danno al DNA e la sua riparazione; in particolare, è stato osservato che la diminuzione dei foci di γ-H2AX correla con la progressione della riparazione delle DSBs. Gli eventi di segnalazione attivati in risposta alle radiazioni ionizzanti dipendono, oltre che dalle caratteristiche genetiche e fisiologiche del sistema biologico osservato, anche dalle condizioni ambientali presenti durante la riparazione del DNA. Per questa ragione abbiamo analizzato e confrontato la risposta cellulare umana alle IR in condizioni diverse di gravità, normale come sulla Terra (1g) e ridotta come nell’ambiente spaziale; in quest’ultimo l’esposizione ai raggi cosmici a cui l’uomo è soggetto durante le missioni spaziali e associata alla riduzione della forza di gravità. L’ambiente spaziale è caratterizzato dalla presenza di radiazioni ionizzanti, nella forma di particelle atomiche cariche che rappresentano il più importante fattore limitante la lunga permanenza dell’uomo nello spazio, ma anche dalla condizione di assenza di peso, che prende il nome di microgravità (10-4–10-6g). In letteratura sono stati riportati alcuni effetti della microgravità osservati in astronauti di ritorno dai voli spaziali, questi riguardano: la soppressione del sistema immunitario, l’atrofia muscolare, problemi cardiovascolari e la demineralizzazione e decalcificazione ossea. Cellule mantenute in coltura durante le missione spaziali e modelli a terra della microgravità mostrano inibizione della proliferazione dei linfociti, soppressione o alterazione della secrezione di citochine, modificazioni del citoscheletro e anche incremento delle aberrazioni cromosomiche e apoptosi. Pertanto, capire se gli effetti della radiazione ionizzante possano essere influenzati dalla microgravità rimane un punto di rilevante importanza nella valutazione dei rischi durante le missioni spaziali. In questo lavoro, la microgravità è stata simulata in laboratorio usando il bioreattore “Rotating Wall Vessel” (Synthecon) messo a punto nei laboratori della NASA a Houston; questo strumento permette di riprodurre un aspetto dei voli spaziali che è l’assenza di peso, condizione che prende il nome di “modeled microgravity” (MMG). Nella prima parte di questo progetto è stata studiata la riparazione delle DSBs in linfociti umani irradiati con raggi gamma e mantenuti durante il tempo di riparazione in 1g o MMG. La formazione e la scomparsa dei foci dell’istone γ-H2AX è stata monitorata a diversi tempi dall’irradiazione mediante immunofluorescenza; nei medesimi campioni è stato anche analizzato l’indice apoptotico e la frammentazione del DNA, quest’ultimo con la tecnica della pulsed-field gel electrophoresis (PFGE) in cui la frazione di DNA rilasciata nel gel (FR) è considerata una misura delle DSBs. I risultati ottenuti confermano che l’incubazione in MMG durante il tempo di riparazione influenza la sopravvivenza cellulare, l’apoptosi e ritarda la riparazione delle DSBs, incrementando l’effetto genotossico delle radiazioni ionizzanti. Sulla base delle osservazioni fatte, si è passati a studiare se la IR e la MMG possono avere un’azione sinergica sulle cellule analizzando i profili di espressione dei microRNAs: regolatori negativi dell’espressione genica. I microRNAs (miRNAs) sono una classe di corti RNA (~22nt) endogeni, che svolgono un ruolo chiave in molti processi cellulari poiché reprimono l’espressione dei mRNA target. Nelle cellule animali, queste molecole vanno a reprimere la traduzione dei geni codificanti proteine legandosi a sequenze complementari nelle regioni non tradotte al 3’ terminale (3’UTR) dei mRNA. Per questo motivo i miRNAs sono coinvolti in numerosi processi biologici come: lo sviluppo, la proliferazione cellulare, l’apoptosi, la funzionalità delle cellule staminali e la tumorigenesi. Scopo: Questo progetto si proponeva di: i) analizzare l’efficienza di riparazione del DNA in condizione di microgravità simulata (MMG), puntando l’attenzione alla cinetica di riparazione delle DSBs; ii) capire se la radiazione ionizzante e la microgravità simulata possono avere un’azione sinergica in cellule umane, confrontando i miRNA radio-responsivi nelle due condizioni di gravità (1g e MMG) Attività svolta: La presenza di foci nucleari dell’istone γ-H2AX e l’indice apoptotico sono stati monitorati in linfociti umani irradiati con raggi γ e non, incubati in 1g e MMG. Negli stessi campioni è stata studiata la riparazione delle DSBs analizzando la frazione di DNA rilasciata (FR) dopo Pulsed-field gel electrophoresis (PFGE). In seguito, usando l’approccio dei microarray con “Human miRNA microarray Kit V2” (Agilent) e della real-time qPCR, sono stati analizzati i profili di espressione dei miRNAs in linfociti umani irradiati con raggi γ e incubati in 1g e MMG. Impiegando poi i microarrays “Whole Human Genome Oligo Microarray” (Agilent) per gli stessi campioni di cellule, è stato possibile determinare i profili di espressione genica; allo scopo di identificare i probabili mRNA target dei miRNA radio-responsivi i dati di espressione dei miRNA e dei mRNA sono stati integrati in un’analisi di anticorrelazione. Infine, per studiare i processi biologici maggiormente coinvolti nella risposta cellulare alle radiazioni ionizzanti è stata eseguita una Gene Ontology analysis (GO) applicata ai miRNA-mRNA target significativamente anti-correlati. Risultati e conclusioni: I risultati ottenuti dallo studio dei foci dell’istone γ-H2AX in PBL irradiati mostrano che il numero medio di foci/nucleo a tempi brevi di riparazione nelle due condizioni di gravità è comparabile. Al contrario, per tempi lunghi, la diminuzione del numero di foci è significativamente differente; infatti, a 24h dall’irradiazione i PBL incubati in 1g presentano 2 foci/nucleo, mentre quelli in MMG 6.4 foci/nucleo. Per verificare che la scomparsa dei foci di γ-H2AX fosse correlata con la riparazione delle DSBs è stata utilizzata la tecnica della PFGE. La cinetica di riparazione delle DSBs è stata analizzata in PBL irradiati e incubati in 1g e MMG; nelle cellule incubate in MMG il contenuto di DNA frammentato era maggiore rispetto alla 1g (FR 77% vs. 33% a 2 h e FR 50% vs. 17% a 6 h, rispettivamente). Probabilmente la MMG influisce sulle modificazioni strutturali della cromatina che avvengono in risposta alla DSBs, diminuendo l’efficienza di riparazione; pertanto, la riparazione delle DSBs che in 1g avviene in poche ore, richiede più tempo in MMG. Nella seconda parte del progetto sono stati analizzati i profili di espressione di miRNA in PBL irradiati con raggi γ e incubati in 1g e MMG. Dai risultati ottenuti è emerso che la radiazione altera i profili di espressione dei miRNA in modo dose e tempo dipendente, in entrambe le condizioni di gravità. L’esposizione ai raggi gamma in 1g altera i profili di espressione dei miRNA, sia a tempi brevi che lunghi, con maggior numero di miRNA radio-responsivi a 24h dopo esposizione alla dose maggiore (2Gy). Dal confronto dei profili di espressione di miRNA in PBL irradiati e mantenuti 24h nelle due condizioni di gravità vengono individuati miRNAs espressi in modo specifico durante l’incubazione in MMG; questi miRNAs vengono probabilmente alterati dall’azione combinata della IR con la MMG con effetto dose-dipendente. Anche le cellule non irradiate ma mantenute 24h in MMG presentano 42 miRNA deregolati rispetto alla 1g. Per far luce sul meccanismo col quale i miRNAs possono modulare alcuni processi biologici in risposta alle radiazioni ionizzanti, sono stati analizzati i profili di espressione di mRNAs negli stessi campioni per i quali sono stati ricavati i profili dei miRNAs. L’analisi di anti-correlazione tra i miRNA e i mRNA differenzialmente espressi e l’analisi computazionale con PITA hanno permesso di predire geni target dei miRNA. Infine, è stata eseguita la Gene Ontology analisi su geni target significativamente anti-correlati, allo scopo di identificare le categorie biologiche di appartenenza. Dai nostri risultati è emerso che alcuni geni sono attivati in PBL irradiati e incubati 24h sia in 1g che MMG, molti di loro sono gravità-specifici. In cellule irradiate con 2Gy e incubate in 1g un grande numero di mRNAs alterati appartiene alle categorie della risposta al danno al DNA (DDR): apoptosi, risposta allo stress, risposta al danno al DNA. Queste categorie non sono risultanti dall’analisi dei PBL irradiati e mantenuti in MMG, dove invece sono alterati processi coinvolti nel differenziamento e attivazione cellulare, sistema immunitario, produzione di citochine ed emopoiesi; tutte caratterizzate da una sostanziale down-regolazione genica. Questo studio fornisce prove che la MMG associata alla radiazione ionizzante porta ad una non appropriata risposta al danno al DNA in linfociti umani, dovuta probabilmente alla perdita di miRNAs radio-responsivi coinvolti nella DDR. Per meglio studiare le funzioni biologiche dei miRNAs in condizione di microgravità simulata è stato necessario puntare l’attenzione sulla validazione dei messageri target predetti e sull’analisi funzionale. Per questa ragione il programma finale di dottorato è stato svolto presso il laboratorio del Prof. Riccardo Dalla-Favera all’“Institute for Cancer Genetics” (Columbia University, New York, USA), per un periodo di sette mesi, allo scopo di acquisire competenze di biologia molecolare che vengono applicate allo studio dei microRNAs.
Findlay, Gordon. "Biogenesis of virulence factors in Vibrio cholerae." Thesis, University of Kent, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294636.
Повний текст джерелаGoecke, Michelle Elisa. "A study of the regulation of expression of dsbA from Salmonella enterica serovar Typhimurium." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ28200.pdf.
Повний текст джерелаMedhi, Darpan K. "The repair of DSBs catalyzed by VMA1 derived endonuclease by homologous recombination during meiosis." Thesis, University of Sheffield, 2013. http://etheses.whiterose.ac.uk/5721/.
Повний текст джерелаSalimbeni, Simona. "Déficience en TDP1 et instabilité génomique dans les cellules non-réplicatives." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30065.
Повний текст джерелаSpinocerebellar ataxia with axonal neuropathy (SCAN1) is a rare recessive neurodegenerative syndrome associated with cerebellar atrophy and peripheral neuropathy. It is caused by a homozygous missense mutation in the tyrosyl-DNA phosphodiesterase-1 (TDP1) gene (A1478G). This results in a substitution of histidine for arginine-493 (H493R) in the TDP1 catalytic site, leading to a reduced TDP1 activity. TDP1 hydrolyses the bond between a DNA 3’-end and a tyrosyl moiety within a trapped topoisomerase I cleavage complex (TOP1cc). TDP1 not only excises trapped TOP1ccs but also processes other 3’-end-blocking lesions, including 3’-phosphoglycolates that result from oxidation. Even so, how TDP1 H493R mutation promotes the SCAN1 phenotype, which is associated with the death of post-mitotic neurons, is unclear. DNA double-strand breaks (DSBs) are infrequent but among the most harmful genomic lesions. Their defective repair can induce cell death, and they have been implicated in the pathogenesis of several human diseases, including neurodegenerative syndromes. Hence, my Ph.D. objective was to investigate whether the SCAN1 phenotype could be related to an accumulation of DSBs in non-replicating cells harboring the H493R mutation of TDP1. The only available models to study the impact of TDP1 H493R mutation were lymphoblastoid cell lines derived from SCAN1 patients compared to those of healthy individuals. Hence, we have generated models of osteosarcoma U2OS cells homozygous for TDP1 H493R or TDP1 KO employing the CRISPR-Cas9 technique. We have also generated primary lung WI38 hTERT fibroblasts TDP1 KO. We found that both TDP1 H493R and TDP1 KO cells accumulate endogenous DSBs, primarily in the G1 phase of the cell cycle compared to S phase. A similar increase of DSBs was observed in quiescent WI38 hTERT cells following depletion of TDP1 with siRNA, suggesting the replication-independent nature of DSBs. Treatment of TDP1 H493R and TDP1 KO cells with camptothecin to induced trapped TOP1ccs, further suggests that accumulation of DSBs could be related to the defective removal of TOP1ccs. Next, we asked whether DSB accumulation in those cells could be related to an increase in DSB production and/or a defect in their repair. Notably, R-loop structures that form co-transcriptionally can induce DSBs in non-replicating cells. We found that TDP1 deficiency modulated R-loop levels at some gene loci, raising the possibility of their implication in DSB formation. Analysis of DSB repair following camptothecin treatment revealed that both TDP1 H493R and TDP1 KO cells were defective in the repair of DSBs in G1 but not in S, with TDP1 H493R having the most pronounced effect. These results suggest that DSBs would accumulate specifically in TDP1-deficient cells that do not undergo replication, due to a defective repair of those breaks. Together, our results provide insights on the etiology of the SCAN1 neurodegenerative syndrome. This work was supported by a PhD fellowship under the French-Italian University VINCI Program 2016
Werner-Rosen, Knut [Verfasser]. "Der subjektive Bedarf an psychologischer Beratung / Psychotherapie von Eltern von Kindern mit DSD / Intersexualität : eine Auswertung der Klinischen Evaluationsstudie von Netzwerk DSD / Intersexualität / Knut Werner-Rosen." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/104683293X/34.
Повний текст джерелаTong, Xinlin. "Mechanisms of action of Dipeptidyl Peptidase 9 in liver cancer." Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/24732.
Повний текст джерелаKyryk, Anzhela. "DSB repair by illegitimate and homologous DNA recombination in Arabidopsis thaliana." [S.l. : s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=96435859X.
Повний текст джерелаGrimstrup, Arne. "An efficient consistency protocol for a DSD-based persistent object system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ62742.pdf.
Повний текст джерелаBurghelea, Andrei E. "Applications of the DSD algorithm with recursive partitioning to nuclear systems." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1406642222.
Повний текст джерелаHulme, Lydia. "The roles of Tel1, Srs2 and Rad6 during meiotic DSB repair." Thesis, University of Sheffield, 2009. http://etheses.whiterose.ac.uk/14522/.
Повний текст джерелаRinaldi, Fabio Cupri. "Estudos estruturais e funcionais das oxidoredutases de pontes dissulfeto da familía DsbA de Xylella fastidiosa." [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/277458.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Instituto de Fisica Gleb Wataghin
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Resumo: As oxidoredutases de pontes dissulfeto da família DsbA são responsáveis pela catálise da formação de pontes dissulfeto em proteínas secretadas para o periplasma, participando do processo de enovelamento de fatores de virulência de diversos organismos. É a proteína com maior potencial de oxidação atualmente caracterizada e tal propriedade é associada às interações eletrostáticas envolvendo resíduos de seu sítio ativo, que apresenta um arranjo Cys-Pro-His-Cys altamente conservado. A bactéria fitopatogênica Xylella fastidiosa possui dois genes adjacentes que codificam duas oxidoredutases pertencentes à família das DsbAs (XfDbsA e XfDbsA2). Embora a XfDbsA conserve o arranjo CPHC, a XfDbsA2 possui a substituição do resíduo histidina, descrito como essencial à atividade da enzima, por alanina (CPAC). Visando a caracterização estrutural e funcional destas proteínas, a estrutura cristalográfica da XfDsbA foi determinada a 1,9 Å de resolução e um modelo por homologia da XfDsbA2 foi construído. Além disso os potenciais de oxidação das enzimas foram determinados por medidas de fluorescência. A estrutura da XfDsbA revelou a presença de um peptídeo ligado próximo a região do sítio ativo em um dos monômeros mostrando, pela primeira vez em uma estrutura a alta resolução, o provável modo de interação da DsbA com um substrato. Os ensaios funcionais revelaram que as DsbAs de X. fastidiosa apresentam potenciais redox similares e ligeiramente superiores ao da homóloga de Escherichia coli. Embora trabalhos sobre a importância do arranjo CPHC têm associado o alto potencial redox das DsbAs à presença do resíduo histidina no sítio ativo, os resultados obtidos para a XfDsbA2 mostraram que a substituição do resíduo de histidina por alanina não afeta seu potencial redox. A análise das interações envolvendo resíduos do sítio ativo mostrou diferenças importantes entre XfDsbA, XfDsbA2 e suas homólogas de E. coli e Vibrio cholerae. Ensaios funcionais com mutantes foram realizados em busca da identificação dos resíduos que possam compensar a ausência da histidina em XfDsbA2. Os resultados obtidos fornecem novas informações sobre o mecanismo molecular dessa família de enzimas
Abstract: Disulfide oxidoreductase DsbA catalyzes disulfide-bond formation in proteins secreted to the periplasm and has been related to the folding process of virulence factors in many organisms. It is the most oxidizing of the thioredoxin-like proteins and DsbA redox power is understood in terms of the electrostatic interactions involving the active site motif CPHC. The plant pathogen Xylella fastidiosa has two chromosomal genes encoding two oxidoreductases belonging to the DsbA family and, in one of them, the canonical motif CPHC is replaced by CPAC. Aiming at the structural and functional characterization of X. fastidiosa DsbAs, the crystal structure of XfDsbA was solved at 1.9 Å resolution and the XfDsbA2 homology model was calculated. We also determined the redox potential of both enzymes by means of fluorescence experiments. The crystal structure of the XfDsbA revealed an electron density corresponding to an 8-mer peptide interacting with the hydrophobic groove on the surface of the monomer C next to the active site. This modeled peptide shows at first time in a high-resolution crystal structure the probable mode of interaction between DsbA and a substrate. Furthermore, the results presented in this work surprisingly show that, despite the absence of the active site histidine in XfDsbA2, both proteins have similar redox potentials. In addition, the structure of XfDsbA revealed critical differences in the interactions involving the active site residues. Biochemical assays with XfDsbA mutants were performed in order to investigate the residues which may be responsible for compensate for the lack of the conserved histidine in XfDsbA2. The results presented contribute to the understanding of DsbA molecular mechanism
Doutorado
Física da Matéria Condensada
Doutor em Ciências
Ishak, Layal. "Etude de la Poly(ADP-ribosyl)ation dans un contexte des cassures double-brins des ADN nucléaire et mitochondriaux chez Drosophila melanogaster." Thesis, Clermont-Ferrand 2, 2016. http://www.theses.fr/2016CLF22685.
Повний текст джерелаBoth nuclear and mitochondrial DNA alterationsarise following exposure to environmental and endogenous stresses. These genomic alterations are various, ranging from base oxidation to DNA strand breaks, single- and double-strand breaks. These damages are highly detrimental to the cell because they can lead to loss of genetic information and thus to cell death. However, cells have developed various mechanisms to counteract this biological issue and to lead up to a complex DNA damage response (DDR). The Poly (ADP- ribosyl) ation (PARylation) is among these DDR systems. This post-translational modification is mainly carried out by PARP and PARG proteins and is characterized by the incorporation of polymers of ADP-ribose on target proteins. The majority of the PARylationfunctions are related to cellular stress response, particulary in response to genomic damages where it is implicated in many DNA integrity pathways such as Base Excision Repair, Non Homologous End Joining and Homologous Recombination. In contrast to the nucleus, PARylation is also described in the mitochondria but its role in mtDNA integrityis still a heavily debate issue, particularly in case of mtDNA DSBs.To understand it, we used Drosophila model wherePARP-B isoform (human PARP-1 ortholog) is the only enzymatically active form in Drosophila PARP family. The aim of this thesis is to study the role of PARylation in response to DSBs induction in nucleus and mitochondrial DNAand then to understand the mechanisms involved in mtDNA integrity and to evaluate the role of PARylation in this process. Our results show that PARylation level remains stable during DSBs induction and also during repair process,contrary to what is shown in Human cells.However, PARP-I and PARP-II mRNA expression increase during repair period. In mitochondria compartment,our data show an increase of mtDNA copy number in presence of mtDNA DSBs. This increased level returns to normal during repair period and seems to be dependent on PARP. All these results suggest that DSBs repair is PARylation independent at the nuclear level but that the presence of PARP is important. In addition, PARP appears to have a role in the regulation of mtDNA replication in response to genotoxic stress
Santos, Clelton Aparecido dos 1984. "Estudos estruturais e funcionais de proteínas relacionadas à patogenicidade de Xylella fastidiosa." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316504.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Xylella fastidiosa é uma bactéria responsável por inúmeras doenças de plantas em culturas economicamente importantes ao redor do mundo, incluindo a clorose variegada dos citros. Após a infecção de seu hospedeiro, as células de X. fastidiosa é apta a formarem uma estrutura de biofilme que bloqueia os vasos xilemáticos, levando a uma condição de estresse hídrico na planta hospedeira e desencadeando o desenvolvimento da doença. Tendo como estímulo a relevância econômica da citricultura para o Brasil e, visando reduzir os prejuízos provocados pelos problemas fitossanitários que acometem esta cultura, foi realizado um consórcio de pesquisa com o intuito de se conhecer completamente o genoma da linhagem 9a5c de X. fastidiosa. Inúmeras proteínas associadas com patogenicidade, adaptação e sobrevivência bacteriana foram identificadas, incluindo XfDsbC (proteína disulfeto isomerase), Xf5'-Nt (5'-nucelotidase), XfTolB (proteína de translocação B) e XfPal (lipoproteína associada ao peptidoglicano) que foram caracterizadas neste estudo. Empregando ferramentas de caracterização de proteínas, aspectos funcionais e estruturais destas quatro proteínas alvos foram avaliados. Dentre os resultados destaca-se a imunodetecção de XfDsbC, Xf5'-Nt, XfTolB e XfPal durante as diferentes fases de formação e desenvolvimento do biofilme de X. fastidiosa, que é tido como o principal mecanismo de patogenicidade deste fitopatógeno, confirmando a predição inicial de tais proteínas como associadas à patogenicidade bacteriana. Adicionalmente, resultados funcionais e estruturais revelaram detalhes finos do papel biológico desempenhado por cada uma das proteínas estudadas. Juntos, os resultados apresentados neste trabalho contribuem para o melhor entendimento de patogenicidade bacteriana, especialmente com respeito ao fitopatógeno X. fastidiosa
Abstract: Xylella fastidiosa is a plant pathogen bacterium responsible for numerous economically important crops diseases around the world, including the citrus variegated chlorosis. Following the host infection, the X. fastidiosa cells are able to form a biofilm structure which block the xylem vessels, leading to a hydric stress condition in the host plant and triggers the disease development. Given the economic relevance of citriculture for Brazil and in order to reduce the damage caused by phytosanitary problems that affect the citrus production, a research consortium was established with the aim to elucidate the complete genome sequence of the X. fastidiosa 9a5c strain. Numerous proteins associated with bacterial pathogenicity, adaptation and survival have been identified, including XfDsbC (protein disulfide isomerase), Xf5'-Nt (5'-nucleotidase), XfTolB (protein translocation B) and XfPal (peptidoglycan-associated lipoprotein) which were characterized in this study. Using tools for protein characterization, structural and functional aspects of these four protein targets were evaluated. Among the results, we highlight the immunodetection of XfDsbC, Xf5'-Nt, XfTolB and XfPal during the different stages of X. fastidiosa biofilm formation and development which is considered the primary mechanism of pathogenicity of this pathogen. These findings, confirming the initial prediction that relates such proteins as associated with bacterial pathogenicity. Additionally, structural and functional results revealed accurate details of the biological role played by each protein studied. Taken together, the findings presented in this study contribute to a better understanding of bacterial pathogenesis, especially with regard to the plant pathogen X. fastidiosa
Doutorado
Genetica de Microorganismos
Doutor em Genetica e Biologia Molecular
Crocetti, Daniela <1975>. "Medicalizing gender: from intersex to DSD, from the laboratory to patient groups." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2011. http://amsdottorato.unibo.it/3282/1/Crocetti_Daniela_tesi.pdf.
Повний текст джерелаTratta dell’intreccio fra genere e medicalizzazione del corpo a partire da uno studio sull’intersessualità, ovvero sui “disturbi della differenziazione sessuale” (DSD). Si tratta di un insieme di sindromi legate allo sviluppo divergente di una delle componenti del sesso biologico. Per la prima volta in Italia, si fa il punto sulla natura, la storia, le rappresentazioni di questa condizione, si esamina il corpo di genere (gendered body), la sua medicalizzazione, s’indaga l’autopercezione dei soggetti in questione.
Crocetti, Daniela <1975>. "Medicalizing gender: from intersex to DSD, from the laboratory to patient groups." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2011. http://amsdottorato.unibo.it/3282/.
Повний текст джерелаTratta dell’intreccio fra genere e medicalizzazione del corpo a partire da uno studio sull’intersessualità, ovvero sui “disturbi della differenziazione sessuale” (DSD). Si tratta di un insieme di sindromi legate allo sviluppo divergente di una delle componenti del sesso biologico. Per la prima volta in Italia, si fa il punto sulla natura, la storia, le rappresentazioni di questa condizione, si esamina il corpo di genere (gendered body), la sua medicalizzazione, s’indaga l’autopercezione dei soggetti in questione.
DI, LILLO ALESSIA. "CAN A PRECISELY-POSITIONED DNA DOUBLE-STRAND BREAK (DSB) ACTIVATE GENE EXPRESSION?" Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/884393.
Повний текст джерелаTakahashi, Yoh-Hei. "Biochemical analyses of the quinone-coupled enzyme, DsbB, of Escherichia coli involved in disulfide bond generation." 京都大学 (Kyoto University), 2007. http://hdl.handle.net/2433/136787.
Повний текст джерелаCESENA, DANIELE. "The RNA processing proteins Xrn1 and Rrp6 regulate DNA damage checkpoint activation and telomere metabolism." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/158272.
Повний текст джерелаGenome instability is one of the most pervasive characteristics of cancer cells. It can be due to DNA repair defects, failure to arrest the cell cycle and loss of telomere-end protection that lead to end-to-end fusion and degradation. Among the many types of DNA damage, the DNA Double Strand Break (DSB) is one of the most severe, because it can cause mutations and chromosomal rearrangements. Eukaryotic cells respond to DSBs by activating a checkpoint that depends on the protein kinases Tel1/ATM and Mec1/ATR, in order to arrest the cell cycle until DSBs are repaired. Mec1/ATR is activated by RPA-coated single-stranded DNA (ssDNA) that arises upon nucleolytic degradation (resection) of the DSB. A similar checkpoint response is triggered when the natural ends of eukaryotic chromosomes lose their protection, resembling and being recognized as DSBs. This protection is provided by specialized nucleoprotein complexes called telomeres. Telomeric DNA consists of repetitive G-rich sequences that terminate with a 3’-ended single-stranded overhang (G-tail), which is important for telomere extension by telomerase. Several proteins, including the CST complex, are necessary to maintain telomere structure and length in both yeast and mammals. Emerging evidences indicate that RNA processing proteins play critical, yet poorly understood, roles in genomic stability and telomere metabolism. We provide evidence that the Saccharomyces cerevisiae RNA decay factors Xrn1, Rrp6 and Trf4 facilitate activation of Mec1/ATR by promoting the generation of RPA-coated ssDNA at intrachromosomal DSBs. Xrn1 and Rrp6 are also required to activate a Mec1/ATR-dependent checkpoint at uncapped telomeres due to loss of the CST component Cdc13. Xrn1 promotes checkpoint activation by facilitating the generation of ssDNA at both DSBs and uncapped telomeres. Xrn1 exerts this function at DSBs by promoting the loading of the MRX complex, whereas how it does at uncapped telomeres remains to be determined. By contrast, DSB resection is not affected by the absence of Rrp6 or Trf4, but their lack impairs the recruitment of RPA, and therefore of Mec1, to the DSB. Rrp6 and Trf4 inactivation affects neither Rad51/Rad52 association nor DSB repair by homologous recombination (HR), suggesting that full Mec1 activation requires higher amount of RPA-coated ssDNA than HR-mediated repair. Finally, we demonstrate that Xrn1 maintains telomere length by promoting the association of Cdc13 to telomeres independently of ssDNA generation and exerts this function by downregulating the RIF1 transcript. Our results provide novel links between RNA processing and genome stability.
VILLA, MATTEO. "Regulation of DNA-end resection at DNA double strand breaks and stalled replication forks." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2018. http://hdl.handle.net/10281/198950.
Повний текст джерелаGenome instability is an hallmark of cancer cells and can be due to DNA damage or replication stress. DNA double strand breaks (DSBs) are the most dangerous type of damage that cells have to manage. In response to DSBs, cells activate an highly conserved mechanism known as DNA damage checkpoint (DDC), whose primary effect is to halt the cell cycle until the damage is repaired. DDC is activated by the apical kinases Tel1/ATM and Mec1/ATR, which phosphorylate and activate the effector kinases Rad53/CHK2 and Chk1/CHK1. The Homologous Recombination (HR)-mediated repair of a DSB starts with the nucleolytic degradation (resection) of the 5’ ends to create long ssDNA tails. In Saccharomyces cerevisiae, resection starts with an endonucleolytic cleavage catalyzed by the MRX complex together with Sae2. More extensive resection relies on two parallel pathways that involve the nucleases Exo1 and Dna2, together with the helicase Sgs1. Resection must be tightly controlled to avoid excessive ssDNA creation. The Ku complex and the checkpoint protein Rad9 negatively regulate resection. While Ku inhibits Exo1, Rad9 restrains nucleolytic degradation by an unknown mechanism. The absence of Sae2 impairs DSB resection and causes prolonged MRX binding at DSB that leads to persistent Tel1 and Rad53-dependent DNA damage checkpoint. SAE2 deleted strains are sensitive to DSBs inducing agents, like camptothecin (CPT). This sensitivity has been associated to the resection defect of sae2∆ cells, but what causes this resection defect and if the enhanced checkpoint signaling contributes to the DNA damage sensitivity of sae2∆ cells is unknown. For these reasons, we tried to identify other possible mechanisms regulating MRX/Sae2 requirement in DSB resection by searching extragenic mutations that suppressed the sensitivity to DNA damaging agents of sae2Δ cells. We identified three mutant alleles (SGS1-G1298R, rad53-Y88H and tel1-N2021D) that suppress both the DNA damage hypersensitivity and the resection defect of sae2∆ cells. We show that Sgs1-G1298R-mediated suppression depends on Dna2 but not on Exo1. Furthermore, not only Sgs1-G1298R suppresses the resection defect of sae2∆ cells but also increases resection efficiency even in a wild type context by escaping Rad9-mediated inhibition. In fact, Rad9 negatively regulates the binding/persistence of Sgs1 at the DSB ends. When inhibition by Rad9 is abolished by the Sgs1-G1298R mutant variant, the requirement for MRX/Sae2 in DSBs resection is reduced. Rad53-Y88H and Tel1-N2021 are loss of function mutant variants that suppress sae2∆ cells sensitivity in a Sgs1-Dna2 dependent manner. Furthermore, abolishing Rad53 and Tel1 kinase activity results in a similar suppression phenotype which does not involve the escape from the checkpoint mediated cell cycle arrest. Rather, defective Rad53 or Tel1 signaling bypasses Sae2 function in DSBs resection by decreasing the amount of Rad9 bound at DSBs. This increases the Sgs1-Dna2 activity that, in turn, can compensate for the lack of Sae2. We propose that persistent Tel1 and Rad53 checkpoint signaling in sae2∆ cells causes DNA damage hypersensitivity and defective DSB resection by increasing the amount of Rad9 that, in turn, inhibits Sgs1-Dna2. Replication stress can induce fork stalling and controlled resection can be a relevant mechanism to allow repair/restart of stalled replication forks. We show that loss of the inhibition that Rad9 exerts on resection exacerbates the sensitivity to replication stress of Mec1 defective yeast cells by exposing stalled replication forks to Dna2-dependent degradation. This Rad9 protective function is independent of checkpoint activation and relies mainly on Rad9-Dpb11 interaction. We propose that Rad9 not only regulates the action of Sgs1-Dna2 at DSBs but also at stalled replication forks, supporting cell viability when the S-phase checkpoint is not fully functional.
Saini, Natalie. "Understanding the mechanisms underlying DSB repair-induced mutagenesis at distant loci in yeast." Diss., Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/51843.
Повний текст джерелаRiches, Lucy C. "Investigating DNA Double Strand Breaks (DSB) in mammalian cells by novel fluorescent reporters." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/1363.
Повний текст джерелаMurphy, Richard F. "Aza-analogues of distyrilbenzene (DSB) synthesis, structures, and properties of 1,4-phenylenediamine bisimines (PDABI)." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/5922.
Повний текст джерелаThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on August 30, 2007) Includes bibliographical references.
Jayaram, Sumithra. "INVESTIGATING ADENOVIRUS INTERACTIONS WITH HOST DOUBLE-STRAND BREAK REPAIR DEFENSES." Miami University / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=miami1133983657.
Повний текст джерелаShankara-, Narayana Nandini. "Clinical Investigations in Andrology." Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/21680.
Повний текст джерелаGrau, Ralf. "Versenkungsdiagenese pelagischer Sedimente unter erhöhtem Wärmefluß, DSPD Legs 68-70, Sites 501/504 und 505 (Panama-Becken, östl. Pazifik) /." München : [Kanzler], 1996. http://www.gbv.de/dms/goettingen/212954113.pdf.
Повний текст джерелаNitschko, Volker [Verfasser], and Klaus [Akademischer Betreuer] Förstemann. "The nuclear export of siRNA precursors via the dsRBD protein Blanks in Drosophila melanogaster / Volker Nitschko ; Betreuer: Klaus Förstemann." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1221062158/34.
Повний текст джерелаKartchner, Laurel Brianne. "Role of the Endoplasmic Reticulum Chaperone dsbA-L Gluthathione S-Transferase Activity in the Assembly of Adipocyte Hormone Adiponectin." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/144537.
Повний текст джерелаLacerda, Fábio de, and Instituto de Engenharia Nuclear. "Conversor DSB-SSB a capacitores chaveados por transformador de Hilbert em tecnologia CMOS de 180nm." Instituto de Engenharia Nuclear, 2017. http://carpedien.ien.gov.br:8080/handle/ien/1870.
Повний текст джерелаMade available in DSpace on 2017-08-07T17:26:37Z (GMT). No. of bitstreams: 1 FABIO DE LACERDA D.pdf: 4651972 bytes, checksum: 40eb0d71a79f39e524da9bb7fc917c63 (MD5) Previous issue date: 2017-03
Este trabalho trata da realização de um circuito integrado analógico para a conversão de sinais com modulação em amplitude de banda dupla (Double Sideband ou DSB) para modulação de banda simples (Single Sideband ou SSB). Implementado por circuitos de tempo discreto a capacitores chaveados, utiliza-se de um filtro com resposta infinita ao impulso (Infinite Input Response ou IIR) para compor um transformador de Hilbert como alternativa a implementações digitais, que se aproveitam da grande capacidade de processamento paralelo dos circuitos digitais para a obtenção do transformador de Hilbert por meio de filtros com resposta finita ao impulso (Finite Impulse Response ou FIR) de ordem elevada. Fabricado em tecnologia CMOS de 180 nm com capacitores do tipo metal-metal (MiM), a adoção de filtros estruturalmente passa-tudo reduz significativamente a sensibilidade do conversor ao descasamento de capacitores. Para alimentação de 1,8 V e sinais diferenciais de até 1 V, resultados experimentais mostram que o conversor atinge taxa de rejeição de imagem (Image Rejection Ratio ou IRR) maior que 39,5 dB para modulação Lower Sideband (LSB) e 38,0 dB para modulação Upper Sideband (USB) para sinais de entrada na faixa de 25% a 75% da frequência da portadora, valores estes superiores a propostas analógicas anteriores e comparáveis a propostas digitais do estado da arte em circuitos integrados. Com área de silício de 1,09 mm2, o conversor consome apenas 17,7 mW para frequência de amostragem de 1 MHz enquanto sua IRR apresentou desvio padrão de apenas 0,5 dB dentre 20 amostras avaliadas.
The realization of an analog integrated circuit for conversion of Double-Sideband (DSB) amplitude-modulated signals into Single-Sideband (SSB) is presented. Implemented by discrete-time switched-capacitor circuits, it adopts an Infinite Impulse Response (IIR) filter to realize a Hilbert transformer as alternative to digital implementations which take advantage of high processing capacity from parallel digital circuits to obtain the Hilbert transformer by means of high-order Finite Impulse Response (FIR) filters. Fabricated in a 180 nm CMOS technology with metal-metal (MiM) capacitors, the use of structurally all-pass filters greatly reduces the converter’s sensitivity to capacitor mismatch. For 1.8 V power supply and 1 V differential input/output signals, experimental results show the converter achieves Image Rejection Ratio (IRR) greater than 39.5 dB for Lower-Sideband (LSB) modulation and 38.0 dB for Upper-Sideband (USB) modulation for input signals ranging from 25% to 75% of the carrier frequency. These figures are higher than previous analog circuit proposals and comparable to digital implementations of state-of-the-art integrated circuits. Its silicon area is 1.09 mm2 and the converter consumes only 17.7 mW for 1 MHz sampling frequency while its IRR presents standard deviation of only 0.5 dB among 20 chip samples.
Mirza, Zainulabedeen Reda. "Control of Shigella sonnei and adhesive invasive Escherichia coli infections with a natural product which inhibits the bacterial oxidoreductase DsbA." Thesis, University of Strathclyde, 2017. http://digitool.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=28637.
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