Дисертації з теми "Cellular RNAs"
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Smith, Nikki. "The role of cellular micro-RNAs in Epstein-Barr virus induced cellular transformation and oncogenesis." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1344/.
Повний текст джерелаKheimar, Ahmed Mahmoud Osman [Verfasser]. "Tumor promoting functions of cellular telomerase RNA and viral RNAs in herpesvirus-induced cancer formation / Ahmed Mahmoud Osman Kheimar." Berlin : Freie Universität Berlin, 2017. http://d-nb.info/1147758247/34.
Повний текст джерелаHewitt, Rachael Nicole. "Investigation of the role of long non-coding RNAs in oncogene induced cellular senescence." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/7143/.
Повний текст джерелаJeon, Young-Jun. "The Roles of Non-Coding RNAs in Solid Tumors." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1426083854.
Повний текст джерелаGeisler, Sarah J. "Decapping of Long Noncoding RNAs Regulates Inducible Genes." Case Western Reserve University School of Graduate Studies / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=case1340141951.
Повний текст джерелаWagner, Simone [Verfasser], and Bettina [Akademischer Betreuer] Kempkes. "Identification of cellular long non-coding RNAs regulated by the EBV nuclear antigen EBNA2 / Simone Wagner ; Betreuer: Bettina Kempkes." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1199265721/34.
Повний текст джерелаRogowski, Karol Jerzy [Verfasser]. "Identification and characterization of non-coding RNAs and their associated proteins involved in cellular stress responses / Karol Jerzy Rogowski." Berlin : Freie Universität Berlin, 2020. http://d-nb.info/1215099606/34.
Повний текст джерелаBalaratnam, Sumirtha. "BIOGENESIS AND FUNCTIONAL APPLICATIONS OF PIWI INTERACTING RNAs (piRNAs)." Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent1531753741509242.
Повний текст джерелаOstler, Jeffery Brent Jr. "Characterization of Pol IV and Pol V-Dependent Non-Coding RNAs Derived from aGeminivirus Genome." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492698361649423.
Повний текст джерелаNavaroli, Deanna M. "Molecular Mechanisms of Endocytosis: Trafficking and Functional Requirements for the Transferrin Receptor, Small Interfering RNAs and Dopamine Transporter: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/592.
Повний текст джерелаNavaroli, Deanna M. "Molecular Mechanisms of Endocytosis: Trafficking and Functional Requirements for the Transferrin Receptor, Small Interfering RNAs and Dopamine Transporter: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/592.
Повний текст джерелаBouckenheimer, Julien. "Rôle fonctionnel des longs ARN non codants dans l'adaptation et la pluripotence des cellules souches en culture." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONT3505.
Повний текст джерелаThe actual and future applications of human pluripotent stem cells (PSC) in the biomedical field are highly promising. Their use for the discovery of new therapeutic drugs through the development of high-throughput screening tests, cytotoxicity tests and in vitro disease modeling has been added to their tremendous interests in regenerative medicine and cellular therapy. As a source of biological material that can be used to restore partially or totally the lost functions of a damaged organ or tissue, or as a source of normal cells to study human development or test putative new drugs, their genomic integrity has to be thoroughly assessed. Therefore, an effective optimization of their culture conditions has to be considered, in order to control the absence of genomic instability and prevent their potential emergence. Any genetic or epigenetic alteration resulting from cell culturing must be detected in order to define and characterize acceptance criteria for scientific and medical purposes.PSC are particularly sensitive to stress resulting from unappropriated passaging techniques, which cause rapid genetic drift. Indeed, our team observed that many genomic abnormalities arise from aggressive single cell, enzymatic based, passaging methods, and that substantial phenotypical changes such as increased survival after cell dissociation and variation in cell shape can then occur.In order to understand the mechanisms governing the emergence of those adverse alterations, the team focused on the consequences resulting from the adaptation of PSC to single-cell dissociation. By using new generation sequencing techniques as RNA-Seq, we compared transcriptomics of PSC passaged by standard techniques (such as mechanical passaging) versus single-cell enzymatic dissociation (such as TRyPLE-based single-cell passaging). This comparison showed that the most striking difference in the gene expression pattern between adapted and non adapted cells concerned the dramatic overexpression of RNAs from a recently discovered class: long non-coding RNAs (lncRNAs).The aim of this thesis work was to determine to which extent some of these lncRNAs were functionally linked to adaptation of PSC. In order to address this matter, we first investigated in silico which lncRNAs were upregulated by single-cell dissociation, and after experimental validation of lncRNA candidates by molecular biology, we performed functional in vitro analysis (notably by siRNA-mediated loss of function) and sought their cellular localization in order to decipher their role in the cellular machinery and their level of implication. Beside this main project, other auxiliary projects were grafted. The observation of major changes in cell phenotype and behavior led to the investigation of the global mechanisms governing these modifications, underlining the potential role of epithelial-to-mesenchymal transition provoked by single-cell dissociation. Finally, the global attractiveness of lncRNAs and the emergence of exponential documentation concerning non-coding RNAs prompted the writing of an extensive review and meta-analysis concerning the implications of lncRNAs during embryo development and in pluripotent stem cells
Conine, Colin C. "Small RNAs and Argonautes Provide a Paternal Epigenetic Memory of Germline Gene Expression to Promote Thermotolerant Male Fertility: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/724.
Повний текст джерелаConine, Colin C. "Small RNAs and Argonautes Provide a Paternal Epigenetic Memory of Germline Gene Expression to Promote Thermotolerant Male Fertility: A Dissertation." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/724.
Повний текст джерелаKolpa, Heather J. "XIST and CoT-1 Repeat RNAs are Integral Components of a Complex Nuclear Scaffold Required to Maintain SAF-A and Modify Chromosome Architecture: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/825.
Повний текст джерелаKolpa, Heather J. "XIST and CoT-1 Repeat RNAs are Integral Components of a Complex Nuclear Scaffold Required to Maintain SAF-A and Modify Chromosome Architecture: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/825.
Повний текст джерелаPalsule, Geeta. "Mechanism and Functional Consequences of Generating and Processing Drosophila RNase P RNA from an Intron." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1555628225881656.
Повний текст джерелаGore, Panter Shamone Robinette. "Genetic and Functional Studies of LociAssociated with Atrial Fibrillation." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1396521127.
Повний текст джерелаHunt, Sarah Louise. "Cellular proteins required for rhinovirus RNA translation." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313880.
Повний текст джерелаBailey, Daniel John. "Cellular proteins in picornavirus replication." Thesis, University of Reading, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298484.
Повний текст джерелаKandan-Kulangara, Febitha. "Poly(ADP-ribose) polymerase-1 (PARP-1) and RNA interference (RNAI) during cell death." Doctoral thesis, Université Laval, 2013. http://hdl.handle.net/20.500.11794/25972.
Повний текст джерелаOsborn, Maire. "Cellular RNA Targeting by Platinum (II) Anticancer Therapeutics." Thesis, University of Oregon, 2014. http://hdl.handle.net/1794/17920.
Повний текст джерелаChan, Annie Yee-Man. "Interactions between the influenza virus RNA polymerase and cellular RNA polymerase II." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670083.
Повний текст джерелаBrown, E. C. "Cellular proteins involved in translation of human rhinovirus RNA." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596963.
Повний текст джерелаTodorova, Tanya (Tanya Todorova). "Function and regulation of PARP13 binding to cellular RNA." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/97789.
Повний текст джерелаCataloged from PDF version of thesis. Vita.
Includes bibliographical references.
Poly(ADP-ribose) polymerase-13 (PARP13) is a member of the PARP family of proteins - enzymes that use NAD+ to synthesize a posttranslational protein modification called poly(ADP-ribose) (PAR). PARPs function in multiple cellular pathways, and recently several members of the family have been implicated in regulating various steps in RNA metabolism, from splicing to translation and decay. PARP1 3 is the best-understood RNA-regulatory PARP. Initially discovered as a host immune factor, PARP13 functions by binding viral transcripts via its four CCCH-type zinc fingers and targeting them for degradation. In the context of the immune response PARP1 3 can also inhibit the translation of its viral targets and enhance the activity of other RNA-binding viral receptors, such as RIG-1. More recently PARP13 was shown to also indirectly regulate the cellular transcriptome by inhibiting the activity of Argonaute 2 (Ago2), a member of the miRNA silencing pathway. While itself catalytically inactive, PARP13 is modified by PAR and can target Ago2 for modification by a yet unknown PARP. However, it remains unclear if RNA binding is required for this function of PARP1 3. Indeed, even though multiple viruses are known to be restricted by PARP13, cellular mRNA targets of PARP13 binding and regulation have not yet been identified. Here we show that PARP1 3 binds endogenous RNA and regulates the cellular transcriptome. We identify TRAILR4 mRNA as the first cellular target of PARP13 regulation and demonstrate that PARP13 represses TRAILR4 expression posttranscriptionally by binding to a specific region in the 3' untranslated region of the transcript and targeting it for degradation in a primarily 3'-5' decay mechanism. By inhibiting the expression of TRAILR4 - a decoy pro-survival receptor of the apoptotic ligand TRAIL, PARP1 3 regulates the cellular response to TRAIL and acts as a pro-apoptotic factor. We also examine possible mechanisms of regulation of PARP1 3 function. We identify the RNA-helicase DHX30 as a constitutive PARP1 3-interacting protein and show that the two proteins co-regulate a subset of cellular transcripts. We further demonstrate that the PAR-binding domain of PARP1 3 inhibits RNA binding, while PARP1 3 interaction with PARP5a and covalent modification with PAR appear to be mutually exclusive with RNA binding.
by Tanya Todorova.
Ph. D.
Mullani, Nowsheen. "An RNA Signature Links Oxidative Stress To Cellular Senescence." Electronic Thesis or Diss., Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2019SORUS560.pdf.
Повний текст джерелаOxidative Stress is one of the routes leading to cellular senescence. While the damages that reactive oxygen species inflict on proteins and DNA are well described, our insight on how transcription may participate in the onset of senescence is still limited. At a transcriptional level, oxidative stress results in accumulation of promoter RNAs (uaRNAs) and enhancer RNAs (eRNAs) as a consequence of defective release of the RNAPII from the chromatin a phenomenon known as RNAPII crawling. We observed that RNAPII crawling was also detected downstream of a small series of genes known to be regulated by HP1Υ at the level of their termination. Exploring this phenomenon yielded an unexpected result in the sense that it revealed an inhibiting effect of hydrogen peroxide on the RNA exosome complex involved in degradation of polyadenylated RNAs. The crawling RNAPII results in the transcription of ALU sequences located in the neighborhood of promoters and enhancers and downstream of intron-less genes and of small series of intron-containing genes. As ALU sequences contain genome encoded A tracts, they should normally be degraded by the RNA exosome. Yet, as oxidative stress also inhibits this RNAse activity, mRNAs containing serendipitously transcribed ALU sequences get stabilized and are detected in the cytoplasm and even polysome fractions. This phenomenon may participate in the onset of the interferon response associated with oxidative stress
Vasale, Jessica J. "Roles of Cellular RNA-Dependent RNA Polymerases in Endogenous Small RNA Pathways in Caenorhabditis elegans: A Dissertation." eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/481.
Повний текст джерелаCordiner, Ross Andrew Alex. "The cellular functions of the microprocessor complex." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25877.
Повний текст джерелаStassinopoulos, Ioannis A. "Interactions of picornavirus internal ribosome entry sites with cellular proteins." Thesis, University of Sussex, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322940.
Повний текст джерелаSchmier, Brad J. "The Molecular Machinery Critical to the Degradation of Cellular RNA." Scholarly Repository, 2012. http://scholarlyrepository.miami.edu/oa_dissertations/714.
Повний текст джерелаTedeschi, Frank A. Tedeschi. "IDENTIFICATION OF CELLULAR RNA BINDING SITES OF DEAD-BOX HELICASES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1531217057171378.
Повний текст джерелаGerst, Catherine. "Epissage in vivo et in vitro de rnas premessagers d'adenovirus-2 : etude des interactions rna - facteurs nucleaires." Université Louis Pasteur (Strasbourg) (1971-2008), 1987. http://www.theses.fr/1987STR13159.
Повний текст джерелаMcNally, Beth Anne. "A role for cytoplasmic PML in the cellular antiviral response." Columbus, Ohio : Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1133377007.
Повний текст джерелаWong, Tsz-lo, and 黃子璐. "Cellular role of miR-143 in cervical cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48274045.
Повний текст джерелаpublished_or_final_version
Pathology
Master
Master of Medical Sciences
Babendure, Jeremy R. "Utilizing RNA structure as a tool in molecular and cellular biology." Diss., Connected to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3190000.
Повний текст джерелаTitle from first page of PDF file (viewed Mar. 6, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 122-131).
Nurmohamed, Salima. "Communication between the Escherichia coli RNA degradative machineries and cellular metabolism." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611286.
Повний текст джерелаDeb, Maharshi Krishna. "Generation of antisense RNAs at convergent gene loci in cells undergoing senescence." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30274.
Повний текст джерелаCellular senescence represents one of the major fail-safe mechanisms that counteracts tumour development is defined as a state of irreversible cell cycle arrest as a consequence of stress response such as oncogenic challenge. Such cells undergoing Oncogene-induced Senescence (OIS) display profound alternation in their epigenome as their chromatin are largely decorated with prominent drivers of constitutive heterochromatin.Antisense RNA-mediated gene regulation has been attributed to play diverse roles in mediating various cellular processes and cell fates per-se. In yeast, histone variant H2A.Z cooperates with RNAi and heterochromatin machinery to regulate antisense transcription at convergent gene loci which can otherwise generate pervasive read-through transcripts owing to improper transcription termination. In mammals, whether such antisense transcripts (occurring by read-through transcription at convergent gene pairs) exist and how they are regulated remains unknown. Interestingly, the depletion of the human H2A.Z histone variant has been reported to induce cellular senescence. We thus wondered if the regulation of particular antisense transcripts at convergent gene pairs occurs in senescence, if their regulation by H2A.Z is conserved in mammals and, if so, if a functional significance can be attributed to these transcripts. To this end we took advantage of a well-established in-vitro OIS model. Briefly, we analysed genome wide strand specific RNA-seq analysis of cells undergoing Oncogene Induced Senescence. This led us to identify numerous convergent gene loci associated with accumulation of transcripts downstream of the designated transcription termination site in senescent cells, and extending to generate an antisense to the next gene located in the opposite strand of the convergent gene pair. We confirmed the RNA-seq data at two of such convergent loci. An RNAi based approach revealed that at least two of these transcripts are generated by transcriptional read-throughs. Hence we designated such pervasive transcripts as Senescence Triggered Antisense Read-through Transcripts (START). Importantly, we further found that the two STARTs for which we performed in depth studies repress the expression of the gene for which they are antisense. Finally, we demonstrate that the histone variant H2A.Z suppresses the accumulation of STARTs in proliferative cells. Since it also prevents senescence induction, this suggests that expression of START is important for cellular senescence. This has lead us to propose a model that human cells undergoing OIS are associated with loss of H2A.Z that leads to the wide spread accumulation of read-through transcripts owing to impaired termination control
Ozes, Ali Rayet. "Targeting the long non coding RNA HOTAIR in cancer." Thesis, Indiana University, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10154781.
Повний текст джерелаOvarian cancer (OC) takes the lives of nearly 14,000 US women every year. Although platinum is one of the most effective drugs in treating ovarian cancer, the development of platinum resistance is one of the biggest challenges facing patients. I have shown that the long non-coding RNA HOTAIR contributes to platinum-resistant OC and determined the regulators and targets of HOTAIR during the platinum-induced DNA damage response. My published data supports the role of HOTAIR in contributing to DNA damage induced cellular senescence and secretion of pro-inflammatory cytokines leading to cisplatin resistance. My unpublished work (under review) analyzed the interaction of HOTAIR with the PRC2, its known interacting partner. In this study, I developed a novel strategy blocking HOTAIR-PRC2 interaction and resensitized ovarian tumors to platinum in mouse studies. The results offer a pre-clinical proof of concept for targeting long non-coding RNAs as a therapeutic approach and may represent a strategy to overcome chemotherapy resistance in tumors exhibiting high expression of HOTAIR, a frequent observation in high grade serous OC.
Singh, Harinder. "CAVEOLAE AS SPATIO-TEMPORAL COMPARTMENTS FOR ROS/RNS GENERATION AND NITROXIDATIVE STRESS SIGNALING." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/275561.
Повний текст джерелаPh.D.
During inflammatory conditions excessive production of reactive oxygen (ROS) and nitrogen species (RNS), peroxynitrite, is implicated in the development of vascular pathologies. Our previous studies showed that both NADPH oxidase enzyme complexes and eNOS localize to endothelial caveolae microdomains. Additionally, caveolae internalization has been shown as an activating mechanism for enzyme eNOS. However, roles of caveolae in ROS/RNS generation and downstream signaling roles in activating endothelial cells are not well known. Hypothesis: Caveolae act as, a) micro-environments in providing spatio-temporal reaction compartments for ROS/RNS generation, tyrosine nitration of proteins, b) platforms to propagate localized nitroxidative signaling in inducing endothelial cell activation and dysfunction (ICAM-1, VCAM-1 expression), and c) intracellular redox signaling endosomes to regulate adhesion molecule expression. Objectives: The aim of the study was to investigate whether, a) caveolae compartmentalize ROS, regulate localized tyrosine nitration of proteins, b) nitroxidative-signaling in the endothelium is compartmentalized in caveolae, c) dynamin-2-dependent internalization of caveoale is important for activating redox signaling, and d) caveolae compartments can be targeted to reduce endothelial ROS Methods and results: Cultured primary bovine aortic endothelial cells were stimulated with TNFα to generate ROS/RNS. Blockade of NADPH oxidase (gp91ds-tat) or scavenging of peroxynitrite (Uric acid) inhibited TNFα-induced protein tyrosine nitration, activation of the NFkB, and upregulation of ICAM-1/VCAM-1 expression. To test the role of caveolae in this process, cultured cells were depleted of caveolin-1 (siRNA). Similar to inhibitors, TNFα failed to induce protein-tyrosine nitration, activate NFkB or enhance adhesion molecule expression in cells lacking caveolin-1. These findings were corroborated in vivo using Cav1KO animals. Our results show that several caveolar residing proteins were nitrated on tyrosine in response to TNFα. Here, immunoprecipitation of cell lysates with an anti-nitrotyrosine antibody revealed Src-family kinases (SFK) in the precipitated fraction. Moreover, SFK nitration was lost in cells depleted of caveolin-1. Given that SFK nitration is associated with enzyme activation, cells were pretreated with PP2 to inhibit SFK activity. We found that PP2 attenuated the NFkB and adhesion molecule pathway activated by TNFα. Depletion of dynamin-2 (Dyn2siRNA) or inhibiting GTPase activity (Dynasore) also showed reductions in ROS generation, NFkB redox signaling and ICAM-1/VCAM-1 expression. Development of caveolae targeting peptide tagged with gp91ds-tat showed inhibitions in compartmentalized ROS production. Conclusions: Caveolae act as sites for ROS/RNS production where resident redox-sensitive second messengers are activated and propagate signals that regulate endothelial inflammatory phenotype. Targeting NADPH oxidase enzyme specifically in caveolae can be used a therapeutic strategy to limit vascular oxidative stress.
Temple University--Theses
Le, Roy Florence. "Clonage et caractérisation de protéines associées à la RNase L. Identification d'ARNm cellulaires régulés par la RNase L." Montpellier 2, 2000. http://www.theses.fr/2000MON20054.
Повний текст джерелаIdris, Jalilah. "Investigating novel roles of RNA binding proteins SAFB1 and SAFB2 in RNA processing and in cellular stress." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.738206.
Повний текст джерелаJeyaraj, Selvi Chrysolyte. "A role for the mRNA-stabilizing protein HuR in protection from cellular ATP depletion." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1186773861.
Повний текст джерелаÖhrmalm, Christina. "Functional characterization of the cellular protein p32 : a protein regulating adenovirus transcription and splicing through targeting of phosphorylation /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6794.
Повний текст джерелаSchonauer, Melissa. "Intersection of RNA Processing and Fatty Acid Synthesis and Attachment in Yeast Mitochondria." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/194674.
Повний текст джерелаMina, Ibarra Leonardo Bruno. "Cellular mRNA decay factors involved in the hepatitis C virus life cycle." Doctoral thesis, Universitat Pompeu Fabra, 2010. http://hdl.handle.net/10803/7215.
Повний текст джерелаSince all (+)RNA viruses need to regulate the exit of the viral genome from the cellular translation machinery to replication and these proteins are conserved from yeast to humans, We hypothesized that the human homologues of Lsm1-7/Dhh1/Pat1 are required for the replication of human (+) RNA viruses. In this work we proved this hypothesis by showing that HCV translation and replication depend on these cellular proteins. Moreover, the requirement of these factors for efficient HCV RNA translation was linked exclusively to the 5´ and 3´ nontranslated regions (NTRs) of the viral genome. Furthermore, the LSm1-7 complex specifically interacts in vitro with essential cis-acting HCV RNA elements located in the NTRs.
El grupo de virus de RNA de cadena de polaridad positiva ((+)RNA) incluye numerosos patógenos de plantas, animales y humanos, tales como el virus de la Hepatitis C (VHC). Sus genomas virales imitan a los RNAm celulares, sin embargo, además de actuar como mensajeros para la traducción de proteínas virales, también actúan como moldes para la replicación viral. Debido a que estas dos funciones son mutuamente excluyentes, un paso clave en la replicación de todos los virus (+) RNA es la salida regulada del RNA genómico desde la maquinaria de traducción celular hacia las complejos de replicación virales. Utilizando un sistema modelo que permite la replicación del virus del mosaico del bromo (VMB), un virus (+) RNA de plantas, en levaduras, nuestro grupo ha demostrado que los activadores de decapping celulares Dhh1, LSm1 y Pat1 juegan un papel clave en este paso. La proteína LSm1 es una subunidad del complejo celular LSm1-7. Hemos demostrado recientemente que dichos complejos interactúan directamente con secuencias específicas en el genoma del VMB y que dichas interacciones regulan la traducción y replicación del VMB. De manera interesante, la proteína homologa de LSm1 en bacterias, Hfq, es necesaria para la replicación del bacteriófago (+) RNA Qβ en E. coli.
Debido a que todos los virus (+) RNA necesitan regular la salida del genoma viral desde la maquinaria traduccional de la célula hacia los complejos de replicación virales, y que las proteínas Dhh1, LSm1-7 y Pat1 están conservadas de levaduras a humanos, nuestra hipótesis es que lo homólogos humanos de Lsm1-7/Dhh1/Pat1 son requeridos para la replicación de virus (+)RNA de humanos. En este trabajo, hemos demostrado esta hipótesis mostrando que la traducción y la replicación del virus de la hepatitis C (VHC) dependen de estas proteínas celulares. Más aún, el requerimiento de estos factores para una eficiente traducción del genoma del VHC está vinculado de manera exclusiva a las regiones no traducidas (RNT) 5´ y 3´ del genome viral. Además, el complejo cellular LSm1-7 interactúa in vitro de manera específica con elementos esenciales del RNA del VHC que actúan en cis localizados en las RNTs.
York, Ashley D. "A study of viral and cellular factors in the regulation of the influenza virus RNA-dependent RNA polymerase." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:5958fafd-4c91-4434-910e-29e2dd0539b9.
Повний текст джерелаMahmoudi, Massoud. "Induction of Interferon Messenger RNA and Expression of Cellular Oncogenes in Human Lymphoblastoid Cells." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc798199/.
Повний текст джерелаChambers, A. "RNA 3' cleavage and polyadenylation in oocytes, eggs and embryos of Xenopus laevis." Thesis, University of Warwick, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380275.
Повний текст джерелаPlakos, Kory. "Platinum-seq: High-throughput mapping of small-molecule platinum adducts on cellular RNA." Thesis, University of Oregon, 2017. http://hdl.handle.net/1794/22269.
Повний текст джерелаRubilar, Guzman Paulina. "Cellular host factors involved in the translation of the HIV-1 genomic RNA." Thesis, Lyon, École normale supérieure, 2015. http://www.theses.fr/2015ENSL1009/document.
Повний текст джерелаHuman Immunodeficiency virus type 1 (HIV-1) is a positive strand RNA virus belonging to the lentivirus genus of the retroviridae family and it is the etiological agent of the pandemic AIDS, which is a major health concern worldwide. Throughout HIV-1 replication cycle, the production of viral proteins depends exclusively on the cellular translational machinery. This is the reason why we have explored the role of some cellular factors that could control HIV-1 translation at different stages. We have focused our studies on the translation of the full length genomic RNA (gRNA), which serves both as genome for viral encapsidation and as a messenger for translation of Gag and Gag-Pol viral polyproteins.1) The role of the RNA helicase DDX3 in HIV-1 translation Initiation The fact that HIV-1 possesses a highly structured 5’ untranslated region (5’UTR) prompted us to speculate that DDX3 may be involved in HIV-1 translation. We used a combination of in vitro and ex-vivo approaches to show that DDX3 was able to bind and form complexes with the 5’-UTR of HIV-1 to assist translation initiation. We also demonstrated that DDX3 can form a complex with initiation factors such as PABP, eIF4G and eIF4E. 2) Programmed Ribosomal Frameshift (PRF) in the genomic RNA of HIV-1Translation of HIV-1 Gag-Pol polyprotein requires a -1 PRF. This mechanism allows the synthesis of Gag and Gag-Pol polyproteins, using the same mRNA template, at ratios of 95 and 5% respectively. Keeping the -1PRF ratio is important as any change leads to reduction in virus infectivity.By means of a dual reporter construct and full provirus replication system we were able to demonstrate that the stress granules associated protein TIAR, controls HIV-1 infectious progeny by regulating the ratio of the HIV-1 PRF