Relevant bibliographies by topics / RNA ; Proteins ; DNA replication

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'RNA ; Proteins ; DNA replication'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "RNA ; Proteins ; DNA replication"

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ZDRAVKOVIĆ, S., M. V. SATARIĆ, and D. VUKOVIĆ. "MODULATION AND DEMODULATION IN DNA MOLECULE." Modern Physics Letters B 20, no. 11 (May 10, 2006): 607–15. http://dx.doi.org/10.1142/s0217984906010706.

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In this paper, we consider the transformation of a breather type soliton in DNA into its demodulated version due to the strong impact of proteins associated with some sequences of DNA chain. These proteins are, for example, RNA polymerase responsible for the formation of m-RNA or initiation protein complex indispensable for chromosome replication.
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Wiedmer, Andreas, Pu Wang, Jing Zhou, Andrew J. Rennekamp, Valeria Tiranti, Massimo Zeviani, and Paul M. Lieberman. "Epstein-Barr Virus Immediate-Early Protein Zta Co-Opts Mitochondrial Single-Stranded DNA Binding Protein To Promote Viral and Inhibit Mitochondrial DNA Replication." Journal of Virology 82, no. 9 (February 27, 2008): 4647–55. http://dx.doi.org/10.1128/jvi.02198-07.

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ABSTRACT Disruption of cellular metabolic processes and usurpation of host proteins are hallmarks of herpesvirus lytic infection. Epstein-Barr virus (EBV) lytic replication is initiated by the immediate-early protein Zta. Zta is a multifunctional DNA binding protein that stimulates viral gene transcription, nucleates a replication complex at the viral origin of lytic replication, and inhibits cell cycle proliferation. To better understand these functions and identify cellular collaborators of Zta, we purified an epitope-tagged version of Zta in cells capable of supporting lytic replication. FLAG-tagged Zta was purified from a nuclear fraction using FLAG antibody immunopurification and peptide elution. Zta-associated proteins were isolated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and identified by mass spectrometry. The Zta-associated proteins included members of the HSP70 family and various single-stranded DNA and RNA binding proteins. The nuclear replication protein A subunits (RPA70 and RPA32) and the human mitochondrial single-stranded DNA binding protein (mtSSB) were confirmed by Western blotting to be specifically enriched in the FLAG-Zta immunopurified complex. mtSSB coimmunoprecipitated with endogenous Zta during reactivation of EBV-positive Burkitt lymphoma and lymphoblastoid cell lines. Small interfering RNA depletion of mtSSB reduced Zta-induced lytic replication of EBV but had only a modest effect on transcription activation function. A point mutation in the Zta DNA binding domain (C189S), which is known to reduce lytic cycle replication, eliminated mtSSB association with Zta. The predominantly mitochondrial localization of mtSSB was shifted to partly nuclear localization in cells expressing Zta. Mitochondrial DNA synthesis and genome copy number were reduced by Zta-induced EBV lytic replication. We conclude that Zta interaction with mtSSB serves the dual function of facilitating viral and blocking mitochondrial DNA replication.
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Ohba, R., K. Matsumoto, and Y. Ishimi. "Induction of DNA replication by transcription in the region upstream of the human c-myc gene in a model replication system." Molecular and Cellular Biology 16, no. 10 (October 1996): 5754–63. http://dx.doi.org/10.1128/mcb.16.10.5754.

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An important relationship between transcription and initiation of DNA replication in both eukaryotes and prokaryotes has been suggested. In an attempt to understand the molecular mechanism of this interaction, we examined whether transcription can induce DNA replication in vitro by constructing a system in which both replication and transcription were combined. Relaxed circular DNA possessing a replication initiation zone located upstream of the human c-myc gene and a T7 promoter near the P1 promoter of the gene was replicated in the presence of T7 RNA polymerase. In our model system, replication was carried out with the proteins required for simian virus 40 DNA replication. DNA synthesis, which was dependent on both T7 RNA polymerase and the replication proteins, was detected mainly in the promoter and upstream regions of the c-myc gene. Blocking RNA synthesis at the initial stage of the reaction severely reduced DNA synthesis, suggesting that RNA chain elongation is required to induce DNA synthesis. The results indicated that transcription can induce DNA replication in the upstream region of the transcribed gene, most likely by introducing negative supercoiling into the region, which results in unwinding of the DNA duplex.
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Barton, Deborah A., Elke F. Roovers, Quentin Gouil, Guilherme C. da Fonseca, Rodrigo S. Reis, Craig Jackson, Robyn L. Overall, Adriana F. Fusaro, and Peter M. Waterhouse. "Live Cell Imaging Reveals the Relocation of dsRNA Binding Proteins Upon Viral Infection." Molecular Plant-Microbe Interactions® 30, no. 6 (June 2017): 435–43. http://dx.doi.org/10.1094/mpmi-02-17-0035-r.

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Viral infection triggers a range of plant responses such as the activation of the RNA interference (RNAi) pathway. The double-stranded RNA binding (DRB) proteins DRB3 and DRB4 are part of this pathway and aid in defending against DNA and RNA viruses, respectively. Using live cell imaging, we show that DRB2, DRB3, and DRB5 relocate from their uniform cytoplasmic distribution to concentrated accumulation in nascent viral replication complexes (VRC) that develop following cell invasion by viral RNA. Inactivation of the DRB3 gene in Arabidopsis by T-DNA insertion rendered these plants less able to repress RNA viral replication. We propose a model for the early stages of virus defense in which DRB2, DRB3, and DRB5 are invasion sensors that relocate to nascent VRC, where they bind to viral RNA and inhibit virus replication.
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Guogas, Laura, James Hogle, and Lee Gehrke. "Origins of Life and the RNA World: Evolution of RNA-Replicase Recognition." Symposium - International Astronomical Union 213 (2004): 321–24. http://dx.doi.org/10.1017/s0074180900193489.

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Central to understanding the origin of life is the elucidation of the first replication mechanism. The RNA World hypothesis suggests that the first self-replicating molecules were RNAs and that DNA later superceded RNA as the genetic material. RNA viruses were not subjected to the same evolutionary pressures as cellular organisms; consequently, they likely possess remnants of earlier replication strategies. Our laboratory investigates how members of the RNA virus family Bromoviridae can have structurally distinct 3' end tags yet are specifically recognized by conserved replication enzymes. This work addresses the idea that 3' tRNA tails were functionally replaced in some viruses by an RNA-protein complex. These viruses may serve as a timeline for the transition from the RNA world to DNA and protein based life.
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Kavanaugh, Gina, Runxiang Zhao, Yan Guo, Kareem N. Mohni, Gloria Glick, Monica E. Lacy, M. Shane Hutson, Manuel Ascano, and David Cortez. "Enhancer of Rudimentary Homolog Affects the Replication Stress Response through Regulation of RNA Processing." Molecular and Cellular Biology 35, no. 17 (June 22, 2015): 2979–90. http://dx.doi.org/10.1128/mcb.01276-14.

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Accurate replication of DNA is imperative for the maintenance of genomic integrity. We identified Enhancer of Rudimentary Homolog (ERH) using a whole-genome RNA interference (RNAi) screen to discover novel proteins that function in the replication stress response. Here we report that ERH is important for DNA replication and recovery from replication stress. ATR pathway activity is diminished in ERH-deficient cells. The reduction in ATR signaling corresponds to a decrease in the expression of multiple ATR pathway genes, including ATR itself. ERH interacts with multiple RNA processing complexes, including splicing regulators. Furthermore, splicing of ATR transcripts is deficient in ERH-depleted cells. Transcriptome-wide analysis indicates that ERH depletion affects the levels of ∼1,500 transcripts, with DNA replication and repair genes being highly enriched among those with reduced expression. Splicing defects were evident in ∼750 protein-coding genes, which again were enriched for DNA metabolism genes. Thus, ERH regulation of RNA processing is needed to ensure faithful DNA replication and repair.
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Rogan, Peter K., Eliseos J. Mucaki, and Ben C. Shirley. "A proposed molecular mechanism for pathogenesis of severe RNA-viral pulmonary infections." F1000Research 9 (August 7, 2020): 943. http://dx.doi.org/10.12688/f1000research.25390.1.

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Background: Certain riboviruses can cause severe pulmonary complications leading to death in some infected patients. We propose that DNA damage induced-apoptosis accelerates viral release, triggered by depletion of host RNA binding proteins (RBPs) from nuclear RNA bound to replicating viral sequences. Methods: Information theory-based analysis of interactions between RBPs and individual sequences in the Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2), Influenza A (H3N1), HIV-1, and Dengue genomes identifies strong RBP binding sites in these viral genomes. Replication and expression of viral sequences is expected to increasingly sequester RBPs - SRSF1 and RNPS1. Ordinarily, RBPs bound to nascent host transcripts prevents their annealing to complementary DNA. Their depletion induces destabilizing R-loops. Chromosomal breakage occurs when an excess of unresolved R-loops collide with incoming replication forks, overwhelming the DNA repair machinery. We estimated stoichiometry of inhibition of RBPs in host nuclear RNA by counting competing binding sites in replicating viral genomes and host RNA. Results: Host RBP binding sites are frequent and conserved among different strains of RNA viral genomes. Similar binding motifs of SRSF1 and RNPS1 explain why DNA damage resulting from SRSF1 depletion is complemented by expression of RNPS1. Clustering of strong RBP binding sites coincides with the distribution of RNA-DNA hybridization sites across the genome. SARS-CoV-2 replication is estimated to require 32.5-41.8 hours to effectively compete for binding of an equal proportion of SRSF1 binding sites in host encoded nuclear RNAs. Significant changes in expression of transcripts encoding DNA repair and apoptotic proteins were found in an analysis of influenza A and Dengue-infected cells in some individuals. Conclusions: R-loop-induced apoptosis indirectly resulting from viral replication could release significant quantities of membrane-associated virions into neighboring alveoli. These could infect adjacent pneumocytes and other tissues, rapidly compromising lung function, causing multiorgan system failure and other described symptoms.
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Rogan, Peter K., Eliseos J. Mucaki, and Ben C. Shirley. "A proposed molecular mechanism for pathogenesis of severe RNA-viral pulmonary infections." F1000Research 9 (January 6, 2021): 943. http://dx.doi.org/10.12688/f1000research.25390.2.

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Background: Certain riboviruses can cause severe pulmonary complications leading to death in some infected patients. We propose that DNA damage induced-apoptosis accelerates viral release, triggered by depletion of host RNA binding proteins (RBPs) from nuclear RNA bound to replicating viral sequences. Methods: Information theory-based analysis of interactions between RBPs and individual sequences in the Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2), Influenza A (H3N2), HIV-1, and Dengue genomes identifies strong RBP binding sites in these viral genomes. Replication and expression of viral sequences is expected to increasingly sequester RBPs - SRSF1 and RNPS1. Ordinarily, RBPs bound to nascent host transcripts prevents their annealing to complementary DNA. Their depletion induces destabilizing R-loops. Chromosomal breakage occurs when an excess of unresolved R-loops collide with incoming replication forks, overwhelming the DNA repair machinery. We estimated stoichiometry of inhibition of RBPs in host nuclear RNA by counting competing binding sites in replicating viral genomes and host RNA. Results: Host RBP binding sites are frequent and conserved among different strains of RNA viral genomes. Similar binding motifs of SRSF1 and RNPS1 explain why DNA damage resulting from SRSF1 depletion is complemented by expression of RNPS1. Clustering of strong RBP binding sites coincides with the distribution of RNA-DNA hybridization sites across the genome. SARS-CoV-2 replication is estimated to require 32.5-41.8 hours to effectively compete for binding of an equal proportion of SRSF1 binding sites in host encoded nuclear RNAs. Significant changes in expression of transcripts encoding DNA repair and apoptotic proteins were found in an analysis of influenza A and Dengue-infected cells in some individuals. Conclusions: R-loop-induced apoptosis indirectly resulting from viral replication could release significant quantities of membrane-associated virions into neighboring alveoli. These could infect adjacent pneumocytes and other tissues, rapidly compromising lung function, causing multiorgan system failure and other described symptoms.
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Dudas, Kathleen C., and Kenneth N. Kreuzer. "UvsW Protein Regulates Bacteriophage T4 Origin-Dependent Replication by Unwinding R-Loops." Molecular and Cellular Biology 21, no. 8 (April 15, 2001): 2706–15. http://dx.doi.org/10.1128/mcb.21.8.2706-2715.2001.

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ABSTRACT The UvsW protein of bacteriophage T4 is involved in many aspects of phage DNA metabolism, including repair, recombination, and recombination-dependent replication. UvsW has also been implicated in the repression of origin-dependent replication at late times of infection, when UvsW is normally synthesized. Two well-characterized T4 origins, ori(uvsY) andori(34), are believed to initiate replication through an R-loop mechanism. Here we provide both in vivo and in vitro evidence that UvsW is an RNA-DNA helicase that catalyzes the dissociation of RNA from origin R-loops. Two-dimensional gel analyses show that the replicative intermediates formed atori(uvsY) persist longer in a uvsWmutant infection than in a wild-type infection. In addition, the inappropriate early expression of UvsW protein results in the loss of these replicative intermediates. Using a synthetic origin R-loop, we also demonstrate that purified UvsW functions as a helicase that efficiently dissociates RNA from R-loops. These and previous results from a number of studies provide strong evidence that UvsW is a molecular switch that allows T4 replication to progress from a mode that initiates from R-loops at origins to a mode that initiates from D-loops formed by recombination proteins.
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Johnson, Kyle L., and L. Andrew Ball. "Induction and Maintenance of Autonomous Flock House Virus RNA1 Replication." Journal of Virology 73, no. 10 (1999): 7933–42. http://dx.doi.org/10.1128/jvi.73.10.7933-7942.1999.

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The nodavirus flock house virus (FHV) has a bipartite, positive-sense, RNA genome that encodes the catalytic subunit of the RNA replicase and the viral capsid protein precursor on separate genomic segments (RNA1 and RNA2, respectively). RNA1 can replicate autonomously when transfected into permissive cells, allowing study of the kinetics of RNA1 replication in the absence of either RNA2 or capsid proteins. However, RNA1 replication ceases ca. 3 days after transfection despite the presence of replication-competent RNA. We examined this inhibition by inducing the expression of RNA1 in cells from a cDNA copy that was under the control of a hormone-regulated RNA polymerase II promoter. This system reproduced the shutoff of RNA replication when DNA-templated primary transcription was turned off. Continued primary transcription partially alleviated the shutoff and maintained the rate of RNA replication for several days at a steady-state level approximately one-third that of the peak rate. After shutoff, RNA replication could be restored by transferring the resulting intracellular RNA to fresh cells or by reinducing primary transcription, indicating that cessation of replication occurred despite the competence of both the viral RNA and the cytoplasmic environment. These data suggest that there is a mechanism by which replication is shut off at late times after transfection, which may reflect the natural endpoint of the replicative cycle.
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Dissertations / Theses on the topic "RNA ; Proteins ; DNA replication"

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Langley, Alexander Richard. "Interactions between non-coding Y RNAs and proteins in the context of the initiation of human chromosomal DNA replication." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609101.

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Hillukkala, T. (Tomi). "Roles of DNA polymerase epsilon and TopBP1 in DNA replication and damage response." Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514282922.

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Abstract During DNA replication cells accurately copy their DNA to transfer the genetic information to daughter cells. DNA polymerases synthesise the new DNA strand using the old strand as a template. Other functions of DNA polymerases are recombination linked and DNA iamage repair linked DNA synthesis, regulation of replication complex formation and regulation of transcription – a process in which the genetic information is transformed into an RNA sequence needed to guide protein synthesis. In this study, the TopBP1 protein was shown to associate with DNA polymerase epsilon. TopBP1 contains eight BRCT domains mediating interactions between phosphorylated proteins and is a human homolog of bakers yeast Dpb11 and fission yeast Cut5. These yeast proteins act on DNA replication and cell cycle arrest after DNA damage. TopBP1 was found to be phosphorylated and expressed in elevated amounts during S phase suggesting an involvement in DNA replication. This was directly demonstrated by DNA synthesis inhibition by a competing TopBP1 fragment and by an antibody targeted to block TopBP1. Ultraviolet irradiation damages DNA and decreases the amount of TopBP1 in the nucleus. The transcription factor Miz-1 was found to associate with TopBP1 and was released from this interaction after UV damage. Free Miz-1 activated the expression of the cell cycle arresting proteins p15 and p21 cooperatively with other transcription factors and allowed extra time for DNA damage repair. TopBP1 was also found to interact with the breast cancer susceptibility protein 1 and both proteins localised together to arrested DNA synthesis apparatuses. The interaction of TopBP1 with the damage recognition and processing protein Rad9 is still further evidence of a link between TopBP1 and DNA damage. DNA polymerase epsilon forms a complex with Cdc45, a protein involved in DNA replication initiation and elongation. This complex does not interact with Cdc45 complexed with DNA polymerase delta, suggesting that these complexes synthesise DNA independently of each other. Our results are in agreement with the view that polymerase epsilon synthesises the first strand of DNA and polymerase delta the other. Finally,DNA polymerase epsilon binds to the RNA synthesising form of RNA polymerase II and nascent transcripts. The physiological meaning of this interaction needs to be determined.
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Tsao, Theresa Tsun-Hui. "Towards the development of transgenic banana bunchy top virus (BBTV)-resistant banana plants : interference with replication." Queensland University of Technology, 2008. http://eprints.qut.edu.au/17031/.

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Banana bunchy top virus (BBTV) causes one of the most devastating diseases of banana. Transgenic virus resistance is now considered one of the most promising strategies to control BBTV. Pathogen-derived resistance (PDR) strategies have been applied successfully to generate plants that are resistant to numerous different viruses, primarily against those viruses with RNA genomes. BBTV is a circular, single-stranded (css) DNA virus of the family Nanoviridae, which is closely related to the family Geminiviridae. Although there are some successful examples of PDR against geminiviruses, PDR against the nanoviruses has not been reported. Therefore, the aim of this thesis was to investigate the potential of BBTV genes to interfere with virus replication when used as transgenes for engineering banana plants resistance to BBTV. The replication initiation protein (Rep) of nanoviruses is the only viral protein essential for viral replication and represents an ideal target for PDR. Therefore, this thesis focused on the effect of wild-type or mutated Rep genes from BBTV satellite DNAs or the BBTV integral genome on the replication of BBTV in banana embryogenic cell suspensions. A new Rep-encoding satellite DNA, designated BBTV DNA-S4, was isolated from a Vietnamese BBTV isolate and characterised. When the effect of DNA-S4 on the replication of BBTV was examined, it was found that DNA-S4 enhanced the replication of BBTV. When the replicative capabilities of DNA-S4 and the previously characterised Rep-encoding BBTV satellite, DNA-S1, were compared, it was found that the amount of DNA-S4 accumulated to higher levels than DNA-S1. The interaction between BBTV and DNA-S1 was also examined. It was found that over-expression of the Rep encoded by DNA-S1 using ubi1 maize polyubiquitin promoter enhanced replication of BBTV. However, when the Rep-encoded by DNA-S1 was expressed by the native S1 promoter (in plasmid pBT1.1-S1), it suppressed the replication of BBTV. Based on this result, the use of DNA-S1 as a possible transgene to generate PDR against BBTV was investigated. The roles of the Rep-encoding and U5 genes of BBTV DNA-R, and the effects of over-expression of these two genes on BBTV replication were also investigated. Three mutants of BBTV DNA-R were constructed; plasmid pUbi-RepOnly-nos contained the ubi1 promoter driving Rep expression from DNA-R, plasmid pUbi-IntOnly-nos contained the ubi1 promoter driving expression of the DNA-R internal gene product (U5), while plasmid pUbi-R.ORF-nos contained the ubi1 promoter driving the expression of both Rep and the internal U5 gene product. The replication of BBTV was found to be significantly suppressed by pUbi-RepOnly-nos, weakly suppressed by pUbi-IntOnly-nos, but strongly enhanced by pUbi-R.ORF-nos. The effect of mutations in three conserved residues within the BBTV Rep on BBTV replication was also assessed. These mutations were all made in the regions in the ATPase motifs and resulted in changes from hydrophilic to hydrophobic residues (i.e. K187→M, D224→I and N268→L). None of these Rep mutants was able to initiate BBTV replication. However, over-expression of Reps containing the K187→M or N268→L mutations significantly suppressed the replication of BBTV. In summary, the Rep constructs that significantly suppressed replication of DNA-R and -C in banana embryogenic cell suspensions have the potential to confer resistance against BBTV by interfering with virus replication. It may be concluded that BBTV satellite DNAs are not ideal for conferring PDR because they did not suppress BBTV replication consistently. Wild-type Rep transcripts and mutated (i.e. K187→M and N248→L) Rep proteins of BBTV DNA-R, however, when over-expressed by a strong promoter, are all promising candidates for generating BBTV-resistant banana plants.
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Tokonzaba, Etienne. "Molecular mechanism of SV40 large tumor antigen helicase /." Connect to abstract via ProQuest. Full text is not available online, 2007.

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Thesis (Ph.D. in Pharmacology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 82-92; 128-134). Online version available via ProQuest Digital Dissertations.
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Leriche, Mélissa. "Mise en évidence d’une interaction entre la protéine 53BP1 et les fragments d’Okazaki." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASS065.

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Le maintien de l’intégrité du génome est un processus crucial à la vie cellulaire. Ce n’est que récemment que les protéines de liaison à l’ARN (« RNA-binding protein » ou RBP) ont été montré être impliquées dans ce processus. En présence d’ADN endommagé, les RBP régulent l’expression des gènes de réponse aux dommages de l’ADN et contrôlent le destin cellulaire. Elles jouent également un rôle plus direct dans la prévention et la réparation des dommages de l’ADN. De plus, des ARN sont présents aux sites de dommages de l’ADN et participent au maintien de l’intégrité du génome. Ainsi, le laboratoire recherche des acteurs protéiques capables de lier directement l’ARN au sein des protéines médiatrices de la réponse aux dommages de l’ADN. Un des candidats est la protéine 53BP1 (p53 binding protein 1) qui contient un domaine de liaison à l’ARN nommé domaine GAR (« Glycine-Arginine Rich »). 53BP1 est un acteur central de la signalisation des cassures double-brin de l’ADN et de la régulation de leur réparation par le processus de jonction d’extrémités non homologues pendant la phase G1 du cycle cellulaire. Le recrutement de 53BP1 aux sites de dommages de l'ADN dépend à la fois d'interactions directes entre 53BP1 et des marques d’histones, mais aussi d’une composante ARN.L’objectif était d’étudier l’interaction entre 53BP1 et l’ARN.Grâce aux méthodes de CLIP (« CrossLinking and ImmunoPrecipitation ») et de 2C (« Complex Capture »), nous avons montré que 53BP1 possède une activité de liaison directe à l'ARN, via son domaine GAR. Nous avons identifié l’acide nucléique interagissant avec 53BP1 comme étant une chimère ARN-ADN constituée d’une partie d’environ 10 ribonucléotides, suivie d’environ 100 désoxyribonucléotides. Ce type de molécule est très similaire à celle des fragments d’Okazaki qui sont impliqués dans l’initiation de la synthèse du brin retardé de la fourche de réplication. Par la méthode de SIRF (« In Situ Protein Interaction with Nascent DNA Replication Forks »), nous avons montré que 53BP1 est présent au niveau de l’ADN naissant, dans un contexte de réplication normal. De plus, la déplétion de la sous-unité catalytique de la primase (PRIM1) qui synthétise l’amorce ARN des fragments d’Okazaki, conduit à la diminution de la présence de 53BP1 à proximité d’ADN naissant. La déplétion de PRIM1 affecte également l’interaction de 53BP1 avec la chimère ARN-ADN in vivo. Ces résultats indiquent que 53BP1 est présent à la fourche de réplication via une interaction directe avec les fragments d’Okazaki. Enfin, sous stress réplicatif induit par l’hydroxyurée, la présence de 53BP1 au niveau de l’ADN naissant est fortement augmentée, indiquant que 53BP1 s’accumule aux fourches de réplication bloquées. L'ensemble de ces résultats montre que 53BP1 est une protéine de liaison aux ARN qui interagit directement avec les fragments d’Okazaki
Maintenance of genome integrity is essential for cell survival. It is only recently that RNA-binding proteins (RBPs) have been shown as fundamental actors in this process. In the presence of DNA damage, RBPs regulate the expression of DNA damage response (DDR) related genes and control cell fate. RBPs also have a more direct role in preventing and repairing DNA damage. Moreover, some RNAs are present at sites of DNA damage and, thus, participate in the maintenance of genome integrity. The laboratory is interested in proteins that are both able to directly bind RNA and involved in DDR. One candidate is the 53BP1 protein (p53 binding protein 1) that contains an RNA-binding domain called GAR domain (Glycin-Arginin Rich). 53BP1 is a key protein mediating the signalling of DNA double-strand breaks and channels DNA repair to the non-homologous end-joining pathway during the G1 phase of the cell cycle. The recruitment of 53BP1 to sites of DNA damage depends on both histones marks and an RNA component.The objective was to study the interaction between 53BP1 and RNA.By using CLIP (CrossLinking and Immunoprecipitation) and 2C (Complex Capture) technologies, we showed that 53BP1 presents a direct RNA-binding activity within its GAR domain. We identified the nucleic acid interacting with 53BP1 as being an RNA-DNA chimera composed of about 10 ribonucleotides, followed by about 100 dexoribonucleotides. This type of entity is highly similar to that of Okazaki fragments, that are involved in the initiation of lagging strand synthesis at replication forks. By using the SIRF method (In Situ Protein Interaction with Nascent DNA Replication Forks), we showed that 53BP1 is localized at sites of newly synthetized DNA, under normal conditions of replication. Furthermore, depletion of the catalytic sub-unit of the primase (PRIM1), that catalyzes the synthesis of the RNA primer of Okazaki fragments, results in a decrease in 53BP1 at sites of newly synthetized DNA. PRIM1 depletion also decreases the interaction between 53BP1 and RNA-DNA chimera in vivo. These results indicate that 53BP1 is localized at the replication fork through a direct interaction with Okazaki fragments. Likewise, under replicative stress induced by hydroxyurea, the presence of 53BP1 at the newly synthetized DNA is increased, indicating that 53BP1 accumulates at stalled replication forks. Altogether, these results show that 53BP1 is an RNA-binding protein that directly interacts with Okazaki fragments
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Pageau, Gayle Jeannette. "Maintenance of Constitutive and Inactive X Heterochromatin in Cancer and a Link to BRCA1: A Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/331.

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The development of cancer is a multi-step process which involves a series of events, including activation of oncogenes and loss of tumor suppressor function, leading to cell immortalization and misregulated proliferation. In the last few years, the importance of epigenetic defects in cancer development has become increasingly recognized. While most epigenetic studies focus on silencing of tumor suppressors, this thesis addresses defects in the maintenance of silenced heterochromatin in cancer, particularly breast cancer. Breast cancer is a leading cause of cancer in women and many familial cases have been linked to mutations in the breast cancer susceptibility genes, BRCA1 and BRCA2. BRCA1 has been linked to DNA repair as well as multiple other cellular processes, including cell cycle checkpoints, ubiquitination, centrosome function, and meiotic silencing of the XY body. This work began with a particular interest in the report that BRCA1 was linked to the failed maintenance of random X-inactivation in female somatic cells, via a role in supporting XIST RNA localization to the inactive X chromosome (Xi). XIST RNA is a non-coding RNA that fully coats or “paints” the Xi and induces its silencing. Work presented in Chapter II substantially clarifies the relationship of BRCA1 to XIST RNA, based on several lines of experimentation. Loss of BRCA1 does not lead to loss of XIST RNA in these studies, nor did reconstitution of HCC1937 BRCA1-/- tumor cells with BRCA1 lead to XIST RNA localization on Xi, although an effect on XIST RNA transcription is possible. Studies of BRCA1 localization with Xi showed that BRCA1 has a limited association with the Xi in ~3-10% of cells, it rarely colocalizes with XIST RNA to a significant extent, but rather is in close apposition to a small part of the XIST RNA/Xi territory. Additionally, analysis of several breast cancer cell lines revealed mislocalization of XIST RNA in some breast cancer cell lines. Many studies have examined BRCA1 foci that form following DNA damage and demonstrated that these are sites of repair. However, whether the numerous large foci consistently present in normal S-phase nuclei were storage sites or had any function was unknown. In Chapter III, I demonstrate that the BRCA1 foci in normal S-phase nuclei associate overwhelmingly with specific heterochromatic regions of the genome. More specifically, BRCA1 foci often associate with centromeric or pericentromeric regions in both human and mouse cells. In human cells BRCA1 foci often appear juxtaposed to centromeric signal, whereas in mouse, BRCA1 often rings or paints the large chromocenters, clusters of DAPI-dense pericentric and centric heterochromatin. Using PCNA and BrdU as markers of replication, I demonstrate that BRCA1 preferentially associates with the chromocenters during their replication, although high-resolution analysis indicates that BRCA1 and PCNA foci rarely directly overlap. Interestingly, cells with defects in BRCA1 were found to have lagging chromosomes and DNA bridges which nearly always contained satellite DNA, which is consistent with the possibility that BRCA1 deficit contributes to failed separation of sister chromatids at the centromere. This is consistent with other recent reports that BRCA1 is necessary for DNA decatenation by topoisomerase II during routine replication and with my demonstration that topoisomerase II also accumulates on pericentric heterochromatin (PCH) during replication. Chapter IV presents recent work which reveals that RNA is commonly expressed from the centric/pericentric heterochromatin and appears to be linked to its replication. In mouse cells RNA from heterochromatic sequences is readily detected using a broad molecular cytological assay for repeat transcription (the COT-1 RNA assay). In addition to a more dispersed nucleoplasmic signal from euchromatic nuclear regions, distinct localized foci of repeat RNA are detected with COT1 probe or pancentromeric probe. Further analysis with the minor satellite (centromere proper) and the major satellite (comprising the larger pericentric heterochromatin) reveals that the large RNA foci often contain these satellite sequences, long thought to be essentially silent. These foci generally associate with the PCH of chromocenters, and produce various patterns similar to BRCA1- including a larger signal partially painting or ringing the chromocenter in a fraction of cells. In conjunction again with PCNA staining, it was possible to determine that the major satellite RNAs associate with the chromocenters during replication. While the satellite RNA co-localizes precisely with PCNA, neither of these co-localizes at high resolution with BRCA1, although they all are present on replicating chromocenters contemporaneously. These findings show that satellite RNAs are more widely expressed in normal cells than previously thought and link their expression to replication of centromere-linked heterochromatin. Finally, Chapter V presents three lines of recent results to support a major concept forwarded in this manuscript: that loss of Xi heterochromatin may reflect defects in the broader heterochromatic compartment, which may be manifest at multiple levels. I provide evidence using two new assays that both the peripheral heterochromatic compartment and the expression and silencing of satellite repeats is commonly compromised in cancer, although this appears to vary among cancer lines or types. The final results connect back to the question with which I began: what maintains XIST RNA localization to the chromosome in normal cells. These results demonstrate for the first time that Aurora B Kinase activity, mediated by Protein Phosphatase 1 (PP1) during interphase, controls the interphase retention and mitotic release of XIST RNA from the chromosome, likely linked to chromatin modifications such as H3Ser10 phosphorylation. As Aurora B Kinase is commonly over-expressed in cancer and is linked to chromatin changes, this exemplifies one type of mechanism whereby broad epigenetic changes in cancer may impact XIST RNA localization and the maintenance of heterochromatin more generally. This thesis represents a melding of cancer biology with the study of X inactivation and heterochromatin, with findings of fundamental interest to both of these fields.
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Pageau, Gayle Jeannette. "Maintenance of Constitutive and Inactive X Heterochromatin in Cancer and a Link to BRCA1: A Dissertation." eScholarship@UMMS, 2006. http://escholarship.umassmed.edu/gsbs_diss/331.

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The development of cancer is a multi-step process which involves a series of events, including activation of oncogenes and loss of tumor suppressor function, leading to cell immortalization and misregulated proliferation. In the last few years, the importance of epigenetic defects in cancer development has become increasingly recognized. While most epigenetic studies focus on silencing of tumor suppressors, this thesis addresses defects in the maintenance of silenced heterochromatin in cancer, particularly breast cancer. Breast cancer is a leading cause of cancer in women and many familial cases have been linked to mutations in the breast cancer susceptibility genes, BRCA1 and BRCA2. BRCA1 has been linked to DNA repair as well as multiple other cellular processes, including cell cycle checkpoints, ubiquitination, centrosome function, and meiotic silencing of the XY body. This work began with a particular interest in the report that BRCA1 was linked to the failed maintenance of random X-inactivation in female somatic cells, via a role in supporting XIST RNA localization to the inactive X chromosome (Xi). XIST RNA is a non-coding RNA that fully coats or “paints” the Xi and induces its silencing. Work presented in Chapter II substantially clarifies the relationship of BRCA1 to XIST RNA, based on several lines of experimentation. Loss of BRCA1 does not lead to loss of XIST RNA in these studies, nor did reconstitution of HCC1937 BRCA1-/- tumor cells with BRCA1 lead to XIST RNA localization on Xi, although an effect on XIST RNA transcription is possible. Studies of BRCA1 localization with Xi showed that BRCA1 has a limited association with the Xi in ~3-10% of cells, it rarely colocalizes with XIST RNA to a significant extent, but rather is in close apposition to a small part of the XIST RNA/Xi territory. Additionally, analysis of several breast cancer cell lines revealed mislocalization of XIST RNA in some breast cancer cell lines. Many studies have examined BRCA1 foci that form following DNA damage and demonstrated that these are sites of repair. However, whether the numerous large foci consistently present in normal S-phase nuclei were storage sites or had any function was unknown. In Chapter III, I demonstrate that the BRCA1 foci in normal S-phase nuclei associate overwhelmingly with specific heterochromatic regions of the genome. More specifically, BRCA1 foci often associate with centromeric or pericentromeric regions in both human and mouse cells. In human cells BRCA1 foci often appear juxtaposed to centromeric signal, whereas in mouse, BRCA1 often rings or paints the large chromocenters, clusters of DAPI-dense pericentric and centric heterochromatin. Using PCNA and BrdU as markers of replication, I demonstrate that BRCA1 preferentially associates with the chromocenters during their replication, although high-resolution analysis indicates that BRCA1 and PCNA foci rarely directly overlap. Interestingly, cells with defects in BRCA1 were found to have lagging chromosomes and DNA bridges which nearly always contained satellite DNA, which is consistent with the possibility that BRCA1 deficit contributes to failed separation of sister chromatids at the centromere. This is consistent with other recent reports that BRCA1 is necessary for DNA decatenation by topoisomerase II during routine replication and with my demonstration that topoisomerase II also accumulates on pericentric heterochromatin (PCH) during replication. Chapter IV presents recent work which reveals that RNA is commonly expressed from the centric/pericentric heterochromatin and appears to be linked to its replication. In mouse cells RNA from heterochromatic sequences is readily detected using a broad molecular cytological assay for repeat transcription (the COT-1 RNA assay). In addition to a more dispersed nucleoplasmic signal from euchromatic nuclear regions, distinct localized foci of repeat RNA are detected with COT1 probe or pancentromeric probe. Further analysis with the minor satellite (centromere proper) and the major satellite (comprising the larger pericentric heterochromatin) reveals that the large RNA foci often contain these satellite sequences, long thought to be essentially silent. These foci generally associate with the PCH of chromocenters, and produce various patterns similar to BRCA1- including a larger signal partially painting or ringing the chromocenter in a fraction of cells. In conjunction again with PCNA staining, it was possible to determine that the major satellite RNAs associate with the chromocenters during replication. While the satellite RNA co-localizes precisely with PCNA, neither of these co-localizes at high resolution with BRCA1, although they all are present on replicating chromocenters contemporaneously. These findings show that satellite RNAs are more widely expressed in normal cells than previously thought and link their expression to replication of centromere-linked heterochromatin. Finally, Chapter V presents three lines of recent results to support a major concept forwarded in this manuscript: that loss of Xi heterochromatin may reflect defects in the broader heterochromatic compartment, which may be manifest at multiple levels. I provide evidence using two new assays that both the peripheral heterochromatic compartment and the expression and silencing of satellite repeats is commonly compromised in cancer, although this appears to vary among cancer lines or types. The final results connect back to the question with which I began: what maintains XIST RNA localization to the chromosome in normal cells. These results demonstrate for the first time that Aurora B Kinase activity, mediated by Protein Phosphatase 1 (PP1) during interphase, controls the interphase retention and mitotic release of XIST RNA from the chromosome, likely linked to chromatin modifications such as H3Ser10 phosphorylation. As Aurora B Kinase is commonly over-expressed in cancer and is linked to chromatin changes, this exemplifies one type of mechanism whereby broad epigenetic changes in cancer may impact XIST RNA localization and the maintenance of heterochromatin more generally. This thesis represents a melding of cancer biology with the study of X inactivation and heterochromatin, with findings of fundamental interest to both of these fields.
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Bailey, Daniel John. "Cellular proteins in picornavirus replication." Thesis, University of Reading, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298484.

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Komori, Hirofumi. "Structural studies on DNA-binding proteins : DNA replication initiator and DNA photolyase." 京都大学 (Kyoto University), 2002. http://hdl.handle.net/2433/150005.

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Antonopoulos, Ioanna H. "CHARACTERIZING RNA TRANSCRIPTION AND DNA REPLICATION VIA RAMAN CRYSTALLOGRAPHY." Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1428076280.

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Books on the topic "RNA ; Proteins ; DNA replication"

1

The molecules of life: DNA, RNA, and proteins. New York: Facts On File, 2009.

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NATO Advanced Study Institute Summer School on the Molecular Basis of Viral Replication (1986 Maratea, Italy). The molecular basis of viral replication. New York: Plenum Press, 1987.

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UCLA, Symposium on Molecular Mechanisms in DNA Replication and Recombination (1989 Keystone Colo ). Molecular mechanisms in DNA replication and recombination: Proceedings of a UCLA Symposium held at Keystone, Colorado, March 27-April 3, 1989. New York: Wiely-Liss, 1990.

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Travers, A. A. DNA-protein interactions. London: Chapman & Hall, 1993.

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Gaston, Kevin. Small DNA tumour viruses. Norfolk, UK: Caister Academic Press, 2012.

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1948-, Tymoczko John L., and Stryer Lubert, eds. Biochemistry. 6th ed. New York, N.Y: W. H. Freeman, 2006.

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Krebs, Jocelyn E. Lewin's genes XI. Burlington, Mass: Jones & Bartlett Learning, 2013.

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C, Richardson Charles, and Lehman I. Robert, eds. Molecular mechanisms in DNA replication and recombination: Proceedings of a UCLA Symposium held at Keystone, Colorado, March 27-April 3, 1989. New York: Wiley-Liss, 1990.

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Lee, Hoyun. Proliferating cell nuclear antigen (PCNA). Trivandrum, Kerala, India: Research Signpost, 2006.

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Artsimovitch, Irina, and Thomas J. Santangelo. Bacterial transcriptional control: Methods and protocols. New York: Humana Press, 2015.

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Book chapters on the topic "RNA ; Proteins ; DNA replication"

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Hübscher, Ulrich. "DNA Replication Fork Proteins." In Methods in Molecular Biology, 19–33. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-815-7_2.

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Sinkovics, Joseph G. "YY Proteins." In RNA/DNA and Cancer, 131–35. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22279-0_8.

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Sinkovics, Joseph G. "Viral and Cellular Proteins Interact." In RNA/DNA and Cancer, 247–50. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22279-0_16.

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Blossey, Ralf. "Biomolecular Structure: DNA, RNA, Proteins." In Computational Biology, 39–82. Second edition. | Boca Raton, Florida : CRC Press, [2020] |: CRC Press, 2019. http://dx.doi.org/10.1201/9780429503672-2.

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Frey, A., T. Chittenden, and A. J. Levine. "Epstein-Barr Virus DNA Replication." In Transforming Proteins of DNA Tumor Viruses, 227–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74578-2_28.

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Collins, Kathleen L., Lome F. Erdile, Sandra K. Randall, Alicia A. R. Russo, Pamela R. Simancek, Christopher B. Umbricht, David M. Virshup, David H. Weinberg, Marc S. Wold, and Thomas J. Kelly. "SV40 DNA Replication with Purified Proteins: Functional Interactions Among the Initiation Proteins." In DNA Replication: The Regulatory Mechanisms, 369–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76988-7_33.

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Hübscher, U., G. Cullmann, P. Thömmes, B. Strack, E. Ferrari, B. Senn, A. Georgaki, T. Weiser, M. W. Berchtold, and V. N. Podust. "Mammalian DNA Helicases, DNA Polymerases and DNA Polymerase Auxiliary Proteins." In DNA Replication and the Cell Cycle, 63–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77040-1_6.

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Tye, B. K., V. Chang, C. Christ, R. Elble, S. Gibson, S. Passmore, and H. Yan. "Proteins Involved in ARS Function in Yeast." In DNA Replication: The Regulatory Mechanisms, 205–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76988-7_19.

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Hass, Cathy S., Ran Chen, and Marc S. Wold. "Detection of Posttranslational Modifications of Replication Protein A." In Single-Stranded DNA Binding Proteins, 193–204. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-032-8_15.

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Theis, James F., and Carol S. Newlon. "Screens for Proteins Binding to the ARS Consensus Sequence." In DNA Replication: The Regulatory Mechanisms, 169–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76988-7_16.

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Conference papers on the topic "RNA ; Proteins ; DNA replication"

1

Young, Paul W. "Student-produced video of role-plays on topics in cell biology and biochemistry: A novel undergraduate group work exercise." In Learning Connections 2019: Spaces, People, Practice. University College Cork||National Forum for the Enhancement of Teaching and Learning in Higher Education, 2019. http://dx.doi.org/10.33178/lc2019.15.

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Group work or cooperative learning is a form of active learning that has potential benefits that extend beyond just being an alternative or improved way of learning course material. For example, Shimazoe and Aldrich (2010) identified six proposed benefits of active learning to students, namely (1) promoting deep learning, (2) helping students earn higher grades, (3) teaching social skills & civic values, (4) teaching higher order thinking skills, (5) promoting personal growth and (6) developing positive attitudes toward autonomous learning. There is evidence for the effectiveness of role-plays both in achieving learning outcomes (Azman, Musa, & Mydin, 2018; Craciun, 2010; Latif, Mumtaz, Mumtaz, & Hussain, 2018; McSharry & Jones, 2000; Yang, Kim, & Noh, 2010), but also in developing desirable graduate attributes such as teamwork, communication and problem solving skills [4]. The importance of such skills is widely touted by employers of science graduates, sometimes more so than discipline-specific knowledge, arguing in favour of the incorporation of role-plays and other forms of cooperative learning into undergraduate science curricula. Role-playing is probably not as widely used in the physical and life sciences as it is in other academic disciplines. In science the most obvious role-play scenarios in which students play the roles of people might be in examining historical figures at the centre of famous scientific discoveries or debates (Odegaard, 2003). In addition, role-plays fit well at the interface between science and other discipline when exploring ethical, legal or commercial implications of scientific discoveries(Chuck, 2011). However, to apply role-play to core topics in science or mathematics the roles that must be played are not those of people but rather of things like particles, forces, elements, atoms, numbers, laws, equations, molecules, cells, organs and so on. The learning scenarios for science-based roleplays in which the characters represented are not people are less obvious, probably explaining why the use of role-plays in science education is less common. Nevertheless, focusing on the life sciences, role-plays in which the characters are organelles in a cell or enzymes involved in fundamental cellular processes like DNA replication, RNA transcription and protein translation have been described for example (Cherif, Siuda, Dianne M. Jedlicka, & Movahedzadeh, 2016; Takemura & Kurabayashi, 2014). The communication of discipline-specific templates and successful models for the application of role-playing in science education is likely to encourage their wider adoption. Here I describe a videoed group role-play assignment that has been developed over a ten-year period of reflective teaching practice. I suggest that this model of videoed group role-plays is a useful cooperative learning format that will allow learners to apply their varied creativity and talents to exploring and explaining diverse scientific topics while simultaneously developing their teamwork skills.
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Yang, Runtao, Chengjin Zhang, Rui Gao, and Lina Zhang. "A machine learning approach to identify DNA replication proteins from sequence-derived features." In 2015 IEEE 28th Canadian Conference on Electrical and Computer Engineering (CCECE). IEEE, 2015. http://dx.doi.org/10.1109/ccece.2015.7129092.

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"PARP1 activation directs RNA binding proteins to DNA damages to form PARG reversible compartments enriched in damaged DNA." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-359.

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Sahin, Ozgur. "High throughput nanomechanical measurements on proteins DNA and RNA with a T-shaped cantilever." In 2009 IEEE/LEOS International Conference on Optical MEMS and Nanophotonics. IEEE, 2009. http://dx.doi.org/10.1109/omems.2009.5338630.

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Lee, C. H., H. Teng, and J. S. Chen. "Atomistic to Continuum Modeling of DNA Molecules." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13157.

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The mechanical properties of DNA has very important biological implication. For example, the bending and twisting rigidities of DNA affect how it wraps around histones to form chromosomes, bends upon interactions with proteins, supercoils during replication process, and packs into the confined space within a virus. Many biologically important processes involving DNA are accompanied by the deformations of double helical structure of DNA.
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Akbar-Khanzadeh, F., M. Jahangir-Blourchian, and M. Valigosky. "17. Ultraviolet Radiation Exposure During Gel Electrophoresis Visualization Used for the Detection of Proteins, DNA and RNA in Research Laboratories." In AIHce 2002. AIHA, 2002. http://dx.doi.org/10.3320/1.2766101.

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Connor, Katherine L., Adrian W. Briggs, Stephen J. Goldfless, Sonia Timberlake, Brian J. Belmont, Christopher R. Clouser, David Koppstein, and Francois Vigneault. "Abstract 1442: Comprehensive TIL profiling by simultaneous DNA barcoding of proteins, RNA and natively paired immune receptors from millions of single cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1442.

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Fortin, Sébastien, Hanane Moussa, Mathieu Gagné-Boulet, Jacques Lacroix, Marie-France Côté, Denis Velic, Joris Pauty, and Jean-Yves Masson. "Abstract 4487: Design, synthesis, and biological activity of N-phenyl ureidobenzenesulfonates (PUB-SOs) as new and innovative small-molecule drugs inhibiting proteins involved in DNA repair/replication mechanisms." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4487.

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Rajput, B., D. Alaimo, A. M. Asselbergs, and E. Reich. "CONSTRUCTION AND EXPRESSION OF HYBRID PLASMINOGEN ACTIVATOR GENES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644412.

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Hybrid plasminogen activator (PA) genes containing fragments of cDNA encoding the non-catalytic part of tissue-PA and the .catalytic domain of urokinase and vice versa were constructed and expressed in Chinese Hamster ovary (CHO) cells. The hybrid nature of the products in stably transformed cells was analyzed at the level of DNA and RNA using probes derived from different regions of the urokinase and tissue-PA cDNAs and at the protein level by means of polyclonal antibodies raised against tissue-PA and urokinase. The hybrid genes made hybrid RNAs and proteins of the expected sizes. The proteins were enzymatically active as determined by zymography and chromogenic enzyme assays and this activity was blocked by the appropriate antibodies. The effect on hybrid PAs of cyanogen bromide cleaved fibrinogen fragments, poly-D-lysine and heparin which are known to affect the activity of tissue-PA and urokinase differently was also studied
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Jubery, Talukder Zaki, Anmiv S. Prabhu, Min Jun Kim, and Prashanta Dutta. "Modeling and Simulation of Translocation Phenomenon in a Solid State Nanopore for Nanoparticle Separation." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-38742.

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Solid state nanopore is a potential candidate for separation of nanoparticles or biomolecules such as proteins, DNA, and RNA. However, efficient separation of particles through nanopores is a challenging task as a number of factors such as externally applied voltage, size and charge density of particle, size and charge density of membrane pore, and the concentration of bulk electrolyte influence the translocation behavior of nanoparticles through pores. This paper uses a mathematical model based on Poisson–Nernst–Plank equations along with Navier-Stokes equations to systematically study these factors. Membrane pore surface charge is found to be a vital parameter in this seperation process. Numerical results reveal that efficient separation of high density lipoprotein (HDL) from low density lipoprotein (LDL) in a 0.2 M KCL solution (resembling blood buffer) through a 150 nm pore is possible if the pore surface charge density is around −4.0 mC/m2.
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Reports on the topic "RNA ; Proteins ; DNA replication"

1

Jackson, Peter K. DNA Replication Initiator Proteins and Genetic Instability: Creating a Mouse Model for Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada392190.

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Hood-DeGrenier, Jennifer. Active Learning Workshops for Teaching Key Topics in Introductory Cell and Molecular Biology: Structure of DNA/RNA, Structure of Proteins, and Cell Division via Mitosis and Meiosis. Genetics Society of America Peer-Reviewed Education Portal (GSA PREP), December 2015. http://dx.doi.org/10.1534/gsaprep.2015.004.

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