Relevant bibliographies by topics / DNA replication

Contents

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

Academic literature on the topic 'DNA replication'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 October 2024

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Journal articles on the topic "DNA replication"

1

Avemann, K., R. Knippers, T. Koller, and J. M. Sogo. "Camptothecin, a specific inhibitor of type I DNA topoisomerase, induces DNA breakage at replication forks." Molecular and Cellular Biology 8, no. 8 (August 1988): 3026–34. http://dx.doi.org/10.1128/mcb.8.8.3026-3034.1988.

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The structure of replicating simian virus 40 minichromosomes, extracted from camptothecin-treated infected cells, was investigated by biochemical and electron microscopic methods. We found that camptothecin frequently induced breaks at replication forks close to the replicative growth points. Replication branches were disrupted at about equal frequencies at the leading and the lagging strand sides of the fork. Since camptothecin is known to be a specific inhibitor of type I DNA topoisomerase, we suggest that this enzyme is acting very near the replication forks. This conclusion was supported by experiments with aphidicolin, a drug that blocks replicative fork movement, but did not prevent the camptothecin-induced breakage of replication forks. The drug teniposide, an inhibitor of type II DNA topoisomerase, had only minor effects on the structure of these replicative intermediates.
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Avemann, K., R. Knippers, T. Koller, and J. M. Sogo. "Camptothecin, a specific inhibitor of type I DNA topoisomerase, induces DNA breakage at replication forks." Molecular and Cellular Biology 8, no. 8 (August 1988): 3026–34. http://dx.doi.org/10.1128/mcb.8.8.3026.

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The structure of replicating simian virus 40 minichromosomes, extracted from camptothecin-treated infected cells, was investigated by biochemical and electron microscopic methods. We found that camptothecin frequently induced breaks at replication forks close to the replicative growth points. Replication branches were disrupted at about equal frequencies at the leading and the lagging strand sides of the fork. Since camptothecin is known to be a specific inhibitor of type I DNA topoisomerase, we suggest that this enzyme is acting very near the replication forks. This conclusion was supported by experiments with aphidicolin, a drug that blocks replicative fork movement, but did not prevent the camptothecin-induced breakage of replication forks. The drug teniposide, an inhibitor of type II DNA topoisomerase, had only minor effects on the structure of these replicative intermediates.
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Swindle, C. Scott, Nianxiang Zou, Brian A. Van Tine, George M. Shaw, Jeffrey A. Engler, and Louise T. Chow. "Human Papillomavirus DNA Replication Compartments in a Transient DNA Replication System." Journal of Virology 73, no. 2 (February 1, 1999): 1001–9. http://dx.doi.org/10.1128/jvi.73.2.1001-1009.1999.

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ABSTRACT Many DNA viruses replicate their genomes at nuclear foci in infected cells. Using indirect immunofluorescence in combination with fluorescence in situ hybridization, we colocalized the human papillomavirus (HPV) replicating proteins E1 and E2 and the replicating origin-containing plasmid to nuclear foci in transiently transfected cells. The host replication protein A (RP-A) was also colocalized to these foci. These nuclear structures were identified as active sites of viral DNA synthesis by bromodeoxyuridine (BrdU) pulse-labeling. Unexpectedly, the great majority of RP-A and BrdU incorporation was found in these HPV replication domains. Furthermore, E1, E2, and RP-A were also colocalized to nuclear foci in the absence of an origin-containing plasmid. These observations suggest a spatial reorganization of the host DNA replication machinery upon HPV DNA replication or E1 and E2 expression. Alternatively, viral DNA replication might be targeted to host nuclear domains that are active during the late S phase, when such domains are limited in number. In a fraction of cells expressing E1 and E2, the promyelocytic leukemia protein, a component of nuclear domain 10 (ND10), was either partially or completely colocalized with E1 and E2. Since ND10 structures were recently hypothesized to be sites of bovine papillomavirus virion assembly, our observation suggests that HPV DNA amplification might be partially coupled to virion assembly.
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Thomas, David C., John D. Roberts, Ralph D. Sabatino, Thomas W. Myers, Cheng Keat Tan, Kathleen M. Downey, Antero G. So, Robert A. Bambara, and Thomas A. Kunkel. "Fidelity of mammalian DNA replication and replicative DNA polymerases." Biochemistry 30, no. 51 (December 1991): 11751–59. http://dx.doi.org/10.1021/bi00115a003.

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Takebayashi, Shin-ichiro, Tyrone Ryba, Kelsey Wimbish, Takuya Hayakawa, Morito Sakaue, Kenji Kuriya, Saori Takahashi, et al. "The Temporal Order of DNA Replication Shaped by Mammalian DNA Methyltransferases." Cells 10, no. 2 (January 29, 2021): 266. http://dx.doi.org/10.3390/cells10020266.

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Multiple epigenetic pathways underlie the temporal order of DNA replication (replication timing) in the contexts of development and disease. DNA methylation by DNA methyltransferases (Dnmts) and downstream chromatin reorganization and transcriptional changes are thought to impact DNA replication, yet this remains to be comprehensively tested. Using cell-based and genome-wide approaches to measure replication timing, we identified a number of genomic regions undergoing subtle but reproducible replication timing changes in various Dnmt-mutant mouse embryonic stem (ES) cell lines that included a cell line with a drug-inducible Dnmt3a2 expression system. Replication timing within pericentromeric heterochromatin (PH) was shown to be correlated with redistribution of H3K27me3 induced by DNA hypomethylation: Later replicating PH coincided with H3K27me3-enriched regions. In contrast, this relationship with H3K27me3 was not evident within chromosomal arm regions undergoing either early-to-late (EtoL) or late-to-early (LtoE) switching of replication timing upon loss of the Dnmts. Interestingly, Dnmt-sensitive transcriptional up- and downregulation frequently coincided with earlier and later shifts in replication timing of the chromosomal arm regions, respectively. Our study revealed the previously unrecognized complex and diverse effects of the Dnmts loss on the mammalian DNA replication landscape.
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Greci, Mark D., and Stephen D. Bell. "Archaeal DNA Replication." Annual Review of Microbiology 74, no. 1 (September 8, 2020): 65–80. http://dx.doi.org/10.1146/annurev-micro-020518-115443.

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It is now well recognized that the information processing machineries of archaea are far more closely related to those of eukaryotes than to those of their prokaryotic cousins, the bacteria. Extensive studies have been performed on the structure and function of the archaeal DNA replication origins, the proteins that define them, and the macromolecular assemblies that drive DNA unwinding and nascent strand synthesis. The results from various archaeal organisms across the archaeal domain of life show surprising levels of diversity at many levels—ranging from cell cycle organization to chromosome ploidy to replication mode and nature of the replicative polymerases. In the following, we describe recent advances in the field, highlighting conserved features and lineage-specific innovations.
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Liu, Guoqi, Michelle Malott, and Michael Leffak. "Multiple Functional Elements Comprise a Mammalian Chromosomal Replicator." Molecular and Cellular Biology 23, no. 5 (March 1, 2003): 1832–42. http://dx.doi.org/10.1128/mcb.23.5.1832-1842.2003.

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ABSTRACT The structure of replication origins in metazoans is only nominally similar to that in model organisms, such as Saccharomyces cerevisiae. By contrast to the compact origins of budding yeast, in metazoans multiple elements act as replication start sites or control replication efficiency. We first reported that replication forks diverge from an origin 5′ to the human c-myc gene and that a 2.4-kb core fragment of the origin displays autonomous replicating sequence activity in plasmids and replicator activity at an ectopic chromosomal site. Here we have used clonal HeLa cell lines containing mutated c-myc origin constructs integrated at the same chromosomal location to identify elements important for DNA replication. Replication activity was measured before or after integration of the wild-type or mutated origins using PCR-based nascent DNA abundance assays. We find that deletions of several segments of the c-myc origin, including the DNA unwinding element and transcription factor binding sites, substantially reduced replicator activity, whereas deletion of the c-myc promoter P1 had only a modest effect. Substitution mutagenesis indicated that the sequence of the DNA unwinding element, rather than the spacing of flanking sequences, is critical. These results identify multiple functional elements essential for c-myc replicator activity.
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Kornberg, A. "DNA replication." Journal of Biological Chemistry 263, no. 1 (January 1988): 1–4. http://dx.doi.org/10.1016/s0021-9258(19)57345-8.

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van der Vliet, P. C. "DNA replication." Current Opinion in Cell Biology 1, no. 3 (June 1989): 481–87. http://dx.doi.org/10.1016/0955-0674(89)90009-4.

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Virshup, D. M. "DNA replication." Current Opinion in Cell Biology 2, no. 3 (June 1990): 453–60. http://dx.doi.org/10.1016/0955-0674(90)90127-z.

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Dissertations / Theses on the topic "DNA replication"

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Carrington, James T. "Post-replicative resolution of under-replication." Thesis, University of Dundee, 2017. https://discovery.dundee.ac.uk/en/studentTheses/f0a89d2a-6ee2-4175-ba65-d58aaaee4e24.

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The evolutionary pressure to prevent re-replication by inactivating licensing during S phase leaves higher-eukaryotes with large genomes, such as human cells, vulnerable to replication stresses. Origins licensed in G1 must be sufficient to complete replication as new origins cannot be licensed in response to irreversible replication fork stalling. Interdisciplinary approaches between cellular biology and biophysics predict that replication of the genome is routinely incomplete in G2, even in the absence of external stressors. The frequency of converging replication forks that never terminate due to irreversible stalling (double fork stall), which result in a segment of unreplicated DNA, was modelled using high quality origin-mapping data in HeLa and IMR-90 cells. From this, hypotheses were generated that related an increase in unreplicated segments of DNA to reduced functional origin number. Presented in this thesis is the confirmation of this relation by quantifying chromosome mis-segregation and DNA damage responses when origin number was reduced using RNAi against licensing factors. The number of ultrafine anaphase bridges and 53BP1 nuclear bodies are in remarkable concordance with the theoretical predictions for the number of double fork stalls, indicating that cells are able to tolerate under-replication through such post-replicative cellular responses. 53BP1 preferentially binds to chromatin associated with large replicons, and functions synergistically with dormant origins to protect the stability of the genome. Additional candidates, inspired by common fragile site research, have also been characterised as responders to spontaneous under-replication, and include FANCD2 and MiDAS, which function in early mitosis to facilitate completion of replication before cells enter anaphase. In conclusion, a series of mechanisms that sequentially function throughout the cell cycle protects the stability of the human genome against inevitable spontaneous under-replication brought about by its large size.
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Rytkönen, A. (Anna). "The role of human replicative DNA polymerases in DNA repair and replication." Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514281381.

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Abstract The maintenance of integrity of the genome is essential for a cell. DNA repair and faithful DNA replication ensure the stability of the genome. DNA polymerases (pols) are the enzymes that synthesise DNA, a process important both in DNA replication and repair. In DNA replication DNA polymerases duplicate the genome during S phase prior to cell division. Pols α, δ, and ε are implicated in chromosomal DNA replication, but their exact function in replication is not yet completely clear. The mechanisms of different repair pathways and proteins involved are not yet completely characterised either. The deeper understanding of DNA repair and replication mechanisms is crucial for our understanding on the function of the cell. The mechanism of repair of DNA double strand breaks (DSBs) by non-homologous end joining (NHEJ) was studied with an in vitro assay. DNA polymerase activity was found to be involved in NHEJ and important in stabilising DNA ends. Antibodies against pol α, but not pol β or ε, decreased NHEJ significantly, which indicates the involvement of pol α in NHEJ. In addition, the removal of proliferating cell nuclear antigen (PCNA) slightly decreased NHEJ activity. The division of labour between pols α, δ, and ε during DNA replication was studied. Results from UV-crosslinking, chromatin association, replication in isolated nuclei, and immunoelectron microscopy (IEM) studies showed that there are temporal differences between the activities and localisations of the pols during S phase. Pol α was active throughout S phase, pol ε was more active at early S phase, whereas the activity of pol δ increased as S phase advanced. These results suggest that pols δ and ε function independently during DNA replication. Pol ε could be crosslinked to nascent RNA, and this labelling was not linked to DNA replication, but rather to transcription. Immunoprecipitation studies indicated that pol ε, but not pols α and δ, associated with RNA polymerase II (RNA pol II). Only the hyperphosphorylated, transcriptionally active RNA pol II was found to associate with pol ε. A large proportion of pol ε and RNA pol II colocalised in cells as determined with immunoelectron microscopy. The interaction between pol ε and RNA pol II suggests that they are involved in a global regulation of transcription and DNA replication.
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Chen, Shuhua. "Multiple mechanisms regulate the human replication factors : replication protein A and DNA polymerase alpha-during DNA replication and DNA repair /." [S.l. : s.n.], 2003.

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Anderson, Mary E. Ph D. (Mary Elizabeth)Massachusetts Institute of Technology. "Regulation of DNA replication and the replication initiator, DnaA, in Bacillus subtilis." Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/121876.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2019
Cataloged from PDF version of thesis. "February 2019."
Includes bibliographical references (pages 118-128).
DNA replication is a highly regulated process across all organisms. Improper regulation of DNA replication can be detrimental. I identified an overinitiating, conditional synthetic lethal mutant of Bacillus subtilis. I isolated suppressors of this mutant and uncovered novel genes associated with DNA replication. These suppressors acted both at the steps of initiation and elongation to overcome the detrimental replication initiation of the synthetic lethal [delta]yabA dnaA 1 mutant. One class of suppressors decreased levels of the replicative helicase, DnaC. I showed that decreased levels of helicase are sufficient to limit replication initiation under fast growth conditions. I also explored the regulation of DnaA as a transcription factor. The replication initiation inhibitor, YabA, binds to DnaA and prevents its cooperative binding at the origin. In addition to its role in replication initiation, DnaA also directly regulates expression of several genes. YabA has been shown to inhibit DnaA binding at several promoters but its effect on DnaA-mediated gene expression is unclear. I found that YabA inhibits sda activation by DnaA but does not significantly affect repression of ywlC by DnaA. Lastly, I showed that YabA appears to stimulate autoregulation of dnaA. This preliminary data illustrates a role for YabA regulation in DnaA-mediated gene expression.
by Mary E. Anderson.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Biology
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Tavares, de Araujo Felipe. "DNA replication and methylation." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37847.

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One of the main questions of modern biology is how our cells interpret our genetic and epigenetic information. DNA methylation is a covalent modification of the genome that is essential for mammalian development and plays an important role in the control of gene expression, genomic imprinting and X-chromosome inactivation (Bird and Wolffe, 1999; Szyf et al., 2000). Furthermore, changes in DNA methylation and DNA methyltransferase 1 (DNMT1) activity have been widely documented in a number of human cancers (Szyf, 1998a; Szyf et al., 2000).
In Escherichia coli, timing and frequency of initiation of DNA replication are controlled by the levels of the bacterial methyltransferase and by the methylation status of its origin of replication (Boye and Lobner-Olesen, 1990; Campbell and Kleckner, 1990). In mammalian cells, however, the importance of methyltransferase activity and of DNA methylation in replication is only now starting to emerge (Araujo et al., 1998; Delgado et al., 1998; DePamphilis, 2000; Knox et al., 2000).
The work described in this thesis focuses mainly on understanding the functional relationship between changes in DNA methylation and DNMT1 activity on mammalian DNA replication. In higher eukaryotes, DNA replication initiates from multiple specific sites throughout the genome (Zannis-Hadjopoulos and Price, 1999). The first part of the thesis describes the identification and characterization of novel in vivo initiation sites of DNA replication within the human dnmt1 locus (Araujo et al., 1999). Subsequently, a study of the temporal relationship between DNA replication and the inheritance of the DNA methylation pattern is presented. We also demonstrate that mammalian origins of replication, similarly to promoters, are differentially methylated (Araujo et al., 1998). We then tested the hypothesis that DNMT1 is a necessary component of the replication machinery. The results presented indicate that inhibition of DNMT1 results in inhibition of DNA replication (Knox et al., 2000). Finally, results are presented, demonstrating that the amino terminal region of DNMT1 is responsible for recognizing hemimethylated CGs, DNMT1's enzymatic target. Taken together, the results presented in this thesis demonstrate that DNMT1 is necessary for proper DNA replication and that DNA methylation may modulate origin function.
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Upton, Amy Louise. "Replication of damaged DNA." Thesis, University of Nottingham, 2009. http://eprints.nottingham.ac.uk/11332/.

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DNA is under constant attack from numerous damaging agents and our cells deal with thousands of lesions every day. With such constant damage it is inevitable that the template will not be completely cleared of lesions before the replication complex arrives. The consequences of the replisome meeting an obstacle will depend upon the nature of the obstacle. I have focussed upon replication in Escherichia coli and the effect of UV-induced lesions, which would block synthesis by the replicative polymerases. It is accepted that a UV lesion in the lagging strand template can be bypassed by the replisome complex, but the consequences of meeting a lesion in the leading strand template remain unclear. A lesion in the leading strand template could block replisome progression and the fork might require extensive processing in order to restart replication. However, it has also been proposed that the replisome could progress past these lesions by re‐priming replication downstream and leaving a gap opposite the lesion. The results of my studies revealed that all modes of synthesis are delayed after UV. I have demonstrated that when synthesis resumed, the majority reflected the combined effects of oriC firing and the initiation of inducible stable DNA replication. These modes of synthesis mask the true extent of the delay in synthesis at existing replication forks. The results also revealed that all synthesis after UV is dependent upon DnaC, suggesting that the replicative helicase and possibly the entire replisome, needs to be reloaded. A functional RecFOR system is required for efficient replication restart, without these proteins replication is capable of resuming but only after a long delay. My data support models proposing that replication forks require extensive processing after meeting a lesion in the leading strand template. Whilst I cannot exclude the possibility that replication forks can progress past some such lesions, my data indicate that they cannot progress past many before stalling. Overall, my results demonstrate the importance of measuring all modes of DNA synthesis when assessing the contribution of any particular protein to recovery after UV irradiation. Thus, although net synthesis in cells lacking RecG appears similar to wild type after UV, the mode of replication is in fact quite different. A dramatic increase in the level of stable DNA replication appears to account for much of the overall synthesis detected and coincides with a major chromosome segregation defect. The importance of stable DNA replication in irradiated recG cells has not previously been considered because the different modes of synthesis were ignored. The significance of this pathology and of the other findings reported in this thesis is discussed in relation to current models of DNA repair and replication restart.
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Borazjani, Gholami Farimah. "Role of replicative primase in lesion bypass during DNA replication." Thesis, University of Sussex, 2017. http://sro.sussex.ac.uk/id/eprint/68762/.

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Maintenance of genome integrity and stability is fundamental for any form of life. This is complicated as DNA is highly reactive and always under attack from a wide range of endogenous and exogenous sources which can lead to different damages in the DNA. To preserve the integrity of DNA replication, cells hav evolved a variety of DNA repair pathways. DNA damage tolerance mechanisms serve as the last line of defence to rescue the stalled replications forks. TLS, error-prone type of DNA damage tolerance, acts to bypass DNA lesions and allows continuation of DNA replication. Surprisingly majority of archaeal species lack canonical TLS polymerases. This poses a question as to how archaea restart stalled replication in the absence of TLS or lesion repair pathways. This thesis establishes that archaeal replicative primase (PriS/L), a member of the archaeo-eukaryotic primase (AEP) superfamily, possessing both primase and polymerase activities, is able to bypass the most common oxidative damages and highly distorting lesions caused by UV radiation. It has been postulated that archaeal replicative polymerases (Pol B and Pol D family Pols) can bind tightly to the deaminated bases uracil and cause replication fork stalling four bases prior to dU. A specific mechanism for resuming replication of uracil containing DNA by PriS/L is suggested in this thesis. In this thesis, we also reported how the enzymatic activities of archaeal PriS/L are regulated. Here, it is demonstrated that in contrast to archaeal replicative polymerases, single-strand binding proteins (RPA) significantly limit the polymerase activity of PriS/L. The remaining results chapter interrogates the possible interactions between PriS/L and RPA. Finally, the attempts to reconstitute an archaeal CMG complex in vitro, with the aim of shedding light on the role of archaeal replicative primase in replication-specific TLS are described.
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Pearson, Christopher Edmund. "DNA cruciforms and mammalian origins of DNA replication." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28503.

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The objective of the research in this thesis is to investigate, at the molecular level, the sequences and/or structures involved in the initiation of mammalian DNA replication and to investigate the protein interactions with DNA cruciforms which have been implicated in the process of replication initiation. Four plasmids containing monkey (CV-1) early replicating nascent origin enriched sequences (ors), which had been shown previously to replicate autonomously in transfected CV-1, COS-7 and HeLa cells, were used in the establishment of an in vitro DNA replication system that uses HeLa cell extracts. The in vitro replication system is dependent upon the presence of an ors sequence, and HeLa cell extracts. Mapping experiments indicate that there is preferential nucleotide incorporation in the ors sequences, suggesting site-specific initiation, and that replication is bidirectional and semiconservative. Electron microscopy confirmed that in vitro initiation occurs within the ors sequence.
Prokaryotic and eukaryotic viral replication origins, mammalian origin enriched sequences (ors) and other mammalian early replicating sequences contain AT-rich sequences and inverted repeats, which have the potential to form bent and cruciform (stem-loop) DNA structures, respectively. Cruciforms have been postulated to form transiently at or near origins to serve as recognition structures for initiator proteins. Using a stable-DNA cruciform as a binding substrate in a band-shift assay, a novel DNA binding activity with specificity for the cruciform-containing DNA and no apparent sequence-specificity was identified in HeLa cell extracts. The activity is protein-dependent and is void of detectable nuclease activity. Cruciform-specific binding was observed to be maximal in early-S phase extracts. A novel cruciform binding protein (CBP) with an apparent molecular weight of 66 kDa was enriched from HeLa cell extracts. Footprinting experiments localized the CBP-DNA cruciform interaction to the four-way junction at the base of the cruciform. CBP appears to interact with the elbow junctions in an asymmetric fashion. Upon CBP binding, structural distortions were observed at the cruciform stems and at a DNA region distal to the junction.
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Schorr, Stephanie. "Replication of Bulky DNA Adducts." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-125267.

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Bennett, Ellen R. (Ellen Ruth). "Activation of papovavirus DNA replication." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=70232.

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To define the viral target sites of cellular permissive factors, simian virus 40-polyomavirus hybrid origins for DNA replication were formed by joining the auxiliary domain of one viral origin to the origin core of the other, and vice versa. The replicative capacity of these constructs were assessed in a number of mouse and monkey cell lines which express the large T antigen of polyomavirus or SV40. The results of this analysis showed that the auxiliary domains of the viral replication origins could substitute for one another in DNA replication, provided that the viral origin core and its cognate large T antigen were present in a permissive cellular milieu. Surprisingly, the large T antigens of the viruses could not substitute for one another, regardless of the species of origin of the host cell, even though the two large T antigens bind to the same sequence motif in vitro. These results suggest that species-specific permissive factors do not interact with the origin auxiliary domains but, rather, with either the origin core, large T antigen, or with both components to effect DNA replication.
To determine whether the minimal sequences that constitute a viral enhancer of gene expression are capable of activating DNA replication, a series of recombinant plasmids, composed of elements and subelements (enhansons) of the SV40 enhancer joined to the late border of the polyomavirus origin core domain, were tested for their capacity to replicate in permissive mouse cells synthesizing polyomavirus large T antigen. The results of these experiments demonstrated that a number of reiterated SV40 minimal enhancer sequences are capable of activating polyomavirus DNA replication and that mutations of elements which impair transcriptional activity also disrupt SV40 enhancer-mediated polyomavirus DNA replication. In addition, when the adenovirus E1A gene, a known repressor of gene expression, was examined for its ability to repress the replication of the plasmids described above, it repressed polyomavirus DNA replication in a sequence non-specific manner.
To determine whether activation surfaces of eukaryotic transcription factors participate in activation of DNA replication, a reporter plasmid was made bearing the binding site for a yeast transcriptional activator, GAL4, positioned near the late side of the polyomavirus origin core domain, and tested for its ability to replicate in mouse cells expressing polyomavirus large T antigen and GAL4. The results of these experiments demonstrated that binding of GAL4 next to the polyomavirus core led to enhanced replication of the reporter plasmid. This enhanced replication was dependent on a GAL4 binding site and the presence of amino acid sequences required for transcriptional activation in mammalian cells. Moreover, fusion proteins formed between the GAL4 DNA binding domain and activation surfaces of other viral transactivators also activated polyomavirus DNA replication whereas deletion mutants of fusion proteins impaired in their ability to activate transcription were poor activators of DNA replication. Together, these results implicate transcription factors as well as other components of the transcriptional machinery in DNA replication, and suggest that activation of transcription and DNA replication may occur by a common mechanism.
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Books on the topic "DNA replication"

1

Adams, R. L. P. DNA replication. Oxford [England]: IRL Press, 1991.

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Halazonetis, Thanos D. DNA Replication & DNA Replication Stress. Washington, DC, USA: American Chemical Society, 2022. http://dx.doi.org/10.1021/acsinfocus.7e5022.

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A, Baker Tania, ed. DNA replication. 2nd ed. New York: W.H. Freeman, 1992.

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L, Campbell Judith, ed. DNA replication. San Diego, Calif: Academic, 1995.

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Vengrova, Sonya, and Jacob Dalgaard, eds. DNA Replication. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2596-4.

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Vengrova, Sonya, and Jacob Z. Dalgaard, eds. DNA Replication. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-815-7.

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Masai, Hisao, and Marco Foiani, eds. DNA Replication. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6955-0.

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1941-, Kelly Thomas J., and Stillman Bruce, eds. Eukaryotic DNA replication. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 1988.

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Julian, Blow J., ed. Eukaryotic DNA replication. Oxford: IRL Press, 1996.

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Alan, Cann, ed. DNA virus replication. Oxford: Oxford University Press, 2000.

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Book chapters on the topic "DNA replication"

1

Zhang, Huidong. "DNA Replication." In DNA Replication - Damage from Environmental Carcinogens, 1–4. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7212-9_1.

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Kaguni, Jon M. "DNA Replication." In Molecular Life Sciences, 1–10. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6436-5_53-2.

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Lygerou, Zoi, K. K. Koutroumpas, and John Lygeros. "DNA Replication." In Encyclopedia of Systems Biology, 610–14. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_40.

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Gooch, Jan W. "DNA Replication." In Encyclopedic Dictionary of Polymers, 888. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13591.

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Kaguni, Jon M. "DNA Replication." In Molecular Life Sciences, 251–59. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-1531-2_53.

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McHenry, Charles S. "DNA Replication." In Emerging Targets in Antibacterial and Antifungal Chemotherapy, 37–67. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3274-3_3.

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Liu, H., J. H. Naismith, and R. T. Hay. "Adenovirus DNA Replication." In Current Topics in Microbiology and Immunology, 131–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05597-7_5.

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Adams, Roger L. P., John T. Knowler, and David P. Leader. "Replication of DNA." In The Biochemistry of the Nucleic Acids, 153–255. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2290-0_6.

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Keshav, Kylie F., and Shonen Yoshida. "Mitochondrial DNA Replication." In Mitochondrial DNA Mutations in Aging, Disease and Cancer, 101–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-12509-0_5.

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Lu, Albert, Peter J. Krell, Just M. Vlak, and George F. Rohrmann. "Baculovirus DNA Replication." In The Baculoviruses, 171–91. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1834-5_7.

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Conference papers on the topic "DNA replication"

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Brieba, Luis G., Mauricio Carbajal, Luis Manuel Montaño, Oscar Rosas-Ortiz, Sergio A. Tomas Velazquez, and Omar Miranda. "Conformational Dynamics in DNA Replication Selectivity." In Advanced Summer School in Physics 2007. AIP, 2007. http://dx.doi.org/10.1063/1.2825116.

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Manturov, Alexey O., and Anton V. Grigoryev. "Synchronization of DNA array replication kinetics." In Saratov Fall Meeting 2015, edited by Elina A. Genina, Valery V. Tuchin, Vladimir L. Derbov, Dmitry E. Postnov, Igor V. Meglinski, Kirill V. Larin, and Alexander B. Pravdin. SPIE, 2016. http://dx.doi.org/10.1117/12.2229623.

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Mindek, Peter, Tobias Klein, and Alfredo De Biasio. "DNA replication of the lagging strand." In SIGGRAPH '23 Electronic Theater: Special Interest Group on Computer Graphics and Interactive Techniques Conference: Electronic Theater. New York, NY, USA: ACM, 2023. http://dx.doi.org/10.1145/3577024.3588981.

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Obeid, Samra, Nina Blatter, and Andreas Marx. "Lost in replication: DNA polymerases encountering non-instructive DNA lesions." In XVth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2011. http://dx.doi.org/10.1135/css201112027.

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Koutroumpas, K., Z. Lygerou, and J. Lygeros. "Parameter Identification for a DNA replication model." In 2008 8th IEEE International Conference on Bioinformatics and BioEngineering (BIBE). IEEE, 2008. http://dx.doi.org/10.1109/bibe.2008.4696726.

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Brückner, L., R. Xu, A. Herrmann, and A. G. Henssen. "Replication stress associated micronucleation of extrachromosomal DNA." In 35. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2024. http://dx.doi.org/10.1055/s-0044-1786559.

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LI, JUNTAO, MAJID ESHAGHI, JIANHUA LIU, and RADHA KRISHNA MURTHY KARUTURI. "NEAR-SIGMOID MODELING TO SIMULTANEOUSLY PROFILE GENOME-WIDE DNA REPLICATION TIMING AND EFFICIENCY IN SINGLE DNA REPLICATION MICROARRAY STUDIES." In The 6th Asia-Pacific Bioinformatics Conference. PUBLISHED BY IMPERIAL COLLEGE PRESS AND DISTRIBUTED BY WORLD SCIENTIFIC PUBLISHING CO., 2007. http://dx.doi.org/10.1142/9781848161092_0039.

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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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Abstract:
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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Shih-Chung Wei, Tsung-Liang Chuang, Kung-Bin Sung, Hui-Hsin Lu, and Chii-Wann Lin. "Metallic tip enhanced fluorescence for DNA replication monitoring." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6609543.

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Koo, Seong Joo, Amaury Ernesto Fernandez-Montalvan, Simon Holton, Oliver von Ahsen, Volker Badock, Sarah Vittori, Christopher J. Ott, James E. Bradner, and Matyas Gorjanacz. "Abstract 4539: ATAD2 mediates DNA replication in cancer." 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.am2016-4539.

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Reports on the topic "DNA replication"

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Meyer, Richard. DNA Replication During Conjugal Transfer of R1162. Fort Belvoir, VA: Defense Technical Information Center, January 2002. http://dx.doi.org/10.21236/ada415172.

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Heimer, Brandon W., Kevin K. Crown, and George David Bachand. Assembling semiconductor nanocomposites using DNA replication technologies. Office of Scientific and Technical Information (OSTI), November 2005. http://dx.doi.org/10.2172/875607.

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Green, Brian M. DNA Damage and Genomic Instability Induced by Inappropriate DNA Re-Replication. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada436928.

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Green, Brian M., and Joachim J. Li. DNA Damage and Genomic Instability Induced by Inappropriate DNA Re-replication. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada467931.

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Green, Brian. DNA Damage and Genomic Instability Induced by Inappropriate DNA Re-replication. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada482750.

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Crown, Kevin K., and George David Bachand. Patterning quantum dot arrays using DNA replication principles. Office of Scientific and Technical Information (OSTI), November 2004. http://dx.doi.org/10.2172/919201.

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Lieberman, Paul. Function of BRCA1 at a DNA Replication Origin. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada429715.

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Chuang, Chen-Hua. Role of DNA Replication Defects in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada541310.

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Chuang, Chen-Hua. Role of DNA Replication Defects in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2009. http://dx.doi.org/10.21236/ada523952.

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Kuo, Shue-Ru, and Thomas Melendy. DNA Replication Arrest and DNA Damage Responses Induced by Alkylating Minor Groove Binders. Fort Belvoir, VA: Defense Technical Information Center, May 2001. http://dx.doi.org/10.21236/ada395141.

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