Database : MEDLINE
Search on : Dna and Replication [Words]
References found : 120350 [refine]
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[PMID]: 29524523
[Au] Autor:Sharma R; Sharma B; Gupta A; Dhar SK
[Ad] Address:Special Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi -110067.
[Ti] Title:Identification of a novel trafficking pathway exporting a replication protein to nucleus via classical secretory pathway in Plasmodium falciparum.
[So] Source:Biochim Biophys Acta;, 2018 Mar 07.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Malaria parasites use an extensive secretory pathway to traffic a number of proteins within itself and beyond. In higher eukaryotes, Endoplasmic Reticulum (ER) membrane bound transcription factors such as SREBP are reported to get processed en route and migrate to nucleus under the influence of specific cues. However, a protein constitutively trafficked to the nucleus via classical secretory pathway has not been reported. Herein, we report the presence of a novel trafficking pathway in an apicomplexan, Plasmodium falciparum where a homolog of an Origin Recognition Complex 2 (Orc2) goes to the nucleus following its association with the ER. Our work highlights the unconventional role of ER in protein trafficking and reports for the first time an ORC homolog getting trafficked through such a pathway to the nucleus where it may be involved in DNA replication and other ancillary functions. Such trafficking pathways may have a profound impact on the cell biology of a malaria parasite and have significant implications in strategizing new antimalarials.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 120350 MEDLINE  
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[PMID]: 29454113
[Au] Autor:Moens MAJ; Pérez-Tris J; Cortey M; Benítez L
[Ad] Address:Department of Biodiversity, Ecology and Evolution, Faculty of Biology, Complutense University of Madrid. Calle José Antonio Nováis 12, 28040 Madrid, Spain; Jocotoco Foundation, Lizardo García E9-104 y Andrés Xaura, Quito, Ecuador. Electronic address: m.moens@bio.ucm.es.
[Ti] Title:Identification of two novel CRESS DNA viruses associated with an Avipoxvirus lesion of a blue-and-gray Tanager (Thraupis episcopus).
[So] Source:Infect Genet Evol;60:89-96, 2018 Feb 14.
[Is] ISSN:1567-7257
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The discovery of circular rep-encoding single stranded (CRESS) DNA viruses has increased spectacularly over the past decade. They represent the smallest animal viruses known worldwide infecting a wide variety of invertebrates and vertebrates in different natural and human-made environments. The extremely low similarity of nucleotide and protein sequences among different CRESS DNA genomes has challenged their classification. Moreover, the existence of capsid proteins (Cp) remains difficult to demonstrate which is crucial to understand the structural properties of these viruses. Here we describe two unclassified CRESS DNA viruses isolated from a cutaneous lesion, caused by a strain of Avipoxvirus, from a blue-and-gray tanager (Thraupis episcopus) in Southern Ecuador. Both viruses present replication-associated proteins (Rep) and one to two open reading frames (ORF), one of which represents a putative Cp. The two new Rep are long proteins characterized by the existence of the several highly conserved amino acid residues characteristic of rolling circle replication. Within the putative Cp we detected intrinsically disordered regions (IDR), potential protein and DNA binding regions, and nuclear localization signals (NLS), providing further evidence of presumed Cp. Despite being found on the same host lesion, both viruses show low similarity between each other (<60%) and other known CRESS DNA viruses. Furthermore, we analyze the evolutionary relationships within the CRESS DNA diversity. Additional sampling is needed to explore the possible pathogenic effects, prevalence and diversity (both phylogenetical and structural) of these viruses in wild bird populations.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 120350 MEDLINE  
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[PMID]: 29438328
[Au] Autor:Kuss-Duerkop SK; Westrich JA; Pyeon D
[Ad] Address:Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA. Sharon.Duerkop@ucdenver.edu.
[Ti] Title:DNA Tumor Virus Regulation of Host DNA Methylation and Its Implications for Immune Evasion and Oncogenesis.
[So] Source:Viruses;10(2), 2018 Feb 13.
[Is] ISSN:1999-4915
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Viruses have evolved various mechanisms to evade host immunity and ensure efficient viral replication and persistence. Several DNA tumor viruses modulate host DNA methyltransferases for epigenetic dysregulation of immune-related gene expression in host cells. The host immune responses suppressed by virus-induced aberrant DNA methylation are also frequently involved in antitumor immune responses. Here, we describe viral mechanisms and virus-host interactions by which DNA tumor viruses regulate host DNA methylation to evade antiviral immunity, which may contribute to the generation of an immunosuppressive microenvironment during cancer development. Recent trials of immunotherapies have shown promising results to treat multiple cancers; however, a significant number of non-responders necessitate identifying additional targets for cancer immunotherapies. Thus, understanding immune evasion mechanisms of cancer-causing viruses may provide great insights for reversing immune suppression to prevent and treat associated cancers.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  4 / 120350 MEDLINE  
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[PMID]: 29523336
[Au] Autor:Ricchetti M
[Ad] Address:Institut Pasteur, Department of Developmental and Stem Cell Biology, Stem Cells and Development, 75724 Cedex15, Paris, France; Team Stability of Nuclear and Mitochondrial DNA, CNRS UMR 3738, 75724, Cedex15, Paris, France. Electronic address: mricch@pasteur.fr.
[Ti] Title:Replication stress in mitochondria.
[So] Source:Mutat Res;, 2018 Feb 01.
[Is] ISSN:1873-135X
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Mitochondrial DNA (mtDNA), which is essential for mitochondrial and cell function, is replicated and transcribed in the organelle by proteins that are entirely coded in the nucleus. Replication of mtDNA is challenged not only by threats related to the replication machinery and orchestration of DNA synthesis, but also by factors linked to the peculiarity of this genome. Indeed the architecture, organization, copy number, and location of mtDNA, which are markedly distinct from the nuclear genome, require ad hoc and complex regulation to ensure coordinated replication. As a consequence sub-optimal mtDNA replication, which results from compromised regulation of these factors, is generally associated with mitochondrial dysfunction and disease. Mitochondrial DNA replication should be considered in the context of the organelle and the whole cell, and not just a single genome or a single replication event. Major threats to mtDNA replication are linked to its dependence on both mitochondrial and nuclear factors, which require exquisite coordination of these crucial subcellular compartments. Moreover, regulation of replication events deals with a dynamic population of multiple mtDNA molecules rather than with a fixed number of genome copies, as it is the case for nuclear DNA. Importantly, the mechanistic aspects of mtDNA replication are still debated. We describe here major challenges for human mtDNA replication, the mechanistic aspects of the process that are to a large extent original, and their consequences on disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 120350 MEDLINE  
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[PMID]: 29523241
[Au] Autor:Garribba L; Wu W; Özer Ö; Bhowmick R; Hickson ID; Liu Y
[Ad] Address:Center for Chromosome Stability, University of Copenhagen, Copenhagen, Denmark.
[Ti] Title:Inducing and Detecting Mitotic DNA Synthesis at Difficult-to-Replicate Loci.
[So] Source:Methods Enzymol;601:45-58, 2018.
[Is] ISSN:1557-7988
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Our conventional understanding of the process of DNA replication is that it occurs in the S-phase of the cell division cycle. However, during investigations into the mechanism by which common fragile sites (CFSs) drive genome instability, we observed that some DNA synthesis was still occurring in early mitosis at these loci. This curious phenomenon of mitotic DNA synthesis (which we now term "MiDAS") appears to be a form of break-induced DNA replication (BIR), a DNA repair process based on homologous recombination that has been characterized in detail only in lower eukaryotes. During MiDAS, it is proposed that parts of the human genome that are not fully replicated when cells enter mitotic prophase complete their replicative cycle at that point. To date, the loci that most depend upon this process are those whose replication can be affected by oncogene-induced DNA replication stress (RS), most notably, CFSs. From our studies, it is clear that the successful completion of MiDAS at CFSs can minimize chromosome missegregation and nondisjunction. Nevertheless, it is still not clear which loci that can undergo MiDAS, whether MiDAS is associated with mutations or genome rearrangements, or whether MiDAS really is a form of BIR. In this review, we describe methods for detecting MiDAS both in prometaphase cells and directly on isolated metaphase chromosomes. In addition, we have included methods for combining MiDAS detection either with immunofluorescence (IF) detection of proteins that are recruited to the MiDAS loci, or with fluorescence in situ hybridization using probes that target specific genomic loci.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review

  6 / 120350 MEDLINE  
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[PMID]: 29523232
[Au] Autor:Elango R; Kockler Z; Liu L; Malkova A
[Ad] Address:University of Iowa, Iowa City, IA, United States.
[Ti] Title:Investigation of Break-Induced Replication in Yeast.
[So] Source:Methods Enzymol;601:161-203, 2018.
[Is] ISSN:1557-7988
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Break-induced replication (BIR) is an important mechanism aimed to repair one-ended double-strand DNA breaks. BIR is initiated by invasion of a broken DNA end into a homologous template followed by DNA synthesis that can proceed for hundreds of kilobases to the end of the chromosome. Unlike S-phase replication, BIR is carried out by a migrating DNA bubble and is associated with conservative inheritance of newly synthesized DNA. The unusual mode of DNA synthesis during BIR leads to an increased level of genetic instabilities including increased mutagenesis and chromosomal rearrangements. Here, we describe our experimental system in yeast Saccharomyces cerevisiae where BIR is initiated by a site-specific DNA break and where the repair involves two copies of chromosome III. This system allows investigation of BIR using genetic and molecular biology approaches, and can be used for characterization of the BIR mechanism, roles of individual proteins in BIR, and for the analysis of genetic instabilities associated with BIR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review

  7 / 120350 MEDLINE  
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[PMID]: 29523231
[Au] Autor:Dwivedi G; Haber JE
[Ad] Address:Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, MA, United States.
[Ti] Title:Assaying Mutations Associated With Gene Conversion Repair of a Double-Strand Break.
[So] Source:Methods Enzymol;601:145-160, 2018.
[Is] ISSN:1557-7988
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:DNA double-strand break (DSB) is a cytotoxic lesion and needs to be repaired immediately. There are several metabolic pathways evolved to repair a DSB. Gene conversion is one of the least error-prone pathway for repair of a DNA DSB. Despite this there is nearly 1000-fold increase in mutation rate associated with gene conversion. Not only higher mutation rate is associated with gene conversion but also there is a very distinct mutation profile compared to spontaneous mutation events. Gene conversion is characterized by the presence of very high frameshift mutation events and other complex mutations that are not present during regular DNA replication. Another DNA DSB repair pathway widely studied is "break-induced replication" (BIR). BIR has been shown to be highly mutagenic in nature. BIR may lead to chromosomal rearrangement and has potential to cause cluster mutations with serious disease implications. In this chapter, the design of assay systems to study various mutation types and experimental procedures to measure specific mutation frequency associated with gene conversion are discussed.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review

  8 / 120350 MEDLINE  
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[PMID]: 29523229
[Au] Autor:Jakobsen KP; Bjergbæk L
[Ad] Address:Aarhus University, Aarhus, Denmark.
[Ti] Title:Using the Flp Recombinase to Induce Site-Specific Protein-DNA Nicks.
[So] Source:Methods Enzymol;601:1-25, 2018.
[Is] ISSN:1557-7988
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A natural and frequent occurring replication insult is generated by the action of DNA Topoisomerase I (Top1). When Top1 gets trapped in a cleavage complex on the DNA, a protein-linked DNA nick (PDN) is generated. Today it is known that PDNs are generated at a high incidence in the cell. If not rapidly removed, PDNs can have a profound impact on cell destiny, as a nick in proliferating cells is passively transformed into a single-ended DSB, when encountered by the replication machinery. A DSB can in turn lead to chromosomal rearrangements and thus jeopardize genome stability if not appropriately repaired. In order to study repair pathways associated with PDNs, we have developed a cellular system (Flp-nick), where we can generate a single PDN at a specific genomic site in the model organism Saccharomyces cerevisiae. The system takes advantages of the Flp recombinase, which catalytically operates like Top1 by generating a nick in the DNA backbone and during this process becomes covalently linked to the DNA. Flp cleaves at well-defined target sites. Thus, a target site has been inserted in the genome and a mutant Flp, which cleaves but do not religate, is expressed. In this way, a single PDN mimicking the one generated by Top1 is induced at a known genomic site. The Flp-nick system allows detailed molecular analysis of repair pathways associated with this type of damage and can be designed to study repair at any genomic context.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review

  9 / 120350 MEDLINE  
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[PMID]: 29523063
[Au] Autor:Letarov AV; Kulikov EE
[Ad] Address:Winogradskii Institute of Microbiology, Biotechnology Federal Research Center, Russian Academy of Sciences, Moscow, 117312, Russia. letarov@gmail.com.
[Ti] Title:Adsorption of Bacteriophages on Bacterial Cells.
[So] Source:Biochemistry (Mosc);82(13):1632-1658, 2017 Dec.
[Is] ISSN:1608-3040
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The biological functions of bacteriophage virions come down to the solution of three basic problems: to provide protection of viral nucleic acid from the factors of extracellular environment, to recognize a host suitable for phage replication, and to provide the delivery of nucleic acid through bacterial cell envelopes. This review considers the main regularities of phage-cell interaction at the initial stages of infection of tailed bacteriophages, from the reversible binding with receptors on the surface to the beginning of phage DNA entry. Data on the structure and functions of the phage adsorption apparatus, the main quantitative characteristics of the adsorption process, and the mechanisms of adaptation of phages and their hosts to each other effective at the stage of adsorption are presented.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process
[do] DOI:10.1134/S0006297917130053

  10 / 120350 MEDLINE  
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[PMID]: 29522991
[Au] Autor:Sharma N; Chakravarthy S; Longley MJ; Copeland WC; Prakash A
[Ad] Address:University of South Alabama, Mitchell Cancer Institute, 1660 Springhill Avenue, Mobile, AL 36604, United States.
[Ti] Title:The C-terminal tail of the NEIL1 DNA glycosylase interacts with the human mitochondrial single-stranded DNA binding protein.
[So] Source:DNA Repair (Amst);65:11-19, 2018 Mar 06.
[Is] ISSN:1568-7856
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The 16.5 kb mitochondrial genome is subjected to damage from reactive oxygen species (ROS) generated in the cell during normal cellular metabolism and external sources such as ionizing radiation and ultraviolet light. ROS cause harmful damage to DNA bases that could result in mutagenesis and various diseases, if not properly repaired. The base excision repair (BER) pathway is the primary pathway involved in maintaining the integrity of mtDNA. Several enzymes that partake in BER within the nucleus have also been identified in the mitochondria. The nei-like (NEIL) DNA glycosylases initiate BER by excising oxidized pyrimidine bases and others such as the ring-opened formamidopyrimidine and the hydantoin lesions. During BER, the NEIL enzymes interact with proteins that are involved with DNA replication and transcription. In the current manuscript, we detected NEIL1 in purified mitochondrial extracts from human cells and showed that NEIL1 interacts with the human mitochondrial single-stranded DNA binding protein (mtSSB) via its C-terminal tail using protein painting, far-western analysis, and gel-filtration chromatography. Finally, we scrutinized the NEIL1-mtSSB interaction in the presence and absence of a partial-duplex DNA substrate using a combination of multi-angle light scattering (MALS) and small-angle X-ray scattering (SAXS). The data indicate that NEIL1 and homotetrameric mtSSB form a larger ternary complex in presence of DNA, however, the tetrameric form of mtSSB gets disrupted by NEIL1 in the absence of DNA as revealed by the formation of a smaller NEIL1-mtSSB complex.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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