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[PMID]:29293521
[Au] Autor:Cambridge JM; Blinkova AL; Salvador Rocha EI; Bode Hernández A; Moreno M; Ginés-Candelaria E; Goetz BM; Hunicke-Smith S; Satterwhite E; Tucker HO; Walker JR
[Ad] Endereço:Department of Molecular Biosciences and Institute for Cell and Molecular Biology, University of Texas, Austin, TX, United States of America.
[Ti] Título:Genomics of Clostridium taeniosporum, an organism which forms endospores with ribbon-like appendages.
[So] Source:PLoS One;13(1):e0189673, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Clostridium taeniosporum, a non-pathogenic anaerobe closely related to the C. botulinum Group II members, was isolated from Crimean lake silt about 60 years ago. Its endospores are surrounded by an encasement layer which forms a trunk at one spore pole to which about 12-14 large, ribbon-like appendages are attached. The genome consists of one 3,264,813 bp, circular chromosome (with 26.6% GC) and three plasmids. The chromosome contains 2,892 potential protein coding sequences: 2,124 have specific functions, 147 have general functions, 228 are conserved but without known function and 393 are hypothetical based on the fact that no statistically significant orthologs were found. The chromosome also contains 101 genes for stable RNAs, including 7 rRNA clusters. Over 84% of the protein coding sequences and 96% of the stable RNA coding regions are oriented in the same direction as replication. The three known appendage genes are located within a single cluster with five other genes, the protein products of which are closely related, in terms of sequence, to the known appendage proteins. The relatedness of the deduced protein products suggests that all or some of the closely related genes might code for minor appendage proteins or assembly factors. The appendage genes might be unique among the known clostridia; no statistically significant orthologs were found within other clostridial genomes for which sequence data are available. The C. taeniosporum chromosome contains two functional prophages, one Siphoviridae and one Myoviridae, and one defective prophage. Three plasmids of 5.9, 69.7 and 163.1 Kbp are present. These data are expected to contribute to future studies of developmental, structural and evolutionary biology and to potential industrial applications of this organism.
[Mh] Termos MeSH primário: Clostridium/genética
Genoma Bacteriano
Esporos Bacterianos
[Mh] Termos MeSH secundário: Clostridium/metabolismo
Filogenia
Prófagos/classificação
Prófagos/genética
Origem de Replicação
Selenoproteínas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Selenoproteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189673


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[PMID]:29330352
[Au] Autor:Fang D; Lengronne A; Shi D; Forey R; Skrzypczak M; Ginalski K; Yan C; Wang X; Cao Q; Pasero P; Lou H
[Ad] Endereço:State Key Laboratory of Agro-Biotechnology, Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Biological Sciences, China Agricultural University, Beijing 100193, China.
[Ti] Título:Dbf4 recruitment by forkhead transcription factors defines an upstream rate-limiting step in determining origin firing timing.
[So] Source:Genes Dev;31(23-24):2405-2415, 2017 12 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Initiation of eukaryotic chromosome replication follows a spatiotemporal program. The current model suggests that replication origins compete for a limited pool of initiation factors. However, it remains to be answered how these limiting factors are preferentially recruited to early origins. Here, we report that Dbf4 is enriched at early origins through its interaction with forkhead transcription factors Fkh1 and Fkh2. This interaction is mediated by the Dbf4 C terminus and was successfully reconstituted in vitro. An interaction-defective mutant, , phenocopies alleles in terms of origin firing. Remarkably, genome-wide replication profiles reveal that the direct fusion of the DNA-binding domain (DBD) of Fkh1 to Dbf4 restores the Fkh-dependent origin firing but interferes specifically with the pericentromeric origin activation. Furthermore, Dbf4 interacts directly with Sld3 and promotes the recruitment of downstream limiting factors. These data suggest that Fkh1 targets Dbf4 to a subset of noncentromeric origins to promote early replication in a manner that is reminiscent of the recruitment of Dbf4 to pericentromeric origins by Ctf19.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Fatores de Transcrição Forkhead/metabolismo
Origem de Replicação/fisiologia
Proteínas de Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Ciclo Celular/genética
Replicação do DNA/genética
Proteínas de Ligação a DNA/metabolismo
Genoma Fúngico/genética
Mutação
Proteínas Nucleares/metabolismo
Transporte Proteico
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/metabolismo
Origem de Replicação/genética
Proteínas de Saccharomyces cerevisiae/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CDC45 protein, S cerevisiae); 0 (Cell Cycle Proteins); 0 (DNA-Binding Proteins); 0 (Dbf4 protein, S cerevisiae); 0 (Fkh1 protein, S cerevisiae); 0 (Fkh2 protein, S cerevisiae); 0 (Forkhead Transcription Factors); 0 (Nuclear Proteins); 0 (Recombinant Fusion Proteins); 0 (Saccharomyces cerevisiae Proteins); 0 (Sld3 protein, S cerevisiae)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE
[do] DOI:10.1101/gad.306571.117


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[PMID]:29208645
[Au] Autor:Mariezcurrena A; Uhlmann F
[Ad] Endereço:Chromosome Segregation Laboratory, The Francis Crick Institute, London NW1 1AT, United Kingdom.
[Ti] Título:Observation of DNA intertwining along authentic budding yeast chromosomes.
[So] Source:Genes Dev;31(21):2151-2161, 2017 11 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA replication of circular genomes generates physically interlinked or catenated sister DNAs. These are resolved through transient DNA fracture by type II topoisomerases to permit chromosome segregation during cell division. Topoisomerase II is similarly required for linear chromosome segregation, suggesting that linear chromosomes also remain intertwined following DNA replication. Indeed, chromosome resolution defects are a frequent cause of chromosome segregation failure and consequent aneuploidies. When and where intertwines arise and persist along linear chromosomes are not known, owing to the difficulty of demonstrating intertwining of linear DNAs. Here, we used excision of chromosomal regions as circular "loop outs" to convert sister chromatid intertwines into catenated circles. This revealed intertwining at replication termination and cohesin-binding sites, where intertwines are thought to arise and persist but not to a greater extent than elsewhere in the genome. Intertwining appears to spread evenly along chromosomes but is excluded from heterochromatin. We found that intertwines arise before replication termination, suggesting that replication forks rotate during replication elongation to dissipate torsion ahead of the forks. Our approach provides previously inaccessible insight into the topology of eukaryotic chromosomes and illuminates a process critical for successful chromosome segregation.
[Mh] Termos MeSH primário: Cromossomos Fúngicos/metabolismo
Replicação do DNA
DNA Fúngico/metabolismo
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Ciclo Celular/metabolismo
Proteínas Cromossômicas não Histona/metabolismo
Segregação de Cromossomos
Estruturas Genéticas
Genoma Fúngico
Heterocromatina/metabolismo
Origem de Replicação/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Chromosomal Proteins, Non-Histone); 0 (DNA, Fungal); 0 (Heterochromatin); 0 (cohesins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1101/gad.305557.117


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[PMID]:28911105
[Au] Autor:Taylor JA; Panis G; Viollier PH; Marczynski GT
[Ad] Endereço:Department of Microbiology and Immunology, McGill University, 3775 University St., Montreal, QC H3A 2B4, Canada.
[Ti] Título:A novel nucleoid-associated protein coordinates chromosome replication and chromosome partition.
[So] Source:Nucleic Acids Res;45(15):8916-8929, 2017 Sep 06.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We searched for regulators of chromosome replication in the cell cycle model Caulobacter crescentus and found a novel DNA-binding protein (GapR) that selectively aids the initiation of chromosome replication and the initial steps of chromosome partitioning. The protein binds the chromosome origin of replication (Cori) and has higher-affinity binding to mutated Cori-DNA that increases Cori-plasmid replication in vivo. gapR gene expression is essential for normal rapid growth and sufficient GapR levels are required for the correct timing of chromosome replication. Whole genome ChIP-seq identified dynamic DNA-binding distributions for GapR, with the strongest associations at the partitioning (parABS) locus near Cori. Using molecular-genetic and fluorescence microscopy experiments, we showed that GapR also promotes the first steps of chromosome partitioning, the initial separation of the duplicated parS loci following replication from Cori. This separation occurs before the parABS-dependent partitioning phase. Therefore, this early separation, whose mechanisms is not known, coincides with the poorly defined mechanism(s) that establishes chromosome asymmetry: C. crescentus chromosomes are partitioned to distinct cell-poles which develop into replicating and non-replicating cell-types. We propose that GapR coordinates chromosome replication with asymmetry-establishing chromosome separation, noting that both roles are consistent with the phylogenetic restriction of GapR to asymmetrically dividing bacteria.
[Mh] Termos MeSH primário: Proteínas de Bactérias/genética
Caulobacter crescentus/genética
Segregação de Cromossomos
Cromossomos Bacterianos/metabolismo
Replicação do DNA
Proteínas de Ligação a DNA/genética
[Mh] Termos MeSH secundário: Proteínas de Bactérias/metabolismo
Caulobacter crescentus/efeitos dos fármacos
Caulobacter crescentus/metabolismo
Divisão Celular/efeitos dos fármacos
Cromossomos Bacterianos/ultraestrutura
Proteínas de Ligação a DNA/metabolismo
Regulação Bacteriana da Expressão Gênica
Mutação
Novobiocina/farmacologia
Plasmídeos/química
Plasmídeos/metabolismo
Origem de Replicação
Rifampina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (DNA-Binding Proteins); 17EC19951N (Novobiocin); VJT6J7R4TR (Rifampin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx596


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[PMID]:28886337
[Au] Autor:Vujanovic M; Krietsch J; Raso MC; Terraneo N; Zellweger R; Schmid JA; Taglialatela A; Huang JW; Holland CL; Zwicky K; Herrador R; Jacobs H; Cortez D; Ciccia A; Penengo L; Lopes M
[Ad] Endereço:Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland.
[Ti] Título:Replication Fork Slowing and Reversal upon DNA Damage Require PCNA Polyubiquitination and ZRANB3 DNA Translocase Activity.
[So] Source:Mol Cell;67(5):882-890.e5, 2017 Sep 07.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA damage tolerance during eukaryotic replication is orchestrated by PCNA ubiquitination. While monoubiquitination activates mutagenic translesion synthesis, polyubiquitination activates an error-free pathway, elusive in mammals, enabling damage bypass by template switching. Fork reversal is driven in vitro by multiple enzymes, including the DNA translocase ZRANB3, shown to bind polyubiquitinated PCNA. However, whether this interaction promotes fork remodeling and template switching in vivo was unknown. Here we show that damage-induced fork reversal in mammalian cells requires PCNA ubiquitination, UBC13, and K63-linked polyubiquitin chains, previously involved in error-free damage tolerance. Fork reversal in vivo also requires ZRANB3 translocase activity and its interaction with polyubiquitinated PCNA, pinpointing ZRANB3 as a key effector of error-free DNA damage tolerance. Mutations affecting fork reversal also induced unrestrained fork progression and chromosomal breakage, suggesting fork remodeling as a global fork slowing and protection mechanism. Targeting these fork protection systems represents a promising strategy to potentiate cancer chemotherapy.
[Mh] Termos MeSH primário: Dano ao DNA
DNA Helicases/metabolismo
Replicação do DNA
DNA de Neoplasias/biossíntese
Neoplasias/enzimologia
Poliubiquitina/metabolismo
Antígeno Nuclear de Célula em Proliferação/metabolismo
Origem de Replicação
[Mh] Termos MeSH secundário: Animais
Sistemas CRISPR-Cas
DNA Helicases/genética
DNA de Neoplasias/genética
DNA de Neoplasias/ultraestrutura
Células HCT116
Células HEK293
Seres Humanos
Cinética
Camundongos
Mutação
Neoplasias/genética
Neoplasias/ultraestrutura
Antígeno Nuclear de Célula em Proliferação/genética
Interferência de RNA
Transfecção
Enzimas de Conjugação de Ubiquitina/genética
Enzimas de Conjugação de Ubiquitina/metabolismo
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Neoplasm); 0 (Proliferating Cell Nuclear Antigen); 120904-94-1 (Polyubiquitin); EC 2.3.2.23 (UBE2N protein, human); EC 2.3.2.23 (Ubiquitin-Conjugating Enzymes); EC 3.6.4.- (DNA Helicases); EC 3.6.4.- (ZRANB3 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


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[PMID]:28854733
[Au] Autor:Zhang Q; Bassetti F; Gherardi M; Lagomarsino MC
[Ad] Endereço:Sorbonne Universités, UPMC Univ Paris 06, UMR 7238, Computational and Quantitative Biology, 4 Place Jussieu, Paris, France.
[Ti] Título:Cell-to-cell variability and robustness in S-phase duration from genome replication kinetics.
[So] Source:Nucleic Acids Res;45(14):8190-8198, 2017 Aug 21.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Genome replication, a key process for a cell, relies on stochastic initiation by replication origins, causing a variability of replication timing from cell to cell. While stochastic models of eukaryotic replication are widely available, the link between the key parameters and overall replication timing has not been addressed systematically. We use a combined analytical and computational approach to calculate how positions and strength of many origins lead to a given cell-to-cell variability of total duration of the replication of a large region, a chromosome or the entire genome. Specifically, the total replication timing can be framed as an extreme-value problem, since it is due to the last region that replicates in each cell. Our calculations identify two regimes based on the spread between characteristic completion times of all inter-origin regions of a genome. For widely different completion times, timing is set by the single specific region that is typically the last to replicate in all cells. Conversely, when the completion time of all regions are comparable, an extreme-value estimate shows that the cell-to-cell variability of genome replication timing has universal properties. Comparison with available data shows that the replication program of three yeast species falls in this extreme-value regime.
[Mh] Termos MeSH primário: Algoritmos
Período de Replicação do DNA/genética
Genoma/genética
Modelos Genéticos
Origem de Replicação/genética
Fase S/genética
[Mh] Termos MeSH secundário: Cromossomos Fúngicos/genética
Biologia Computacional/métodos
Cinética
Saccharomyces cerevisiae/citologia
Saccharomyces cerevisiae/genética
Saccharomycetales/citologia
Saccharomycetales/genética
Schizosaccharomyces/citologia
Schizosaccharomyces/genética
Especificidade da Espécie
Processos Estocásticos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx556


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[PMID]:28781123
[Au] Autor:Gardner NJ; Gillespie PJ; Carrington JT; Shanks EJ; McElroy SP; Haagensen EJ; Frearson JA; Woodland A; Blow JJ
[Ad] Endereço:Centre for Gene Regulation & Expression, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
[Ti] Título:The High-Affinity Interaction between ORC and DNA that Is Required for Replication Licensing Is Inhibited by 2-Arylquinolin-4-Amines.
[So] Source:Cell Chem Biol;24(8):981-992.e4, 2017 Aug 17.
[Is] ISSN:2451-9456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In late mitosis and G , origins of DNA replication must be "licensed" for use in the upcoming S phase by being encircled by double hexamers of the minichromosome maintenance proteins MCM2-7. A "licensing checkpoint" delays cells in G until sufficient origins have been licensed, but this checkpoint is lost in cancer cells. Inhibition of licensing can therefore kill cancer cells while only delaying normal cells in G . In a high-throughput cell-based screen for licensing inhibitors we identified a family of 2-arylquinolin-4-amines, the most potent of which we call RL5a. The binding of the origin recognition complex (ORC) to origin DNA is the first step of the licensing reaction. We show that RL5a prevents ORC forming a tight complex with DNA that is required for MCM2-7 loading. Formation of this ORC-DNA complex requires ATP, and we show that RL5a inhibits ORC allosterically to mimic a lack of ATP.
[Mh] Termos MeSH primário: Aminas/farmacologia
Replicação do DNA/efeitos dos fármacos
DNA/metabolismo
Complexo de Reconhecimento de Origem/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Regulação Alostérica
Aminas/química
Aminas/metabolismo
Animais
Proteínas de Ciclo Celular/antagonistas & inibidores
Proteínas de Ciclo Celular/química
Proteínas de Ciclo Celular/metabolismo
Linhagem Celular Tumoral
Cromatina/química
Cromatina/metabolismo
Seres Humanos
Proteínas de Manutenção de Minicromossomo/química
Proteínas de Manutenção de Minicromossomo/metabolismo
Proteínas Nucleares/química
Proteínas Nucleares/metabolismo
Complexo de Reconhecimento de Origem/antagonistas & inibidores
Quinolinas/farmacologia
Origem de Replicação/genética
Tiazóis/farmacologia
Xenopus
Proteínas de Xenopus/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amines); 0 (CDC6 protein, human); 0 (CDT1 protein, human); 0 (Cell Cycle Proteins); 0 (Chromatin); 0 (Nuclear Proteins); 0 (Origin Recognition Complex); 0 (Quinolines); 0 (RO 3306); 0 (Thiazoles); 0 (Xenopus Proteins); 8L70Q75FXE (Adenosine Triphosphate); 9007-49-2 (DNA); EC 3.6.4.12 (Minichromosome Maintenance Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE


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[PMID]:28757209
[Au] Autor:Kolinjivadi AM; Sannino V; De Antoni A; Zadorozhny K; Kilkenny M; Técher H; Baldi G; Shen R; Ciccia A; Pellegrini L; Krejci L; Costanzo V
[Ad] Endereço:DNA Metabolism Laboratory, IFOM, FIRC Institute for Molecular Oncology, 20139 Milan, Italy.
[Ti] Título:Smarcal1-Mediated Fork Reversal Triggers Mre11-Dependent Degradation of Nascent DNA in the Absence of Brca2 and Stable Rad51 Nucleofilaments.
[So] Source:Mol Cell;67(5):867-881.e7, 2017 Sep 07.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brca2 deficiency causes Mre11-dependent degradation of nascent DNA at stalled forks, leading to cell lethality. To understand the molecular mechanisms underlying this process, we isolated Xenopus laevis Brca2. We demonstrated that Brca2 protein prevents single-stranded DNA gap accumulation at replication fork junctions and behind them by promoting Rad51 binding to replicating DNA. Without Brca2, forks with persistent gaps are converted by Smarcal1 into reversed forks, triggering extensive Mre11-dependent nascent DNA degradation. Stable Rad51 nucleofilaments, but not RPA or Rad51 mutant proteins, directly prevent Mre11-dependent DNA degradation. Mre11 inhibition instead promotes reversed fork accumulation in the absence of Brca2. Rad51 directly interacts with the Pol α N-terminal domain, promoting Pol α and δ binding to stalled replication forks. This interaction likely promotes replication fork restart and gap avoidance. These results indicate that Brca2 and Rad51 prevent formation of abnormal DNA replication intermediates, whose processing by Smarcal1 and Mre11 predisposes to genome instability.
[Mh] Termos MeSH primário: Proteína BRCA2/metabolismo
Replicação do DNA
DNA/biossíntese
Rad51 Recombinase/metabolismo
Proteínas de Xenopus/metabolismo
Xenopus laevis/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína BRCA2/genética
Sítios de Ligação
DNA/genética
DNA Helicases/genética
DNA Helicases/metabolismo
DNA Polimerase I/metabolismo
DNA Polimerase III/metabolismo
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Endodesoxirribonucleases/genética
Endodesoxirribonucleases/metabolismo
Exodesoxirribonucleases/genética
Exodesoxirribonucleases/metabolismo
Feminino
Instabilidade Genômica
Seres Humanos
Proteína Homóloga a MRE11
Masculino
Mutação
Ligação Proteica
Rad51 Recombinase/genética
Origem de Replicação
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
Fatores de Tempo
Proteínas de Xenopus/genética
Xenopus laevis/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BRCA2 Protein); 0 (DNA-Binding Proteins); 0 (MRE11A protein, human); 0 (Saccharomyces cerevisiae Proteins); 0 (Xenopus Proteins); 9007-49-2 (DNA); EC 2.7.7.- (DNA Polymerase I); EC 2.7.7.- (DNA Polymerase III); EC 2.7.7.- (RAD51 protein, Xenopus); EC 2.7.7.- (RAD51 protein, human); EC 2.7.7.- (Rad51 Recombinase); EC 2.7.7.- (SMARCAL1 protein, human); EC 3.1.- (Endodeoxyribonucleases); EC 3.1.- (Exodeoxyribonucleases); EC 3.1.- (MRE11 Homologue Protein); EC 3.1.- (MRE11 protein, S cerevisiae); EC 3.6.4.- (DNA Helicases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE


  9 / 3376 MEDLINE  
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[PMID]:28735897
[Au] Autor:Dungrawala H; Bhat KP; Le Meur R; Chazin WJ; Ding X; Sharan SK; Wessel SR; Sathe AA; Zhao R; Cortez D
[Ad] Endereço:Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN, USA.
[Ti] Título:RADX Promotes Genome Stability and Modulates Chemosensitivity by Regulating RAD51 at Replication Forks.
[So] Source:Mol Cell;67(3):374-386.e5, 2017 Aug 03.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RAD51 promotes homology-directed repair (HDR), replication fork reversal, and stalled fork protection. Defects in these functions cause genomic instability and tumorigenesis but also generate hypersensitivity to cancer therapeutics. Here we describe the identification of RADX as an RPA-like, single-strand DNA binding protein. RADX is recruited to replication forks, where it prevents fork collapse by regulating RAD51. When RADX is inactivated, excessive RAD51 activity slows replication elongation and causes double-strand breaks. In cancer cells lacking BRCA2, RADX deletion restores fork protection without restoring HDR. Furthermore, RADX inactivation confers chemotherapy and PARP inhibitor resistance to cancer cells with reduced BRCA2/RAD51 pathway function. By antagonizing RAD51 at forks, RADX allows cells to maintain a high capacity for HDR while ensuring that replication functions of RAD51 are properly regulated. Thus, RADX is essential to achieve the proper balance of RAD51 activity to maintain genome stability.
[Mh] Termos MeSH primário: DNA de Neoplasias/biossíntese
Resistência a Medicamentos Antineoplásicos
Instabilidade Genômica
Neoplasias/tratamento farmacológico
Inibidores de Poli(ADP-Ribose) Polimerases/farmacologia
Rad51 Recombinase/metabolismo
Origem de Replicação
[Mh] Termos MeSH secundário: Células A549
Animais
Proteína BRCA2/genética
Proteína BRCA2/metabolismo
Sistemas CRISPR-Cas
Quebras de DNA de Cadeia Dupla
Reparo do DNA
DNA de Neoplasias/química
DNA de Neoplasias/genética
Relação Dose-Resposta a Droga
Resistência a Medicamentos Antineoplásicos/genética
Regulação Neoplásica da Expressão Gênica
Células HEK293
Seres Humanos
Camundongos
Modelos Moleculares
Mutação
Neoplasias/enzimologia
Neoplasias/genética
Neoplasias/patologia
Ligação Proteica
Interferência de RNA
Rad51 Recombinase/genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BRCA2 Protein); 0 (BRCA2 protein, human); 0 (DNA, Neoplasm); 0 (Poly(ADP-ribose) Polymerase Inhibitors); EC 2.7.7.- (RAD51 protein, human); EC 2.7.7.- (Rad51 Recombinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE


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[PMID]:28717046
[Au] Autor:Riera A; Barbon M; Noguchi Y; Reuter LM; Schneider S; Speck C
[Ad] Endereço:DNA Replication Group, Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, London W12 0NN, United Kingdom.
[Ti] Título:From structure to mechanism-understanding initiation of DNA replication.
[So] Source:Genes Dev;31(11):1073-1088, 2017 Jun 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA replication results in the doubling of the genome prior to cell division. This process requires the assembly of 50 or more protein factors into a replication fork. Here, we review recent structural and biochemical insights that start to explain how specific proteins recognize DNA replication origins, load the replicative helicase on DNA, unwind DNA, synthesize new DNA strands, and reassemble chromatin. We focus on the minichromosome maintenance (MCM2-7) proteins, which form the core of the eukaryotic replication fork, as this complex undergoes major structural rearrangements in order to engage with DNA, regulate its DNA-unwinding activity, and maintain genome stability.
[Mh] Termos MeSH primário: Replicação do DNA/fisiologia
[Mh] Termos MeSH secundário: Animais
Cromatina/metabolismo
DNA Helicases/metabolismo
Replicação do DNA/genética
Evolução Molecular
Instabilidade Genômica/genética
Seres Humanos
Proteínas de Manutenção de Minicromossomo/genética
Proteínas de Manutenção de Minicromossomo/metabolismo
Origem de Replicação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chromatin); EC 3.6.4.- (DNA Helicases); EC 3.6.4.12 (Minichromosome Maintenance Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1101/gad.298232.117



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