Base de dados : MEDLINE
Pesquisa : D08.811.399.403 [Categoria DeCS]
Referências encontradas : 322 [refinar]
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[PMID]:28973473
[Au] Autor:Benedetti F; Racko D; Dorier J; Burnier Y; Stasiak A
[Ad] Endereço:Center for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland.
[Ti] Título:Transcription-induced supercoiling explains formation of self-interacting chromatin domains in S. pombe.
[So] Source:Nucleic Acids Res;45(17):9850-9859, 2017 Sep 29.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The question of how self-interacting chromatin domains in interphase chromosomes are structured and generated dominates current discussions on eukaryotic chromosomes. Numerical simulations using standard polymer models have been helpful in testing the validity of various models of chromosome organization. Experimental contact maps can be compared with simulated contact maps and thus verify how good is the model. With increasing resolution of experimental contact maps, it became apparent though that active processes need to be introduced into models to recapitulate the experimental data. Since transcribing RNA polymerases are very strong molecular motors that induce axial rotation of transcribed DNA, we present here models that include such rotational motors. We also include into our models swivels and sites for intersegmental passages that account for action of DNA topoisomerases releasing torsional stress. Using these elements in our models, we show that transcription-induced supercoiling generated in the regions with divergent-transcription and supercoiling relaxation occurring between these regions are sufficient to explain formation of self-interacting chromatin domains in chromosomes of fission yeast (S. pombe).
[Mh] Termos MeSH primário: DNA Topoisomerases/química
DNA Fúngico/química
DNA Super-Helicoidal/química
RNA Polimerases Dirigidas por DNA/química
Schizosaccharomyces/genética
Transcrição Genética
[Mh] Termos MeSH secundário: Fenômenos Biomecânicos
Cromatina/química
Cromatina/metabolismo
Cromossomos Fúngicos/química
Cromossomos Fúngicos/metabolismo
DNA Topoisomerases/genética
DNA Topoisomerases/metabolismo
DNA Fúngico/genética
DNA Fúngico/metabolismo
DNA Super-Helicoidal/genética
DNA Super-Helicoidal/metabolismo
RNA Polimerases Dirigidas por DNA/genética
RNA Polimerases Dirigidas por DNA/metabolismo
Regulação Fúngica da Expressão Gênica
Simulação de Dinâmica Molecular
Rotação
Schizosaccharomyces/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (DNA, Fungal); 0 (DNA, Superhelical); EC 2.7.7.6 (DNA-Directed RNA Polymerases); EC 5.99.1.- (DNA Topoisomerases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx716


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[PMID]:28763648
[Au] Autor:Yuan Z; Chen S; Chen C; Chen J; Chen C; Dai Q; Gao C; Jiang Y
[Ad] Endereço:Department of Chemistry, Tsinghua University, Beijing, 100084, PR China; The Ministry-Province Jointly Constructed Base for State Key Lab-Shenzhen Key Laboratory of Chemical Biology, The Graduate School at Shenzhen, Tsinghua University, Shenzhen, 518055, PR China.
[Ti] Título:Design, synthesis and biological evaluation of 4-amidobenzimidazole acridine derivatives as dual PARP and Topo inhibitors for cancer therapy.
[So] Source:Eur J Med Chem;138:1135-1146, 2017 Sep 29.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:PARP-1 could repair the DNA damages induced by Topo inhibitors, therefore inhibiting Topo and PARP-1 simultaneously might be able to overcome resistance and improve outcomes. In this study a series of 4-amidobenzimidazole acridines were designed and synthesized as dual Topo and PARP-1 inhibitors. Compound 11l displayed good inhibitory activities against Topo and PARP-1, as well as significantly inhibited cancer cells proliferation. Further mechanistic evaluations indicated that 11l treatment in MCF-7 cells induced accumulated DNA double-strand breaks, prompted remarkable apoptosis, and caused prominent G0/G1 cell cycle arrest. Moreover, 11l greatly suppressed tumor growth in mice, and displayed favorable metabolic properties in liver microsomes. Our study suggested that single agents inhibiting Topo and PARP concurrently might be an alternative for cancer therapy and 11l represented a potential lead compound for development of antitumor agents.
[Mh] Termos MeSH primário: Acridinas/farmacologia
Antineoplásicos/farmacologia
DNA Topoisomerases/metabolismo
Desenho de Drogas
Poli(ADP-Ribose) Polimerase-1/antagonistas & inibidores
Inibidores de Poli(ADP-Ribose) Polimerases/farmacologia
Inibidores da Topoisomerase/farmacologia
[Mh] Termos MeSH secundário: Acridinas/síntese química
Acridinas/química
Antineoplásicos/síntese química
Antineoplásicos/química
Apoptose/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Estrutura Molecular
Poli(ADP-Ribose) Polimerase-1/metabolismo
Inibidores de Poli(ADP-Ribose) Polimerases/síntese química
Inibidores de Poli(ADP-Ribose) Polimerases/química
Relação Estrutura-Atividade
Inibidores da Topoisomerase/síntese química
Inibidores da Topoisomerase/química
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acridines); 0 (Antineoplastic Agents); 0 (Poly(ADP-ribose) Polymerase Inhibitors); 0 (Topoisomerase Inhibitors); EC 2.4.2.30 (PARP1 protein, human); EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1); EC 5.99.1.- (DNA Topoisomerases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE


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[PMID]:28528358
[Au] Autor:Cuya SM; Bjornsti MA; van Waardenburg RCAM
[Ad] Endereço:Department of Pharmacology and Toxicology, University of Alabama at Birmingham, 155 Volker Hall, 1720 2nd Ave. S., Birmingham, AL, 35294-0019, USA.
[Ti] Título:DNA topoisomerase-targeting chemotherapeutics: what's new?
[So] Source:Cancer Chemother Pharmacol;80(1):1-14, 2017 Jul.
[Is] ISSN:1432-0843
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:To resolve the topological problems that threaten the function and structural integrity of nuclear and mitochondrial genomes and RNA molecules, human cells encode six different DNA topoisomerases including type IB enzymes (TOP1 and TOP1mt), type IIA enzymes (TOP2α and TOP2ß) and type IA enzymes (TOP3α and TOP3ß). DNA entanglements and the supercoiling of DNA molecules are regulated by topoisomerases through the introduction of transient enzyme-linked DNA breaks. The covalent topoisomerase-DNA complexes are the cellular targets of a diverse group of cancer chemotherapeutics, which reversibly stabilize these reaction intermediates. Here we review the structure-function and catalytic mechanisms of each family of eukaryotic DNA topoisomerases and the topoisomerase-targeting agents currently approved for patient therapy or in clinical trials, and highlight novel developments and challenges in the clinical development of these agents.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
DNA Topoisomerases/metabolismo
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Quebras de DNA
Desenho de Drogas
Seres Humanos
Mitocôndrias/enzimologia
Mitocôndrias/genética
Terapia de Alvo Molecular
Neoplasias/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); EC 5.99.1.- (DNA Topoisomerases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170522
[St] Status:MEDLINE
[do] DOI:10.1007/s00280-017-3334-5


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[PMID]:28355294
[Au] Autor:Hou GX; Liu P; Yang J; Wen S
[Ad] Endereço:Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in Southern China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
[Ti] Título:Mining expression and prognosis of topoisomerase isoforms in non-small-cell lung cancer by using Oncomine and Kaplan-Meier plotter.
[So] Source:PLoS One;12(3):e0174515, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA topoisomerases are essential to modulate DNA topology during various cellular genetic processes. The expression and distinct prognostic value of topoisomerase isoforms in non-small-cell lung cancer (NSCLC) is not well established. In the current study, we have examined the mRNA expression of topoisomerase isoforms by using Oncomine analysis and investigated their prognostic value via the Kaplan-Meier plotter database in NSCLC patients. Our analysis indicated that the expression level of topoisomerases in lung cancer was higher compared with normal tissues. Especially, high expression of two topoisomerase isoforms, TOP2A and TOP3A, was found to be correlated to worse overall survival (OS) in all NSCLC and lung adenocarcinoma (Ade) patients, but not in lung squamous cell carcinoma (SCC) patients. In a contrast, high expression of isoforms TOP1 and TOP2B indicated better OS in all NSCLC and Ade, but not in SCC patients. Meanwhile, high expression of TOP1MT and TOP3B was not correlated with OS in NSCLC patients. Furthermore, we also demonstrated a relationship between topoisomerase isoforms and the clinicopathological features for the NSCLC patients, such as grades, clinical stages, lymph node status, smoking status, gender, chemotherapy and radiotherapy. These results support that TOP2A and TOP3A are associated with worse prognosis in NSCLC patients. In addition, our study also shows that TOP1 and TOP2B contribute to favorable prognosis in NSCLC patients. The exact prognostic significance of TOP1MT and TOP3B need to be further elucidated. Comprehensive evaluation of expression and prognosis of topoisomerase isoforms will be a benefit for the better understanding of heterogeneity and complexity in the molecular biology of NSCLC, paving a way for more accurate prediction of prognosis and discovery of potential drug targets for NSCLC patients.
[Mh] Termos MeSH primário: Adenocarcinoma/enzimologia
Biomarcadores Tumorais/metabolismo
Carcinoma de Células Escamosas/enzimologia
DNA Topoisomerases/metabolismo
Neoplasias Pulmonares/enzimologia
[Mh] Termos MeSH secundário: Adenocarcinoma/diagnóstico
Adenocarcinoma/mortalidade
Biomarcadores Tumorais/genética
Carcinoma de Células Escamosas/diagnóstico
Carcinoma de Células Escamosas/mortalidade
DNA Topoisomerases/genética
Mineração de Dados
Bases de Dados de Ácidos Nucleicos
Expressão Gênica
Perfilação da Expressão Gênica
Seres Humanos
Estimativa de Kaplan-Meier
Neoplasias Pulmonares/diagnóstico
Neoplasias Pulmonares/mortalidade
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 5.99.1.- (DNA Topoisomerases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174515


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[PMID]:28345463
[Au] Autor:James AR; Unnikrishnan BS; Priya R; Joseph MM; Manojkumar TK; Raveendran Pillai K; Shiji R; Preethi GU; Kusumakumary P; Sreelekha TT
[Ad] Endereço:1 Laboratory of Biopharmaceuticals and Nanomedicine, Division of Cancer Research, Regional Cancer Centre (RCC), Thiruvananthapuram, India.
[Ti] Título:Computational and mechanistic studies on the effect of galactoxyloglucan: Imatinib nanoconjugate in imatinib resistant K562 cells.
[So] Source:Tumour Biol;39(3):1010428317695946, 2017 Mar.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Imatinib mesylate, a BCR/ABL fusion protein inhibitor, is the first-line treatment against chronic myelogenous leukemia. In spite of its advantageous viewpoints, imatinib still has genuine impediments like undesirable side effects and tumor resistance during chemotherapy. Nanoparticles with sustainable release profile will help in targeted delivery of anticancer drugs while minimizing deleterious side effects and drug resistance. The use of biopolymers like galactoxyloglucan (PST001) for the fabrication of imatinib mesylate nanoparticles could impart its use in overcoming multidrug resistance in chronic myelogenous leukemia patients with minimal side effects. This study involved in the synthesis of PST-Imatinib nanoconjugates with appreciable drug payload and excellent cytotoxicity against drug-resistant chronic myelogenous leukemia cell line (K562) in comparison with free drug. The use of bioinformatics tool revealed better binding affinity for the drug-polysaccharide complex than the drug alone with three proteins: 3QX3 (Topoisomerase), 1M17 (EGFR tyrosine kinase domain), and 3QRJ (ABL1 kinase domain). Assessment of the biochemical, hematological, and histopathological parameters in mice upheld the security and adequacy of the nanoconjugate compared to free drug. Although perspective investigations are warranted, in a condition like drug resistance in leukemia, this nanoconjugate would display a productive approach in cancer therapeutics.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Preparações de Ação Retardada/uso terapêutico
Glucanos/uso terapêutico
Mesilato de Imatinib/uso terapêutico
Leucemia Mielogênica Crônica BCR-ABL Positiva/tratamento farmacológico
Nanoconjugados/uso terapêutico
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
DNA Topoisomerases/genética
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Seres Humanos
Células K562
Proteínas Tirosina Quinases/genética
Receptor do Fator de Crescimento Epidérmico/genética
Proteínas Recombinantes de Fusão/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Delayed-Action Preparations); 0 (Glucans); 0 (Nanoconjugates); 0 (Recombinant Fusion Proteins); 8A1O1M485B (Imatinib Mesylate); EC 2.7.10.1 (EGFR protein, mouse); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 5.99.1.- (DNA Topoisomerases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170407
[Lr] Data última revisão:
170407
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317695946


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[PMID]:28283390
[Au] Autor:Gao C; Qi S; Liu K; Li D; Jin C; Duan S; Zhang M; Chen M
[Ad] Endereço:College of Agronomy, Northwest A&F University, Yangling, Shaanxi 712100, China.
[Ti] Título:Functional characterization of Brassica napus DNA topoisomerase Iα-1 and its effect on flowering time when expressed in Arabidopsis thaliana.
[So] Source:Biochem Biophys Res Commun;486(1):124-129, 2017 Apr 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies have shown that DNA topoisomerase Iα (AtTOP1α) has specific developmental functions during growth and development in Arabidopsis thaliana. However, little is known about the roles of DNA topoisomerases in the closely related and commercially important plant, rapeseed (Brassica napus). Here, the full-length BnTOP1α-1 coding sequence was cloned from the A2 subgenome of the Brassica napus inbred line L111. We determine that all BnTOP1α paralogs showed differing patterns of expression in different organs of L111, and that when expressed in tobacco leaves as a fusion protein with green fluorescent protein, BnTOP1α-1 localized to the nucleus. We further showed that ectopic expression of BnTOP1α-1 in the A. thaliana top1α-7 mutant fully complemented the early flowering phenotype of the mutant. Moreover, altered expression levels in top1α-7 seedlings of several key genes controlling flowering time were restored to wild type levels by ectopic expression of BnTOP1α-1. These results provide valuable insights into the roles of rapeseed DNA topoisomerases in flowering time, and provide a promising target for genetic manipulation of this commercially significant process in rapeseed.
[Mh] Termos MeSH primário: Arabidopsis/genética
Brassica napus/genética
DNA Topoisomerases/genética
Flores/genética
Proteínas de Plantas/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Arabidopsis/enzimologia
Brassica napus/enzimologia
Núcleo Celular/enzimologia
Núcleo Celular/genética
DNA Topoisomerases/metabolismo
Flores/metabolismo
Perfilação da Expressão Gênica
Regulação Enzimológica da Expressão Gênica
Regulação da Expressão Gênica de Plantas
Teste de Complementação Genética
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Microscopia Confocal
Mutação
Folhas de Planta/enzimologia
Folhas de Planta/genética
Proteínas de Plantas/metabolismo
Plantas Geneticamente Modificadas
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Homologia de Sequência de Aminoácidos
Fatores de Tempo
Tabaco/enzimologia
Tabaco/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant Proteins); 147336-22-9 (Green Fluorescent Proteins); EC 5.99.1.- (DNA Topoisomerases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170312
[St] Status:MEDLINE


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[PMID]:28120712
[Au] Autor:Müller S
[Ad] Endereço:Institut Curie, PSL Research University, Organic Synthesis and Cell Biology Group, CNRS UMR3666, INSERM U1143, 26 rue d'Ulm, 75248 Paris Cedex 05. France.
[Ti] Título:DNA Damage-inducing Compounds: Unraveling their Pleiotropic Effects Using High Throughput Sequencing.
[So] Source:Curr Med Chem;24(15):1558-1585, 2017.
[Is] ISSN:1875-533X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Compounds causing DNA damage have been used widely in molecular biology and some are used as therapeutic agents in cancer therapy. In most cases, their cellular response is pleiotropic, making it challenging to develop these agents efficiently for potential therapeutic use. Furthermore, this means that such compounds can also affect healthy tissues, which is a major drawback for the use in therapy. Thus, dissecting and understanding not only their molecular mode of action, but also identifying all their cellular targets is critical. With the advent of high throughput DNA sequencing technologies our understanding of the genomic targets of such compounds has increased significantly over recent years. This review gives an overview of some well-studied DNA-damaging agents and dissects what is known about their molecular mode of action, their cellular response and use in clinical settings. It then describes how high throughput-sequencing approaches can be used (a) to study DNAdamaging compounds and (b) to gain insight into their biological activity in vivo.
[Mh] Termos MeSH primário: Antineoplásicos/toxicidade
Dano ao DNA
[Mh] Termos MeSH secundário: Alquilantes/uso terapêutico
Alquilantes/toxicidade
Antineoplásicos/uso terapêutico
Dano ao DNA/efeitos dos fármacos
Reparo do DNA
DNA Topoisomerases/química
DNA Topoisomerases/metabolismo
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Neoplasias/tratamento farmacológico
Neoplasias/patologia
Bibliotecas de Moléculas Pequenas/química
Bibliotecas de Moléculas Pequenas/uso terapêutico
Bibliotecas de Moléculas Pequenas/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alkylating Agents); 0 (Antineoplastic Agents); 0 (Small Molecule Libraries); EC 5.99.1.- (DNA Topoisomerases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.2174/0929867324666170124143710


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[PMID]:28120709
[Au] Autor:Blasiak J
[Ad] Endereço:Department of Molecular Genetics, University of Lodz, Lodz, Poland.
[Ti] Título:DNA-Damaging Anticancer Drugs - A Perspective for DNA Repair- Oriented Therapy.
[So] Source:Curr Med Chem;24(15):1488-1503, 2017.
[Is] ISSN:1875-533X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:DNA-damaging drugs in cancer present two main problems: therapeutic resistance and side effects and both can associate with DNA repair, which can be targeted in cancer therapy. Bleomycin (BLM) induces complex DNA damages, including strand breaks, base loss and 3'-phosphoglycolate (3'PG) residues repaired by several pathways, but 3'PGs must be processed to the 3'-OH ends, usually by tyrosyl-DNA phosphodiesterase 1 (Tdp1). Therefore, targeting Tdp1 can improve anticancer therapy with BLM. Mitomycin C (MMC) produces a variety of adducts with DNA, including inter-strand cross-links (ICLs) and Xeroderma pigmentosum (XP) proteins, including XPG, XPE and XPF can be crucial for the initial stage of ICL repair, so they can be targeted by inhibitors to increase toxicity of MMC in cancer cells. Although these proteins are essential for nucleotide excision repair (NER), their decreased activity may not be fatal in normal cells as almost all NER substrates can be repaired by other pathways. Four-stranded DNA, resulted mainly from guanine quadruplexes (G-4s), are highly overexpressed at the end of telomeres, where they can inhibit telomerase, hence stabilization G-4s at the telomeres ends can hamper proliferation of cancer cells. Quadruplexes are also found in the promoters of genes important for cancer and are resolved by DNA helicases, which can be targeted in cancer along with stabilization of quadruplexes. As cancer cells often have defects in DNA repair pathway(s), they can be subjected by synthetic lethality, with the most promising results with poly(ADP-ribose) polymerase 1 (PARP-1) and DNA-dependent protein kinase, catalytic subunit (DNA-PKCS).
[Mh] Termos MeSH primário: Antibióticos Antineoplásicos/toxicidade
Dano ao DNA/efeitos dos fármacos
Reparo do DNA
[Mh] Termos MeSH secundário: Antibióticos Antineoplásicos/uso terapêutico
Bleomicina/uso terapêutico
Bleomicina/toxicidade
DNA Topoisomerases/química
DNA Topoisomerases/metabolismo
Quadruplex G/efeitos dos fármacos
Seres Humanos
Neoplasias/tratamento farmacológico
Neoplasias/patologia
Diester Fosfórico Hidrolases/química
Diester Fosfórico Hidrolases/metabolismo
Inibidores da Topoisomerase/química
Inibidores da Topoisomerase/uso terapêutico
Inibidores da Topoisomerase/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (Topoisomerase Inhibitors); 11056-06-7 (Bleomycin); EC 3.1.4.- (Phosphoric Diester Hydrolases); EC 5.99.1.- (DNA Topoisomerases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.2174/0929867324666170124145557


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[PMID]:28060558
[Au] Autor:Barutcu AR; Lian JB; Stein JL; Stein GS; Imbalzano AN
[Ad] Endereço:a Department of Cell and Developmental Biology , University of Massachusetts Medical School , Worcester , MA , USA.
[Ti] Título:The connection between BRG1, CTCF and topoisomerases at TAD boundaries.
[So] Source:Nucleus;8(2):150-155, 2017 Mar 04.
[Is] ISSN:1949-1042
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The eukaryotic genome is partitioned into topologically associating domains (TADs). Despite recent advances characterizing TADs and TAD boundaries, the organization of these structures is an important dimension of genome architecture and function that is not well understood. Recently, we demonstrated that knockdown of BRG1, an ATPase driving the chromatin remodeling activity of mammalian SWI/SNF enzymes, globally alters long-range genomic interactions and results in a reduction of TAD boundary strength. We provided evidence suggesting that this effect may be due to BRG1 affecting nucleosome occupancy around CTCF sites present at TAD boundaries. In this review, we elaborate on our findings and speculate that BRG1 may contribute to the regulation of the structural and functional properties of chromatin at TAD boundaries by affecting the function or the recruitment of CTCF and DNA topoisomerase complexes.
[Mh] Termos MeSH primário: Adenosina Trifosfatases/metabolismo
DNA Topoisomerases/metabolismo
Genômica
Proteínas Repressoras/metabolismo
[Mh] Termos MeSH secundário: Animais
Fator de Ligação a CCCTC
Seres Humanos
Nucleossomos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CCCTC-Binding Factor); 0 (CTCF protein, human); 0 (Nucleosomes); 0 (Repressor Proteins); EC 3.6.1.- (Adenosine Triphosphatases); EC 5.99.1.- (DNA Topoisomerases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE
[do] DOI:10.1080/19491034.2016.1276145


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[PMID]:27997856
[Au] Autor:Rendosová M; Vargová Z; Kuchár J; Sabolová D; Levoca S; Kudlácová J; Paulíková H; Hudecová D; Helebrandtová V; Almási M; Vilková M; Dusek M; Bobálová D
[Ad] Endereço:Department of Inorganic Chemistry, Faculty of Science, P. J. Safárik University, Moyzesova 11, SK-041 54 Kosice, Slovak Republic.
[Ti] Título:New silver complexes with bioactive glycine and nicotinamide molecules - Characterization, DNA binding, antimicrobial and anticancer evaluation.
[So] Source:J Inorg Biochem;168:1-12, 2017 Mar.
[Is] ISSN:1873-3344
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study introduces a pair of newly synthesized silver complexes, [Ag (HGly) ] (NO ) (1) and [Ag(Nam) ]NO ·H O (2) (Gly - glycine, Nam - nicotinamide), that were prepared and characterized by relevant methods in solid state (elemental, spectral, thermal and structural analysis) and their stability in solution was verified by H NMR measurements. Moreover, suitable reaction conditions were observed by potentiometry depending on pH in case of binary system Ag-Gly. X-ray analysis confirmed argentophilic interactions in complex 1 with an Ag1-Ag2 distance of 2.8018(6) Å. Antimicrobial testing indicates higher growth inhibition effect of complex 1 than complex 2. Moreover the effectivity of both complexes against bacteria (Staphylococcus aureus and Escherichia coli) is superior (or similar) to that of the commercially available Ag(I) sulfadiazine, AgSD (used, for example, in Dermazine cream). The binding of the Ag(I) complexes to calf thymus DNA was investigated using electronic absorption, fluorescence and circular dichroism spectrophotometry. The Stern-Volmer quenching constants obtained from the linear quenching plot were estimated in the range from 2.01×10 to 20.34×10 M . The results of topoisomerase I and topoisomerase II (Topo I and Topo II) inhibition assay suggested that complex 2 inhibits the enzyme activity of both enzymes at a concentration of 2µM. The cytotoxicity of both complexes on L1210 leukemia cells was revealed to be approximately three times higher than that of cisplatin. Moreover, the new Ag(I) complexes also induced apoptosis of the leukemia cells. The high DNA binding activity of these complexes is considered to be responsible for their cytotoxic effects.
[Mh] Termos MeSH primário: Bactérias/efeitos dos fármacos
Complexos de Coordenação/farmacologia
DNA/metabolismo
Glicina/química
Niacinamida/química
Prata/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Infecciosos/química
Anti-Infecciosos/farmacologia
Antineoplásicos/química
Antineoplásicos/farmacologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Complexos de Coordenação/química
Cristalografia por Raios X
DNA/química
DNA Topoisomerases/metabolismo
Ativação Enzimática/efeitos dos fármacos
Concentração Inibidora 50
Camundongos
Prata/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Infective Agents); 0 (Antineoplastic Agents); 0 (Coordination Complexes); 25X51I8RD4 (Niacinamide); 3M4G523W1G (Silver); 9007-49-2 (DNA); EC 5.99.1.- (DNA Topoisomerases); TE7660XO1C (Glycine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE



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