Base de dados : MEDLINE
Pesquisa : D08.811.150.280.260.240 [Categoria DeCS]
Referências encontradas : 1092 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 110 ir para página                         

  1 / 1092 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27796281
[Au] Autor:Zhou L; Bu Y; Liang Y; Zhang F; Zhang H; Li S
[Ad] Endereço:Department of Hematology, The First People's Hospital, Jining, Shandong, China (mainland).
[Ti] Título:Epstein-Barr Virus (EBV)-BamHI-A Rightward Transcript (BART)-6 and Cellular MicroRNA-142 Synergistically Compromise Immune Defense of Host Cells in EBV-Positive Burkitt Lymphoma.
[So] Source:Med Sci Monit;22:4114-4120, 2016 Oct 31.
[Is] ISSN:1643-3750
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND This study was designed to explore the molecular mechanism underlying the effect of cellular miRNAs and EBV miRNA upon the expression of targets such as PTEN, and their involvement in the pathogenesis of Burkitt lymphoma. MATERIAL AND METHODS In this study, we examined several differentially expressed cellular miRNAs in EBV-positive versus EBV-negative Burkett lymphoma tissue samples, and confirmed PTEN as targets of cellular miR-142 by using a bioinformatics tool, luciferase reporter system, oligo transfection, real-time PCR, and Western blot analysis. RESULTS We further confirmed the binding site of miR-142 in the 3'UTR of the target genes, and established the negative regulatory relationship between miRNA and mRNAs with luciferase activity assay. To verify the regulatory relationship between the miRNAs and PTEN, we evaluated the expression of PTEN in the tissue samples, and found that PTEN was downregulated in EBV- positive Burkett lymphoma. Additionally, lymphoma cells were transfected with EBV-BART-6-3p and miR-142 and we found that EBV-BART-6-3p and miR-142 synergistically reduced expression of IL-6R and PTEN. Furthermore, we also examined viability of the cells in each treatment group, and showed that EBV-BART-6-3p and miR-142 synergistically promoted proliferation of the cells. CONCLUSIONS These findings improve our knowledge about the role of miR-142/EBV-BART-6-3p and their target, PTEN, in the development of Burkett lymphoma; they could be novel therapeutic targets for the treatment of EBV-positive Burkett lymphoma.
[Mh] Termos MeSH primário: Linfoma de Burkitt/imunologia
Linfoma de Burkitt/virologia
Infecções por Vírus Epstein-Barr/imunologia
Herpesvirus Humano 4/imunologia
MicroRNAs/imunologia
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Linfoma de Burkitt/genética
Linfoma de Burkitt/patologia
Linhagem Celular Tumoral
Proliferação Celular
Desoxirribonuclease BamHI/genética
Desoxirribonuclease BamHI/metabolismo
Regulação para Baixo
Infecções por Vírus Epstein-Barr/genética
Infecções por Vírus Epstein-Barr/patologia
Infecções por Vírus Epstein-Barr/virologia
Perfilação da Expressão Gênica
Herpesvirus Humano 4/genética
Herpesvirus Humano 4/metabolismo
Seres Humanos
MicroRNAs/biossíntese
MicroRNAs/genética
MicroRNAs/metabolismo
PTEN Fosfo-Hidrolase/genética
PTEN Fosfo-Hidrolase/metabolismo
RNA Viral/genética
Análise de Sequência de RNA
Proteínas Virais/genética
Proteínas Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (BHRF1 protein, Human herpesvirus 4); 0 (MIRN142 microRNA, human); 0 (MicroRNAs); 0 (RNA, Viral); 0 (Viral Proteins); EC 3.1.21.- (Deoxyribonuclease BamHI); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE


  2 / 1092 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27147748
[Au] Autor:Verhoeven RJ; Tong S; Zhang G; Zong J; Chen Y; Jin DY; Chen MR; Pan J; Chen H
[Ad] Endereço:State Key Laboratory for Emerging Infectious Diseases, Department of Microbiology and the Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The University of Hong Kong, Hong Kong SAR, People's Republic of China.
[Ti] Título:NF-κB Signaling Regulates Expression of Epstein-Barr Virus BART MicroRNAs and Long Noncoding RNAs in Nasopharyngeal Carcinoma.
[So] Source:J Virol;90(14):6475-88, 2016 Jul 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Epstein-Barr virus (EBV) expresses few viral proteins in nasopharyngeal carcinoma (NPC) but high levels of BamHI-A rightward transcripts (BARTs), which include long noncoding RNAs (lncRNAs) and BART microRNAs (miRNAs). It is hypothesized that the mechanism for regulation of BARTs may relate to EBV pathogenesis in NPC. We showed that nuclear factor-κB (NF-κB) activates the BART promoters and modulates the expression of BARTs in EBV-infected NPC cells but that introduction of mutations into the putative NF-κB binding sites abolished activation of BART promoters by NF-κB. Binding of p50 subunits to NF-κB sites in the BART promoters was confirmed in electrophoretic mobility shift assays (EMSA) and further demonstrated in vivo using chromatin immunoprecipitation (ChIP) analysis. Expression of BART miRNAs and lncRNAs correlated with NF-κB activity in EBV-infected epithelial cells, while treatment of EBV-harboring NPC C666-1 cells with aspirin (acetylsalicylic acid [ASA]) and the IκB kinase inhibitor PS-1145 inhibited NF-κB activity, resulting in downregulation of BART expression. Expression of EBV LMP1 activates BART promoters, whereas an LMP1 mutant which cannot induce NF-κB activation does not activate BART promoters, further supporting the idea that expression of BARTs is regulated by NF-κB signaling. Expression of LMP1 is tightly regulated in NPC cells, and this study confirmed that miR-BART5-5p downregulates LMP1 expression, suggesting a feedback loop between BART miRNA and LMP1-mediated NF-κB activation in the NPC setting. These findings provide new insights into the mechanism underlying the deregulation of BARTs in NPC and identify a regulatory loop through which BARTs support EBV latency in NPC. IMPORTANCE: Nasopharyngeal carcinoma (NPC) cells are ubiquitously infected with Epstein-Barr virus (EBV). Notably, EBV expresses very few viral proteins in NPC cells, presumably to avoid triggering an immune response, but high levels of EBV BART miRNAs and lncRNAs which exhibit complex functions associated with EBV pathogenesis. The mechanism for regulation of BARTs is critical for understanding NPC oncogenesis. This study provides multiple lines of evidence to show that expression of BARTs is subject to regulation by NF-κB signaling. EBV LMP1 is a potent activator of NF-κB signaling, and we demonstrate that LMP1 can upregulate expression of BARTs through NF-κB signaling and that BART miRNAs are also able to downregulate LMP1 expression. It appears that aberrant NF-κB signaling and expression of BARTs form an autoregulatory loop for maintaining EBV latency in NPC cells. Further exploration of how targeting NF-κB signaling interrupts EBV latency in NPC cells may reveal new options for NPC treatment.
[Mh] Termos MeSH primário: Desoxirribonuclease BamHI/genética
Infecções por Vírus Epstein-Barr/virologia
Regulação Viral da Expressão Gênica
MicroRNAs/genética
NF-kappa B/metabolismo
Neoplasias Nasofaríngeas/genética
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Carcinoma
Herpesvirus Humano 4/patogenicidade
Seres Humanos
NF-kappa B/genética
Neoplasias Nasofaríngeas/patologia
Neoplasias Nasofaríngeas/virologia
Regiões Promotoras Genéticas/genética
RNA Viral/genética
Transdução de Sinais
Células Tumorais Cultivadas
Proteínas da Matriz Viral/genética
Proteínas da Matriz Viral/metabolismo
Latência Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EBV-associated membrane antigen, Epstein-Barr virus); 0 (MicroRNAs); 0 (NF-kappa B); 0 (RNA, Long Noncoding); 0 (RNA, Viral); 0 (Viral Matrix Proteins); EC 3.1.21.- (Deoxyribonuclease BamHI)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160506
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.00613-16


  3 / 1092 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26687717
[Au] Autor:Morozova N; Sabantsev A; Bogdanova E; Fedorova Y; Maikova A; Vedyaykin A; Rodic A; Djordjevic M; Khodorkovskii M; Severinov K
[Ad] Endereço:Peter the Great St. Petersburg Polytechnic University, St. Petersburg, 195251, Russia.
[Ti] Título:Temporal dynamics of methyltransferase and restriction endonuclease accumulation in individual cells after introducing a restriction-modification system.
[So] Source:Nucleic Acids Res;44(2):790-800, 2016 Jan 29.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Type II restriction-modification (R-M) systems encode a restriction endonuclease that cleaves DNA at specific sites, and a methyltransferase that modifies same sites protecting them from restriction endonuclease cleavage. Type II R-M systems benefit bacteria by protecting them from bacteriophages. Many type II R-M systems are plasmid-based and thus capable of horizontal transfer. Upon the entry of such plasmids into a naïve host with unmodified genomic recognition sites, methyltransferase should be synthesized first and given sufficient time to methylate recognition sites in the bacterial genome before the toxic restriction endonuclease activity appears. Here, we directly demonstrate a delay in restriction endonuclease synthesis after transformation of Escherichia coli cells with a plasmid carrying the Esp1396I type II R-M system, using single-cell microscopy. We further demonstrate that before the appearance of the Esp1396I restriction endonuclease the intracellular concentration of Esp1396I methyltransferase undergoes a sharp peak, which should allow rapid methylation of host genome recognition sites. A mathematical model that satisfactorily describes the observed dynamics of both Esp1396I enzymes is presented. The results reported here were obtained using a functional Esp1396I type II R-M system encoding both enzymes fused to fluorescent proteins. Similar approaches should be applicable to the studies of other R-M systems at single-cell level.
[Mh] Termos MeSH primário: Enzimas de Restrição-Modificação do DNA/metabolismo
Análise de Célula Única/métodos
[Mh] Termos MeSH secundário: Metilases de Modificação do DNA/genética
Metilases de Modificação do DNA/metabolismo
Enzimas de Restrição-Modificação do DNA/análise
Enzimas de Restrição-Modificação do DNA/genética
Desoxirribonuclease BamHI/genética
Desoxirribonuclease BamHI/metabolismo
Escherichia coli/genética
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Microscopia de Fluorescência
Modelos Biológicos
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA Restriction-Modification Enzymes); 0 (Luminescent Proteins); 0 (Recombinant Proteins); 0 (red fluorescent protein); EC 2.1.1.- (DNA Modification Methylases); EC 3.1.21.- (Deoxyribonuclease BamHI)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151222
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkv1490


  4 / 1092 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26423217
[Au] Autor:Zhou C; Xie Z; Gao L; Liu C; Ai J; Zhang L; Shen K
[Ad] Endereço:Virology Laboratory, Capital Medical University Affiliated Beijing Children's Hospital.
[Ti] Título:Profiling of EBV-Encoded microRNAs in EBV-Associated Hemophagocytic Lymphohistiocytosis.
[So] Source:Tohoku J Exp Med;237(2):117-26, 2015 10.
[Is] ISSN:1349-3329
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis (EBV-HLH) is a life-threatening complication of EBV infection. MicroRNAs (miRNAs) were small non-coding RNA, and EBV could encode miRNAs that are involved in the progression of infection. However, the profiles of EBV-miRNAs in EBV-HLH were unknown. Here, we aimed to profile the expression of EBV-miRNAs in children with EBV-HLH by analyzing 44 known EBV-miRNAs, encoded within the BamHI fragment H rightward open reading frame 1 (BHRF1) and the BamHI-A region rightward transcript (BART), in plasma and cellular targets by real-time quantitative PCR. The study included 15 children with EBV-HLH, 15 children with infectious mononucleosis (IM), and 15 healthy controls. CD8(+) T cells were found to be the cellular target of EBV infection in EBV-HLH, while CD19(+) B cells were infected with EBV in IM. We also found the greater levels of several miRNAs encoded by BART in EBV-HLH, compared to those in IM and healthy controls, whereas the levels of BHRF1 miRNAs were lower than those in IM. The profile and pattern of EBV-miRNAs in EBV-HLH indicated that EBV could display type II latency in EBV-HLH. Importantly, the level of plasma miR-BART16-1 continued decreasing during the whole chemotherapy, suggesting that plasma miR-BART16-1 could be a potential biomarker for monitoring EBV-HLH progression. The pathogenesis of EBV-HLH might be attributed to the abundance of EBV-miRNAs in EBV-HLH. These findings help elucidate the roles of EBV miRNAs in EBV-HLH, enabling the understanding of the basis of this disease and providing clues for its treatment.
[Mh] Termos MeSH primário: Infecções por Vírus Epstein-Barr/complicações
Herpesvirus Humano 4/genética
Linfo-Histiocitose Hemofagocítica/etiologia
MicroRNAs/genética
RNA Viral/genética
[Mh] Termos MeSH secundário: Biomarcadores
Linfócitos T CD8-Positivos/química
Linfócitos T CD8-Positivos/metabolismo
Portador Sadio/virologia
Criança
Pré-Escolar
Desoxirribonuclease BamHI/genética
Infecções por Vírus Epstein-Barr/tratamento farmacológico
Infecções por Vírus Epstein-Barr/mortalidade
Feminino
Seres Humanos
Mononucleose Infecciosa/virologia
Linfo-Histiocitose Hemofagocítica/tratamento farmacológico
Linfo-Histiocitose Hemofagocítica/mortalidade
Masculino
Reação em Cadeia da Polimerase
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (MicroRNAs); 0 (RNA, Viral); EC 3.1.21.- (Deoxyribonuclease BamHI)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151002
[St] Status:MEDLINE
[do] DOI:10.1620/tjem.237.117


  5 / 1092 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26311882
[Au] Autor:Marquitz AR; Mathur A; Edwards RH; Raab-Traub N
[Ad] Endereço:Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
[Ti] Título:Host Gene Expression Is Regulated by Two Types of Noncoding RNAs Transcribed from the Epstein-Barr Virus BamHI A Rightward Transcript Region.
[So] Source:J Virol;89(22):11256-68, 2015 Nov.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: In Epstein-Barr virus-infected epithelial cancers, the alternatively spliced BamHI A rightward transcripts (BARTs) are the most abundant viral polyadenylated RNA. The BART introns form the template for the production of 44 microRNAs (miRNAs), and the spliced and polyadenylated exons form nuclear non-protein-coding RNAs. Analysis of host cell transcription by RNA-seq during latency in AGS cells identified a large number of reproducibly changed genes. Genes that were downregulated were enriched for BART miRNA targets. Bioinformatics analysis predicted activation of the myc pathway and downregulation of XBP1 as likely mediators of the host transcriptional changes. Effects on XBP1 activity were not detected in these cells; however, myc activation was confirmed through use of a myc-responsive luciferase reporter. To identify potential regulatory properties of the spliced, polyadenylated BART RNAs, a full-length cDNA clone of one of the BART isoforms was obtained and expressed in the Epstein-Barr virus (EBV)-negative AGS cells. The BART cDNA transcript remained primarily nuclear yet induced considerable and consistent changes in cellular transcription, as profiled by RNA-seq. These transcriptional changes significantly overlapped the transcriptional changes induced during latent EBV infection of these same cells, where the BARTs are exclusively nuclear and do not encode proteins. These data suggest that the nuclear BART RNAs are functional long noncoding RNAs (lncRNAs). The abundant expression of multiple forms of noncoding RNAs that contribute to growth regulation without expression of immunogenic proteins would be an important mechanism for viral oncogenesis in the presence of a functional immune system. IMPORTANCE: Infection with Epstein-Barr virus (EBV) is nearly ubiquitous in the human population; however, it does contribute to the formation of multiple types of cancer. In immunocompromised patients, EBV causes multiple types of lymphomas by expressing viral oncogenes that promote growth and survival of infected B lymphocytes. EBV-positive gastric carcinoma does not require immune suppression, and the viral oncoproteins that are frequent targets for an immunological response are not expressed. This study demonstrates using transcriptional analysis that the expression of various classes of viral non-protein-coding RNAs likely contribute to the considerable changes in the host transcriptional profile in the AGS gastric cancer cell line. This is the first report to show that the highly expressed polyadenylated BamHI A rightward transcripts (BART) viral transcript in gastric carcinoma is in fact a functional viral long noncoding RNA. These studies provide new insight into how EBV can promote transformation in the absence of viral protein expression.
[Mh] Termos MeSH primário: Regulação Viral da Expressão Gênica
Herpesvirus Humano 4/genética
MicroRNAs/genética
RNA Longo não Codificante/genética
Transcrição Genética/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Linhagem Celular Tumoral
Proteínas de Ligação a DNA/biossíntese
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Desoxirribonuclease BamHI/metabolismo
Regulação para Baixo
Infecções por Vírus Epstein-Barr/virologia
Seres Humanos
Proteínas Proto-Oncogênicas c-myc/metabolismo
RNA Mensageiro/genética
RNA Viral/genética
Fatores de Transcrição de Fator Regulador X
Análise de Sequência de RNA
Neoplasias Gástricas/virologia
Fatores de Transcrição/biossíntese
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Proteína 1 de Ligação a X-Box
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (MYC protein, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Long Noncoding); 0 (RNA, Messenger); 0 (RNA, Viral); 0 (Regulatory Factor X Transcription Factors); 0 (Transcription Factors); 0 (X-Box Binding Protein 1); 0 (XBP1 protein, human); EC 3.1.21.- (Deoxyribonuclease BamHI)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150828
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.01492-15


  6 / 1092 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25523862
[Au] Autor:Lou J; Liu S; Tu W; Dai Z
[Ad] Endereço:Jiangsu Collaborative Innovation Center of Biomedical Functional Materials and Jiangsu Key Laboratory of Biofunctional Materials, College of Chemistry and Materials Science, Nanjing Normal University , Nanjing, 210023, P. R. China.
[Ti] Título:Graphene quantums dots combined with endonuclease cleavage and bidentate chelation for highly sensitive electrochemiluminescent DNA biosensing.
[So] Source:Anal Chem;87(2):1145-51, 2015 Jan 20.
[Is] ISSN:1520-6882
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A novel strategy for highly sensitive electrochemiluminescence (ECL) detection of DNA was proposed based on site-specific cleavage of BamHI endonuclease combined with the excellent ECL activity of graphene quantum dots (GQDs) and bidentate chelation of the dithiocarbamate DNA (DTC-DNA) probe assembly. The difference between photoluminescence and ECL spectral peaks suggested that a negligible defect existed on the GQDs surface for generation of an ECL signal. The formed DTC-DNA was directly attached to the gold surface by bidentate anchoring (S-Au-S bonds), which conferred a strong affinity between the ligands and the gold surface, increasing the robustness of DNA immobilization on the gold surface. BamHI endonuclease site-specifically recognized and cleaved the duplex symmetrical sequence, which made the double-stranded DNA fragments and GQDs break off from the electrode surface, inducing a decrease of the ECL signal. Using hepatitis C virus-1b genotype complementary DNA (HCV-1b cDNA) as a model, a novel signal-off ECL DNA biosensor was developed based on variation of the ECL intensity before and after digestion of the DNA hybrid. Electrochemical impedance spectroscopy confirmed the successful fabrication of the ECL DNA biosensor. This ECL biosensor for HCV-1b cDNA determination exhibited a linear range from 5 fM to 100 pM with a detection limit of 0.45 fM at a signal-to-noise ratio of 3 and showed satisfactory selectivity and good stability, which validated the feasibility of the designed strategy. The proposed strategy may be conveniently combined with other specific biological recognition events for expansion of the biosensing application, especially in clinical diagnoses.
[Mh] Termos MeSH primário: Técnicas Biossensoriais/métodos
DNA Viral/análise
Desoxirribonuclease BamHI/metabolismo
Técnicas Eletroquímicas/métodos
Grafite/química
Hepacivirus/genética
Medições Luminescentes/métodos
Pontos Quânticos
[Mh] Termos MeSH secundário: Quelantes/metabolismo
DNA Complementar/genética
DNA Viral/genética
Hepatite C/diagnóstico
Hepatite C/genética
Hepatite C/virologia
Seres Humanos
Limite de Detecção
Razão Sinal-Ruído
Tiocarbamatos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chelating Agents); 0 (DNA, Complementary); 0 (DNA, Viral); 0 (Thiocarbamates); 7782-42-5 (Graphite); EC 3.1.21.- (Deoxyribonuclease BamHI)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:150121
[Lr] Data última revisão:
150121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141220
[St] Status:MEDLINE
[do] DOI:10.1021/ac5037318


  7 / 1092 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:25503135
[Au] Autor:Arzuman L; Beale P; Yu JQ; Proschogo N; Huq F
[Ad] Endereço:Discipline of Biomedical Science, Sydney Medical School, The University of Sydney, Cumberland Campus, Lidcombe, NSW, Australia.
[Ti] Título:Synthesis of a monofunctional platinum compound and its activity alone and in combination with phytochemicals in ovarian tumor models.
[So] Source:Anticancer Res;34(12):7077-90, 2014 Dec.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Currently used platinum drugs fail to provide long-term cure for ovarian cancer mainly because of acquired drug resistance. In this study, a new monofunctional planaramineplatinum(II) complex, namely tris(8-hydroxyquinoline)monochloroplatinum(II) chloride (coded as LH3), was synthesised and investigated for its activity against human ovarian A2780, cisplatin-resistant A2780 (A2780(cisR)) and ZD0473-resistant A2780 (A2780(ZD0473R)) cancer cell lines, alone and in combination with the phytochemicals curcumin, genistein and resveratrol. Cellular levels of glutathione in A2780 and A2780(cisR) cell lines before and after treatment with LH3 and its combinations with genistein and curcumin were also determined. Interaction of the compounds with salmon sperm DNA, pBR322 plasmid DNA and damage to DNA in A2780 and A2780(cisR) cells due to interaction with LH3-alone and in combination with phytochemicals were also investigated. LH3 was found to be much more active than cisplatin against the resistant tumor models and greatest synergism in activity was observed when combinations of LH3 with genistein and curcumin were administered as a bolus. For combinations of LH3 with the phytochemicals, platinum accumulation and the level of Pt-DNA binding were found to be greater in the resistant A2780(cisR) cell line than in the parental A2780 cell line. Greater activity of LH3 than cisplatin against the resistant ovarian cell lines indicates that it may have the potential for development as a novel anticancer drug and that its combination with phytochemicals can serve to further enhance drug efficacy.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Compostos Organoplatínicos/farmacologia
Neoplasias Ovarianas/tratamento farmacológico
Compostos Fitoquímicos/farmacologia
Compostos de Platina/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Cisplatino/farmacologia
Curcumina/farmacologia
DNA/efeitos dos fármacos
Fragmentação do DNA/efeitos dos fármacos
Desoxirribonuclease BamHI/metabolismo
Avaliação Pré-Clínica de Medicamentos
Resistência a Medicamentos Antineoplásicos
Sinergismo Farmacológico
Feminino
Genisteína/farmacologia
Glutationa/análise
Seres Humanos
Compostos Organoplatínicos/síntese química
Neoplasias Ovarianas/patologia
Plasmídeos/efeitos dos fármacos
Plasmídeos/genética
Compostos de Platina/síntese química
Estilbenos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Organoplatinum Compounds); 0 (Phytochemicals); 0 (Platinum Compounds); 0 (Stilbenes); 0 (amminedichloro(2-methylpyridine)platinum(II)); 0 (tris(8-hydroxyquinoline)monochloroplatinum(II)); 9007-49-2 (DNA); DH2M523P0H (Genistein); EC 3.1.21.- (Deoxyribonuclease BamHI); GAN16C9B8O (Glutathione); IT942ZTH98 (Curcumin); Q20Q21Q62J (Cisplatin); Q369O8926L (resveratrol)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:141216
[Lr] Data última revisão:
141216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141216
[St] Status:MEDLINE


  8 / 1092 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:25116617
[Au] Autor:Tong Z; Zhao B; Zhao G; Shang H; Guan Y
[Ad] Endereço:Key Laboratory of Medical Cell Biology (Ministry of Education), Department of Biochemistry and Molecular Biology, China Medical University, Shenyang, Liaoning, China 110001.
[Ti] Título:2'-O-methyl nucleotide modified DNA substrates influence the cleavage efficiencies of BamHI and BglII.
[So] Source:J Biosci;39(4):621-30, 2014 Sep.
[Is] ISSN:0973-7138
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:Induction of endonucleolytic DNA cleavage is an essential event that links the initiating stimuli to the final effects of cells. The cleavage efficiency and thus the final yield could be affected by many factors, including structures of DNA substrates, composite structures of enzymes-substrates or enzymes-nucleic analogs and so on. However, it is not clear whether a nucleotide derivative-substituted in DNA substrates can influence the efficiency of enzymatic cleavage. To investigate the effect of sugar pucker conformation on DNA-protein interactions, we used 2'-O-methyl modified nucleotides (OMeN) to modify DNA substrates of isocaudemers BamHI and BglII in this study, and used FRET assay as an efficient method for analysis of enzyme cleavage. Experimental results demonstrated that OMeN-substituted recognition sequences influenced the cleavage rates significantly in a position-dependent manner. OMeN substitutions can reduce the cleavage as expected. Surprisingly, OMeN substitutions can also enhance the cleavage rates. The kinetics parameters of Vmax and Km have been obtained by fitting the Michaelis-Menten kinetic equation. These 2'- OMe nucleotides could behave as a regulatory element to modulate the enzymatic activity in vitro, and this property could enrich our understanding about the endonuclease cleavage mechanism and enhance our ability to regulate the enzymatic cleavage efficiency for applications in synthetic biology.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Clivagem do DNA
DNA/química
Desoxirribonuclease BamHI/metabolismo
Desoxirribonucleases de Sítio Específico do Tipo II/metabolismo
[Mh] Termos MeSH secundário: Adenosina/análogos & derivados
Adenosina/química
Citidina/análogos & derivados
Citidina/química
DNA/metabolismo
Transferência Ressonante de Energia de Fluorescência
Guanosina/análogos & derivados
Guanosina/química
Cinética
Oligonucleotídeos/genética
Timidina/análogos & derivados
Timidina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2'-O-methylthymidine); 0 (Bacterial Proteins); 0 (Oligonucleotides); 02YX82IHZ5 (2'-O-methyladenosine); 12133JR80S (Guanosine); 58970-16-4 (2'-O-methylcytidine); 5CSZ8459RP (Cytidine); 9007-49-2 (DNA); EC 3.1.21.- (Deoxyribonuclease BamHI); EC 3.1.21.4 (BglII endonuclease); EC 3.1.21.4 (Deoxyribonucleases, Type II Site-Specific); K72T3FS567 (Adenosine); VC2W18DGKR (Thymidine); W722H4PA1S (2'-O-methylguanosine)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140814
[St] Status:MEDLINE


  9 / 1092 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:24895130
[Au] Autor:Sommers JA; Banerjee T; Hinds T; Wan B; Wold MS; Lei M; Brosh RM
[Ad] Endereço:From the Laboratory of Molecular Gerontology, Biomedical Research Center, NIA, National Institutes of Health, Baltimore, Maryland 21224.
[Ti] Título:Novel function of the Fanconi anemia group J or RECQ1 helicase to disrupt protein-DNA complexes in a replication protein A-stimulated manner.
[So] Source:J Biol Chem;289(29):19928-41, 2014 Jul 18.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Understanding how cellular machinery deals with chromosomal genome complexity is an important question because protein bound to DNA may affect various cellular processes of nucleic acid metabolism. DNA helicases are at the forefront of such processes, yet there is only limited knowledge how they remodel protein-DNA complexes and how these mechanisms are regulated. We have determined that representative human RecQ and Fe-S cluster DNA helicases are potently blocked by a protein-DNA interaction. The Fanconi anemia group J (FANCJ) helicase partners with the single-stranded DNA-binding protein replication protein A (RPA) to displace BamHI-E111A bound to duplex DNA in a specific manner. Protein displacement was dependent on the ATPase-driven function of the helicase and unique properties of RPA. Further biochemical studies demonstrated that the shelterin proteins TRF1 and TRF2, which preferentially bind the telomeric repeat found at chromosome ends, effectively block FANCJ from unwinding the forked duplex telomeric substrate. RPA, but not the Escherichia coli single-stranded DNA-binding protein or shelterin factor Pot1, stimulated FANCJ ejection of TRF1 from the telomeric DNA substrate. FANCJ was also able to displace TRF2 from the telomeric substrate in an RPA-dependent manner. The stimulation of helicase-catalyzed protein displacement is also observed with the DNA helicase RECQ1, suggesting a conserved functional interaction of RPA-interacting helicases. These findings suggest that partnerships between RPA and interacting human DNA helicases may greatly enhance their ability to dislodge proteins bound to duplex DNA, an activity that is likely to be highly relevant to their biological roles in DNA metabolism.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
DNA/metabolismo
Proteínas de Grupos de Complementação da Anemia de Fanconi/metabolismo
RecQ Helicases/metabolismo
Proteína de Replicação A/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Sequência de Bases
DNA/química
DNA/genética
Desoxirribonuclease BamHI/metabolismo
Exodesoxirribonucleases/metabolismo
Seres Humanos
Substâncias Macromoleculares/química
Substâncias Macromoleculares/metabolismo
Conformação de Ácido Nucleico
Ligação Proteica
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Proteína de Replicação A/genética
Especificidade por Substrato
Proteína 1 de Ligação a Repetições Teloméricas/metabolismo
Helicase da Síndrome de Werner
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BACH1 protein, human); 0 (Basic-Leucine Zipper Transcription Factors); 0 (Fanconi Anemia Complementation Group Proteins); 0 (Macromolecular Substances); 0 (RPA1 protein, human); 0 (Recombinant Proteins); 0 (Replication Protein A); 0 (Telomeric Repeat Binding Protein 1); 9007-49-2 (DNA); EC 3.1.- (Exodeoxyribonucleases); EC 3.1.21.- (Deoxyribonuclease BamHI); EC 3.6.1.- (RECQL protein, human); EC 3.6.4.12 (RecQ Helicases); EC 3.6.4.12 (WRN protein, human); EC 3.6.4.12 (Werner Syndrome Helicase)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140605
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M113.542456


  10 / 1092 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:24718258
[Au] Autor:Shu Z; Li J; Mu N; Gao Y; Huang T; Zhang Y; Wang Z; Li M; Hao Q; Li W; He L; Zhang C; Zhang W; Xue X; Zhang Y
[Ad] Endereço:State Key Laboratory of Cancer Biology, Department of Biopharmaceutics, School of Pharmacy, Fourth Military Medical University, Xi'an 710032, China.
[Ti] Título:Expression, purification and characterization of galectin-1 in Escherichia coli.
[So] Source:Protein Expr Purif;99:58-63, 2014 Jul.
[Is] ISSN:1096-0279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:As a member of beta-galactoside-binding proteins family, Galectin-1 (Gal-1) contains a single carbohydrate recognition domain, by means of which it can bind glycans both as a monomer and as a homodimer. Gal-1 is implicated in modulating cell-cell and cell-matrix interactions and may act as an autocrine negative growth factor that regulates cell proliferation. Besides, it can also suppress TH1 and TH17 cells by regulating dendritic cell differentiation or suppress inflammation via IL-10 and IL-27. In the present study, Gal-1 monomer and concatemer (Gal-1â‘¡), which can resemble Gal-1 homodimer, were expressed in Escherichia coli and their bioactivities were analyzed. The results of this indicate that both Gal-1 and Gal-1â‘¡ were expressed in E. coli in soluble forms with a purity of over 95% after purifying with ion-exchange chromatography. Clearly, both Gal-1 and Gal-1â‘¡ can effectively promote erythrocyte agglutination in hemagglutinating activity assays and inhibit Jurkat cell proliferation in MTT assays. All these data demonstrate that bacterially-expressed Gal-1 and Gal-1â‘¡ have activities similar to those of wild type human Gal-1 whereas the bioactivity of concatemer Gal-1â‘¡ was stronger than those of the bacterially-expressed and wild type human Gal.
[Mh] Termos MeSH primário: DNA Concatenado/farmacologia
Galectina 1/biossíntese
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
DNA Concatenado/isolamento & purificação
Desoxirribonuclease BamHI/metabolismo
Escherichia coli/metabolismo
Galectina 1/isolamento & purificação
Galectina 1/farmacologia
Hemaglutinação/efeitos dos fármacos
Seres Humanos
Células Jurkat
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/isolamento & purificação
Proteínas Recombinantes/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Concatenated); 0 (Galectin 1); 0 (LGALS1 protein, human); 0 (Recombinant Proteins); EC 3.1.21.- (Deoxyribonuclease BamHI)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:140602
[Lr] Data última revisão:
140602
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140411
[St] Status:MEDLINE



página 1 de 110 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde