Base de dados : MEDLINE
Pesquisa : D08.811.277.352.335.350.250 [Categoria DeCS]
Referências encontradas : 6589 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 659 ir para página                         

  1 / 6589 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29372800
[Au] Autor:Abdurashitov MA; Degtyarev SK
[Ti] Título:[Use of site-specific DNA endonucleases in genome-wide studies of human DNA].
[So] Source:Genetika;53(1):3-11, 2017 Jan.
[Is] ISSN:0016-6758
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:During the last decades, site-specific DNA endonucleases have served as a key instrument to study primary structure of DNA and genetic engineering. Here, we describe examples of these enzyme uses in genome-wide analysis of human DNA including restriction endonucleases involvement during sample preparation for sequencing using NGS devices, as well as visualization of cleavage of DNA repeats by endonucleases. The first studies on application of DNA endonucleases in the rapidly developing area of epigenetic analysis of genomes, which is facilitated by the recent discovery of a new class of enzymes, 5-methylcytosinedependent site-specific DNA endonucleases, are of special interest.
[Mh] Termos MeSH primário: DNA/química
DNA/genética
Desoxirribonuclease I/química
Genoma Humano
Estudo de Associação Genômica Ampla/métodos
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
9007-49-2 (DNA); EC 3.1.21.1 (Deoxyribonuclease I)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE


  2 / 6589 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28458013
[Au] Autor:Wang S; He Z; Li D; Zhang B; Li M; Li W; Zhu W; Xing X; Zeng X; Wang Q; Dong G; Xiao Y; Chen W; Chen L
[Ad] Endereço:Department of Toxicology, Guangzhou Key Laboratory of Environmental Pollution and Health Risk Assessment, School of Public Health, Sun Yat-sen University, Guangzhou, China.
[Ti] Título:Aberrant methylation of RUNX3 is present in Aflatoxin B -induced transformation of the L02R cell line.
[So] Source:Toxicology;385:1-9, 2017 06 15.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Chronic exposure to aflatoxin B (AFB ) is linked to the development of hepatocellular carcinoma (HCC). To identify differentially methylated genes involved in AFB -induced cell transformation, we analyzed DNA methylation patterns in immortal human hepatocyte L02 cells expressing an oncogenic H-Ras allele (L02R cells) and AFB -transformed L02R (L02RT-AFB ) cells by performing genome-wide methylation profiling. We treated L02R cells with 0.3µM AFB weekly and observed a transformed phenotype at the 17th week post-treatment. The transformed cells (L02RT-AFB ) could grow in an anchorage independent fashion and form tumors in immunodeficient mice. qRT-PCR was performed to examine whether gene methylation led to a reduction in gene expression of methylated candidate genes. As a result, the expression of the following seven genes including JUNB, RUNX3, NAV1, CXCR4, RARRES1, INTS1, and POLL was down-regulated in transformed L02RT-AFB cells. The reduction of gene expression of these genes could be reversed by treatment of 5-azadeoxycytidine. The methylated CpG sites of RUNX3 genes were verified using bisulfite sequencing PCR (BSP) assay. Furthermore, a dynamic change in RUNX3 methylation was observed over the course of AFB -induced cell transformation, which was corresponded to the alteration of gene expression and the extent of DNA damage. In vitro study showed that methylation of RUNX3 tended to abate in L02R cells treated with AFB for a short-term period of time. Notably, hypermethylation of RUNX3 appeared in 70% (14/20) of human hepatocellular carcinomas. Moreover, LINE-1 hypomethylation and dynamic changes of DNMTs, TETs and MeCP2 expression were also observed during AFB -induced transformation. Taken together, these observations suggest that aberrant methylation of RUNX3 and LINE-1 might be involved in AFB -induced carcinogenesis.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Transformação Celular Neoplásica/genética
Subunidade alfa 3 de Fator de Ligação ao Core/genética
Neoplasias Hepáticas/genética
[Mh] Termos MeSH secundário: Adulto
Aflatoxina B1
Carcinoma Hepatocelular/metabolismo
Linhagem Celular
Ensaio Cometa
Subunidade alfa 3 de Fator de Ligação ao Core/metabolismo
Metilação de DNA
Desoxirribonuclease I/genética
Feminino
Seres Humanos
Neoplasias Hepáticas/metabolismo
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 3 Subunit); 0 (Runx3 protein, human); 9N2N2Y55MH (Aflatoxin B1); EC 3.1.21.1 (Deoxyribonuclease I); EC 3.1.21.1 (LINE-1 endonuclease, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  3 / 6589 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29190833
[Au] Autor:Horvei KD; Pedersen HL; Fismen S; Thiyagarajan D; Schneider A; Rekvig OP; Winkler TH; Seredkina N
[Ad] Endereço:RNA and Molecular Pathology Research Group, Department of Medical Biology, Faculty of Health Sciences, UIT-The Arctic University of Norway, Tromsø, Norway.
[Ti] Título:Lupus nephritis progression in FcγRIIB-/-yaa mice is associated with early development of glomerular electron dense deposits and loss of renal DNase I in severe disease.
[So] Source:PLoS One;12(11):e0188863, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:FcγRIIB-/-yaa mice develop severe lupus glomerulonephritis due to lack of an inhibitory immune cell receptor combined with a Y-chromosome linked autoimmune accelerator mutation. In the present study, we have investigated nephritis development and progression in FcγRIIB-/-yaa mice to find shared features with NZB/NZW F1 lupus prone mice and human disease. We sacrificed 25 male FcγRIIB-/-yaa mice at various disease stages, and grouped them according to activity and chronicity indices for lupus nephritis. Glomerular morphology and localization of electron dense deposits containing IgG were further determined by immune electron microscopy. Renal DNase I and pro-inflammatory cytokine mRNA levels were measured by real-time quantitative PCR. DNase I protein levels was assessed by immunohistochemistry and zymography. Our results demonstrate early development of electron dense deposits containing IgG in FcγRIIB-/-yaa mice, before detectable levels of serum anti-dsDNA antibodies. Similar to NZB/NZW F1, electron dense deposits in FcγRIIB-/-yaa progressed from being confined to the mesangium in the early stage of lupus nephritis to be present also in capillary glomerular basement membranes. In the advanced stage of lupus nephritis, renal DNase I was lost on both transcriptional and protein levels, which has previously been shown in NZB/NZW F1 mice and in human disease. Although lupus nephritis appears on different genetic backgrounds, our findings suggest similar processes when comparing different murine models and human lupus nephritis.
[Mh] Termos MeSH primário: Desoxirribonuclease I/metabolismo
Glomérulos Renais/patologia
Nefrite Lúpica/patologia
Receptores de IgG/genética
[Mh] Termos MeSH secundário: Animais
Progressão da Doença
Imunoglobulina G/metabolismo
Glomérulos Renais/enzimologia
Glomérulos Renais/metabolismo
Túbulos Renais/metabolismo
Nefrite Lúpica/metabolismo
Masculino
Glicoproteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Receptor 7 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fcgr2b protein, mouse); 0 (Immunoglobulin G); 0 (Membrane Glycoproteins); 0 (Receptors, IgG); 0 (Tlr7 protein, mouse); 0 (Toll-Like Receptor 7); EC 3.1.21.1 (Deoxyribonuclease I)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188863


  4 / 6589 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29031777
[Au] Autor:Jia C; Huai C; Ding J; Hu L; Su B; Chen H; Lu D
[Ad] Endereço:School of Life Science, Fudan University, 2005 Songhu Road, Shanghai 200438, China.
[Ti] Título:New applications of CRISPR/Cas9 system on mutant DNA detection.
[So] Source:Gene;641:55-62, 2018 Jan 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The detection of mutant DNA is critical for precision medicine, but low-frequency DNA mutation is very hard to be determined. CRISPR/Cas9 is a robust tool for in vivo gene editing, and shows the potential for precise in vitro DNA cleavage. Here we developed a DNA mutation detection system based on CRISPR/Cas9 that can detect gene mutation efficiently even in a low-frequency condition. The system of CRISPR/Cas9 cleavage in vitro showed a high accuracy similar to traditional T7 endonuclease I (T7E1) assay in estimating mutant DNA proportion in the condition of normal frequency. The technology was further used for low-frequency mutant DNA detection of EGFR and HBB somatic mutations. To the end, Cas9 was employed to cleave the wild-type (WT) DNA and to enrich the mutant DNA. Using amplified fragment length polymorphism analysis (AFLPA) and Sanger sequencing, we assessed the sensitivity of CRISPR/Cas9 cleavage-based PCR, in which mutations at 1%-10% could be enriched and detected. When combined with blocker PCR, its sensitivity reached up to 0.1%. Our results suggested that this new application of CRISPR/Cas9 system is a robust and potential method for heterogeneous specimens in the clinical diagnosis and treatment management.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas/genética
DNA/análise
Subunidades de Hemoglobina/genética
Reação em Cadeia da Polimerase/métodos
Receptor do Fator de Crescimento Epidérmico/genética
[Mh] Termos MeSH secundário: Análise do Polimorfismo de Comprimento de Fragmentos Amplificados
Carcinoma Pulmonar de Células não Pequenas
DNA/genética
Desoxirribonuclease I/genética
Células HEK293
Seres Humanos
Neoplasias Pulmonares
Mutação/genética
Taxa de Mutação
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hemoglobin Subunits); 9007-49-2 (DNA); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.1.21.1 (Deoxyribonuclease I)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE


  5 / 6589 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29049320
[Au] Autor:Kakumanu A; Velasco S; Mazzoni E; Mahony S
[Ad] Endereço:Center for Eukaryotic Gene Regulation, Department of Biochemistry & Molecular Biology, The Pennsylvania State University, University Park, PA, United States of America.
[Ti] Título:Deconvolving sequence features that discriminate between overlapping regulatory annotations.
[So] Source:PLoS Comput Biol;13(10):e1005795, 2017 Oct.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genomic loci with regulatory potential can be annotated with various properties. For example, genomic sites bound by a given transcription factor (TF) can be divided according to whether they are proximal or distal to known promoters. Sites can be further labeled according to the cell types and conditions in which they are active. Given such a collection of labeled sites, it is natural to ask what sequence features are associated with each annotation label. However, discovering such label-specific sequence features is often confounded by overlaps between the labels; e.g. if regulatory sites specific to a given cell type are also more likely to be promoter-proximal, it is difficult to assess whether motifs identified in that set of sites are associated with the cell type or associated with promoters. In order to meet this challenge, we developed SeqUnwinder, a principled approach to deconvolving interpretable discriminative sequence features associated with overlapping annotation labels. We demonstrate the novel analysis abilities of SeqUnwinder using three examples. Firstly, SeqUnwinder is able to unravel sequence features associated with the dynamic binding behavior of TFs during motor neuron programming from features associated with chromatin state in the initial embryonic stem cells. Secondly, we characterize distinct sequence properties of multi-condition and cell-specific TF binding sites after controlling for uneven associations with promoter proximity. Finally, we demonstrate the scalability of SeqUnwinder to discover cell-specific sequence features from over one hundred thousand genomic loci that display DNase I hypersensitivity in one or more ENCODE cell lines.
[Mh] Termos MeSH primário: Anotação de Sequência Molecular
Sequências Reguladoras de Ácido Nucleico/genética
Software
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Linhagem Celular
Linhagem da Célula/genética
Cromatina/genética
Cromatina/metabolismo
Biologia Computacional/métodos
Desoxirribonuclease I/genética
Desoxirribonuclease I/metabolismo
Células-Tronco Embrionárias/citologia
Células-Tronco Embrionárias/metabolismo
Regulação da Expressão Gênica
Loci Gênicos
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Regiões Promotoras Genéticas
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (Transcription Factors); EC 3.1.21.1 (Deoxyribonuclease I)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1005795


  6 / 6589 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29022941
[Au] Autor:Cooper J; Ding Y; Song J; Zhao K
[Ad] Endereço:Systems Biology Center, Division of Intramural Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA.
[Ti] Título:Genome-wide mapping of DNase I hypersensitive sites in rare cell populations using single-cell DNase sequencing.
[So] Source:Nat Protoc;12(11):2342-2354, 2017 Nov.
[Is] ISSN:1750-2799
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Increased chromatin accessibility is a feature of cell-type-specific cis-regulatory elements; therefore, mapping of DNase I hypersensitive sites (DHSs) enables the detection of active regulatory elements of transcription, including promoters, enhancers, insulators and locus-control regions. Single-cell DNase sequencing (scDNase-seq) is a method of detecting genome-wide DHSs when starting with either single cells or <1,000 cells from primary cell sources. This technique enables genome-wide mapping of hypersensitive sites in a wide range of cell populations that cannot be analyzed using conventional DNase I sequencing because of the requirement for millions of starting cells. Fresh cells, formaldehyde-cross-linked cells or cells recovered from formalin-fixed paraffin-embedded (FFPE) tissue slides are suitable for scDNase-seq assays. To generate scDNase-seq libraries, cells are lysed and then digested with DNase I. Circular carrier plasmid DNA is included during subsequent DNA purification and library preparation steps to prevent loss of the small quantity of DHS DNA. Libraries are generated for high-throughput sequencing on the Illumina platform using standard methods. Preparation of scDNase-seq libraries requires only 2 d. The materials and molecular biology techniques described in this protocol should be accessible to any general molecular biology laboratory. Processing of high-throughput sequencing data requires basic bioinformatics skills and uses publicly available bioinformatics software.
[Mh] Termos MeSH primário: Mapeamento Cromossômico/métodos
Desoxirribonuclease I/metabolismo
Análise de Sequência de DNA/métodos
Análise de Célula Única/métodos
[Mh] Termos MeSH secundário: Animais
Apoptose
Linfócitos T CD8-Positivos/imunologia
Eletroforese em Gel de Ágar
Seres Humanos
Camundongos
Células NIH 3T3
Projetos Piloto
Reação em Cadeia da Polimerase
Estatística como Assunto
Sítio de Iniciação de Transcrição
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.1.21.1 (Deoxyribonuclease I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1038/nprot.2017.099


  7 / 6589 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28941814
[Au] Autor:Basher MA; Rahman KM; Jackson PJM; Thurston DE; Fox KR
[Ad] Endereço:Biological Sciences, Life Sciences Building 85, University of Southampton, Southampton SO17 1BJ, UK.
[Ti] Título:Sequence-selective binding of C8-conjugated pyrrolobenzodiazepines (PBDs) to DNA.
[So] Source:Biophys Chem;230:53-61, 2017 Nov.
[Is] ISSN:1873-4200
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:DNA footprinting and melting experiments have been used to examine the sequence-specific binding of C8-conjugates of pyrrolobenzodiazepines (PBDs) and benzofused rings including benzothiophene and benzofuran, which are attached using pyrrole- or imidazole-containing linkers. The conjugates modulate the covalent attachment points of the PBDs, so that they bind best to guanines flanked by A/T-rich sequences on either the 5'- or 3'-side. The linker affects the binding, and pyrrole produces larger changes than imidazole. Melting studies with 14-mer oligonucleotide duplexes confirm covalent attachment of the conjugates, which show a different selectivity to anthramycin and reveal that more than one ligand molecule can bind to each duplex.
[Mh] Termos MeSH primário: Benzodiazepinas/química
DNA/química
Pirróis/química
[Mh] Termos MeSH secundário: Antramicina/química
Antramicina/metabolismo
Sequência de Bases
Benzodiazepinas/metabolismo
Sítios de Ligação
DNA/metabolismo
Pegada de DNA
Desoxirribonuclease I/metabolismo
Guanina/química
Simulação de Dinâmica Molecular
Conformação de Ácido Nucleico
Desnaturação de Ácido Nucleico
Oligonucleotídeos/química
Oligonucleotídeos/metabolismo
Pirróis/metabolismo
Espectrometria de Fluorescência
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oligonucleotides); 0 (Pyrroles); 0 (pyrrolo(2,1-c)(1,4)benzodiazepine); 0WZD9Y66WN (Anthramycin); 12794-10-4 (Benzodiazepines); 5Z93L87A1R (Guanine); 9007-49-2 (DNA); EC 3.1.21.1 (Deoxyribonuclease I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


  8 / 6589 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28911123
[Au] Autor:Lubock NB; Zhang D; Sidore AM; Church GM; Kosuri S
[Ad] Endereço:Department of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, CA, USA.
[Ti] Título:A systematic comparison of error correction enzymes by next-generation sequencing.
[So] Source:Nucleic Acids Res;45(15):9206-9217, 2017 Sep 06.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Gene synthesis, the process of assembling gene-length fragments from shorter groups of oligonucleotides (oligos), is becoming an increasingly important tool in molecular and synthetic biology. The length, quality and cost of gene synthesis are limited by errors produced during oligo synthesis and subsequent assembly. Enzymatic error correction methods are cost-effective means to ameliorate errors in gene synthesis. Previous analyses of these methods relied on cloning and Sanger sequencing to evaluate their efficiencies, limiting quantitative assessment. Here, we develop a method to quantify errors in synthetic DNA by next-generation sequencing. We analyzed errors in model gene assemblies and systematically compared six different error correction enzymes across 11 conditions. We find that ErrASE and T7 Endonuclease I are the most effective at decreasing average error rates (up to 5.8-fold relative to the input), whereas MutS is the best for increasing the number of perfect assemblies (up to 25.2-fold). We are able to quantify differential specificities such as ErrASE preferentially corrects C/G transversions whereas T7 Endonuclease I preferentially corrects A/T transversions. More generally, this experimental and computational pipeline is a fast, scalable and extensible way to analyze errors in gene assemblies, to profile error correction methods, and to benchmark DNA synthesis methods.
[Mh] Termos MeSH primário: Técnicas de Química Sintética/normas
DNA/síntese química
Genes Sintéticos
Sequenciamento de Nucleotídeos em Larga Escala
[Mh] Termos MeSH secundário: Benchmarking
DNA/genética
Desoxirribonuclease I/genética
Desoxirribonuclease I/metabolismo
Proteínas de Escherichia coli/genética
Proteínas de Escherichia coli/metabolismo
Proteína MutS de Ligação de DNA com Erro de Pareamento/genética
Proteína MutS de Ligação de DNA com Erro de Pareamento/metabolismo
Oligodesoxirribonucleotídeos/química
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Escherichia coli Proteins); 0 (Oligodeoxyribonucleotides); 9007-49-2 (DNA); EC 3.1.21.1 (Deoxyribonuclease I); EC 3.6.1.3 (MutS DNA Mismatch-Binding Protein); EC 3.6.1.3 (MutS protein, E coli)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx691


  9 / 6589 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28732013
[Au] Autor:Luo M; Yang S; Li X; Liu P; Xue J; Zhou X; Su K; Xu X; Qing Y; Qiu J; Li Y
[Ad] Endereço:School of Public Health and Management, Chongqing Medical University, Chongqing, China.
[Ti] Título:The KP1_4563 gene is regulated by the cAMP receptor protein and controls type 3 fimbrial function in Klebsiella pneumoniae NTUH-K2044.
[So] Source:PLoS One;12(7):e0180666, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Klebsiella pneumoniae (K. pneumoniae) is an opportunistic pathogen that can adhere to host cells or extracellular matrix via type 1 and type 3 fimbriae. KP1_4563 is a gene encoding a hypothetical protein in K. pneumoniae NTUH-K2044. KP1_4563 is located between the type 1 and type 3 fimbrial gene clusters and is likely associated with fimbrial function given its putative conserved domains of unknown function (DUF1471). Cyclic AMP receptor protein (CRP) regulates virulence-related gene expression and is a crucial transcriptional regulator in many bacteria. The predicted DNA recognition motif of CRP is present in the KP1_4563 promoter region. This study aimed to investigate the function of KP1_4563 in fimbriae and its transcriptional regulation mechanism by CRP. We generated Kp-Δ4563 mutant and complementation strains. We utilized phenotype and adhesion assays to evaluate the role of KP1_4563 in fimbriae. We conducted quantitative RT-PCR (qRT-PCR), LacZ fusion, electrophoretic mobility shift, and DNase I footprinting assays to study the transcriptional regulation of KP1_4563 gene by CRP. We found that KP1_4563 negatively regulates the function of type 3 fimbriae. Compared with NTUH-K2044, the absence of KP1_4563 enhanced the ability of Kp-Δ4563 to adhere to A549 cells. CRP negatively regulates KP1_4563 by directly binding to its promoter region. KP1_4563 plays an important role in type 3 fimbrial function. This novel insight will assist in the development of strategies for preventing K. pneumoniae infection.
[Mh] Termos MeSH primário: Proteína Receptora de AMP Cíclico/metabolismo
Proteínas de Fímbrias/metabolismo
Klebsiella pneumoniae/genética
Klebsiella pneumoniae/metabolismo
[Mh] Termos MeSH secundário: Aderência Bacteriana/fisiologia
Pegada de DNA
Desoxirribonuclease I/metabolismo
Ensaio de Desvio de Mobilidade Eletroforética
Escherichia coli
Regulação da Expressão Gênica/fisiologia
Testes de Hemaglutinação
Óperon Lac
Mananas/química
Fenótipo
Reação em Cadeia da Polimerase em Tempo Real
Saccharomyces cerevisiae
Deleção de Sequência
Transcrição Genética/fisiologia
beta-Galactosidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic AMP Receptor Protein); 0 (Mannans); 147680-16-8 (Fimbriae Proteins); EC 3.1.21.1 (Deoxyribonuclease I); EC 3.2.1.23 (beta-Galactosidase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180666


  10 / 6589 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28686857
[Au] Autor:Shooshtari P; Huang H; Cotsapas C
[Ad] Endereço:Department of Neurology, Yale School of Medicine, New Haven, CT 06511, USA; Program in Medical and Population Genetics and Stanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA.
[Ti] Título:Integrative Genetic and Epigenetic Analysis Uncovers Regulatory Mechanisms of Autoimmune Disease.
[So] Source:Am J Hum Genet;101(1):75-86, 2017 Jul 06.
[Is] ISSN:1537-6605
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genome-wide association studies in autoimmune and inflammatory diseases (AID) have uncovered hundreds of loci mediating risk. These associations are preferentially located in non-coding DNA regions and in particular in tissue-specific DNase I hypersensitivity sites (DHSs). While these analyses clearly demonstrate the overall enrichment of disease risk alleles on gene regulatory regions, they are not designed to identify individual regulatory regions mediating risk or the genes under their control, and thus uncover the specific molecular events driving disease risk. To do so we have departed from standard practice by identifying regulatory regions which replicate across samples and connect them to the genes they control through robust re-analysis of public data. We find significant evidence of regulatory potential in 78/301 (26%) risk loci across nine autoimmune and inflammatory diseases, and we find that individual genes are targeted by these effects in 53/78 (68%) of these. Thus, we are able to generate testable mechanistic hypotheses of the molecular changes that drive disease risk.
[Mh] Termos MeSH primário: Doenças Autoimunes/genética
Epigênese Genética
Sequências Reguladoras de Ácido Nucleico/genética
[Mh] Termos MeSH secundário: Alelos
Cromossomos Humanos Par 6/genética
Desoxirribonuclease I/metabolismo
Loci Gênicos
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Inflamação/genética
Especificidade de Órgãos/genética
Mapeamento Físico do Cromossomo
Reprodutibilidade dos Testes
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.1.21.1 (Deoxyribonuclease I)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE



página 1 de 659 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