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  1 / 163 MEDLINE  
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[PMID]:27214048
[Au] Autor:Chavez A; Tuttle M; Pruitt BW; Ewen-Campen B; Chari R; Ter-Ovanesyan D; Haque SJ; Cecchi RJ; Kowal EJK; Buchthal J; Housden BE; Perrimon N; Collins JJ; Church G
[Ad] Endereço:Wyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, Massachusetts, USA.
[Ti] Título:Comparison of Cas9 activators in multiple species.
[So] Source:Nat Methods;13(7):563-567, 2016 Jul.
[Is] ISSN:1548-7105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Several programmable transcription factors exist based on the versatile Cas9 protein, yet their relative potency and effectiveness across various cell types and species remain unexplored. Here, we compare Cas9 activator systems and examine their ability to induce robust gene expression in several human, mouse, and fly cell lines. We also explore the potential for improved activation through the combination of the most potent activator systems, and we assess the role of cooperativity in maximizing gene expression.
[Mh] Termos MeSH primário: Proteínas Associadas a CRISPR/metabolismo
Drosophila melanogaster/metabolismo
Transativadores/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Drosophila melanogaster/genética
Genes vpr
Engenharia Genética
Seres Humanos
Camundongos
Fatores de Transcrição/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRISPR-Associated Proteins); 0 (Trans-Activators); 0 (Transcription Factors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160524
[St] Status:MEDLINE
[do] DOI:10.1038/nmeth.3871


  2 / 163 MEDLINE  
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[PMID]:26160407
[Au] Autor:Rawson JM; Landman SR; Reilly CS; Mansky LM
[Ad] Endereço:Institute for Molecular Virology, University of Minnesota, Minneapolis, MN, USA. rawso018@umn.edu.
[Ti] Título:HIV-1 and HIV-2 exhibit similar mutation frequencies and spectra in the absence of G-to-A hypermutation.
[So] Source:Retrovirology;12:60, 2015 Jul 10.
[Is] ISSN:1742-4690
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Human immunodeficiency virus type 2 (HIV-2) is often distinguished clinically by lower viral loads, reduced transmissibility, and longer asymptomatic periods than for human immunodeficiency virus type 1 (HIV-1). Differences in the mutation frequencies of HIV-1 and HIV-2 have been hypothesized to contribute to the attenuated progression of HIV-2 observed clinically. RESULTS: To address this hypothesis, we performed Illumina sequencing of multiple amplicons prepared from cells infected with HIV-1 or HIV-2, resulting in ~4.7 million read pairs and the identification of ~200,000 mutations after data processing. We observed that: (1) HIV-2 displayed significantly lower total mutation, substitution, and transition mutation frequencies than that of HIV-1, along with a mutation spectrum markedly less biased toward G-to-A transitions, (2) G-to-A hypermutation consistent with the activity of APOBEC3 proteins was observed for both HIV-1 and HIV-2 despite the presence of Vif, (3) G-to-A hypermutation was significantly higher for HIV-1 than for HIV-2, and (4) HIV-1 and HIV-2 total mutation frequencies were not significantly different in the absence of G-to-A hypermutants. CONCLUSIONS: Taken together, these data demonstrate that HIV-2 exhibits a distinct mutational spectrum and a lower mutation frequency relative to HIV-1. However, the observed differences were primarily due to reduced levels of G-to-A hypermutation for HIV-2. These findings suggest that HIV-2 may be less susceptible than HIV-1 to APOBEC3-mediated hypermutation, but that the fidelities of other mutational sources (such as reverse transcriptase) are relatively similar for HIV-1 and HIV-2. Overall, these data imply that differences in replication fidelity are likely not a major contributing factor to the unique clinical features of HIV-2 infection.
[Mh] Termos MeSH primário: Infecções por HIV/virologia
HIV-1/genética
HIV-2/genética
Taxa de Mutação
Mutação Puntual
Replicação Viral/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Citosina Desaminase/genética
Genes vpr
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Análise de Sequência de DNA
Produtos do Gene vif do Vírus da Imunodeficiência Humana/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (vif Gene Products, Human Immunodeficiency Virus); EC 3.5.4.1 (APOBEC3 protein, human); EC 3.5.4.1 (Cytosine Deaminase)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150711
[St] Status:MEDLINE
[do] DOI:10.1186/s12977-015-0180-6


  3 / 163 MEDLINE  
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[PMID]:25264057
[Au] Autor:Doi N; Adachi A; Nomaguchi M
[Ad] Endereço:Department of Microbiology, Institute of Health Biosciences, the University of Tokushima Graduate School.
[Ti] Título:Growth properties of macaque-tropic HIV-1 clones carrying vpr/vpx genes derived from simian immunodeficiency viruses in place of their vpr regions.
[So] Source:J Med Invest;61(3-4):374-9, 2014.
[Is] ISSN:1349-6867
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:We have previously generated a macaque-tropic human immunodeficiency virus type 1 (HIV-1mt) clone designated MN4/LSDQgtu by genetic manipulation from a parental virus that replicates poorly in rhesus macaque cells. In rhesus cell line M1.3S and peripheral blood mononuclear cells (PBMCs), MN4/LSDQgtu grows comparably to a standard simian immunodeficiency virus clone derived from the rhesus macaque (SIVmac239) that can induce the acquired immunodeficiency syndrome (AIDS) in the animals. In this study, we further modified the Vpr-coding region of MN4/LSDQgtu genome by introducing vpr gene of an SIV clone from the greater spot-nosed monkey (SIVgsn166) or vpx gene of SIVmac239 to generate four new clones for determining functional importance of the central genomic area. Furthermore, two clones with an additional Gag-p6 mutation were made to ensure the virion-packaging of Vpx. In addition, accessory gene mutant clones of MN4/LSDQgtu with a frame-shift mutation, including a vpr mutant, were constructed and their growth properties were examined. Infection experiments showed that newly constructed viruses all grew poorly to various degrees in M1.3S cells, relative to MN4/LSDQgtu. Together with the previous data, our results here show that vpr/vpx gene in the appropriate context of HIV-1 genome is critical for viral growth ability.
[Mh] Termos MeSH primário: Genes vpr/fisiologia
HIV-1/crescimento & desenvolvimento
Vírus da Imunodeficiência Símia/genética
Proteínas Virais Reguladoras e Acessórias/genética
[Mh] Termos MeSH secundário: Animais
HIV-1/genética
Seres Humanos
Macaca mulatta
Proteínas Virais Reguladoras e Acessórias/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (VPX protein, Simian immunodeficiency virus); 0 (Viral Regulatory and Accessory Proteins)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:140929
[Lr] Data última revisão:
140929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140930
[St] Status:MEDLINE


  4 / 163 MEDLINE  
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[PMID]:24368332
[Au] Autor:Lucas SJ; Bastas K; Budak H
[Ad] Endereço:Sabanci University, Faculty of Engineering & Natural Sciences, Istanbul, Turkey.
[Ti] Título:Exploring the interaction between small RNAs and R genes during Brachypodium response to Fusarium culmorum infection.
[So] Source:Gene;536(2):254-64, 2014 Feb 25.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The present study aims to investigate small RNA interactions with putative disease response genes in the model grass species Brachypodium distachyon. The fungal pathogen Fusarium culmorum (Fusarium herein) and phytohormone salicylic acid treatment were used to induce the disease response in Brachypodium. Initially, 121 different putative disease response genes were identified using bioinformatic and homology based approaches. Computational prediction was used to identify 33 candidate new miRNA coding sequences, of which 9 were verified by analysis of small RNA sequence libraries. Putative Brachypodium miRNA target sites were identified in the disease response genes, and a subset of which were screened for expression and possible miRNA interactions in 5 different Brachypodium lines infected with Fusarium. An NBS-LRR family gene, 1g34430, was polymorphic among the lines, forming two major genotypes, one of which has its miRNA target sites deleted, resulting in altered gene expression during infection. There were siRNAs putatively involved in regulation of this gene, indicating a role of small RNAs in the B. distachyon disease response.
[Mh] Termos MeSH primário: Brachypodium/genética
Fusariose/genética
Genes vpr/genética
MicroRNAs/genética
RNA Interferente Pequeno/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Brachypodium/microbiologia
Biologia Computacional/métodos
Fusariose/microbiologia
Fusarium
Dados de Sequência Molecular
Polimorfismo Genético/genética
Alinhamento de Sequência
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Small Interfering)
[Em] Mês de entrada:1404
[Cu] Atualização por classe:140114
[Lr] Data última revisão:
140114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131226
[St] Status:MEDLINE


  5 / 163 MEDLINE  
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[PMID]:24324167
[Au] Autor:Harris CJ; Slootweg EJ; Goverse A; Baulcombe DC
[Ad] Endereço:Department of Plant Sciences, University of Cambridge, Cambridge CB2 3EA, United Kingdom.
[Ti] Título:Stepwise artificial evolution of a plant disease resistance gene.
[So] Source:Proc Natl Acad Sci U S A;110(52):21189-94, 2013 Dec 24.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genes encoding plant nucleotide-binding leucine-rich repeat (NB-LRR) proteins confer dominant resistance to diverse pathogens. The wild-type potato NB-LRR protein Rx confers resistance against a single strain of potato virus X (PVX), whereas LRR mutants protect against both a second PVX strain and the distantly related poplar mosaic virus (PopMV). In one of the Rx mutants there was a cost to the broad-spectrum resistance because the response to PopMV was transformed from a mild disease on plants carrying wild-type Rx to a trailing necrosis that killed the plant. To explore the use of secondary mutagenesis to eliminate this cost of broad-spectrum resistance, we performed random mutagenesis of the N-terminal domains of this broad-recognition version of Rx and isolated four mutants with a stronger response against the PopMV coat protein due to enhanced activation sensitivity. These mutations are located close to the nucleotide-binding pocket, a highly conserved structure that likely controls the "switch" between active and inactive NB-LRR conformations. Stable transgenic plants expressing one of these versions of Rx are resistant to the strains of PVX and the PopMV that previously caused trailing necrosis. We conclude from this work that artificial evolution of NB-LRR disease resistance genes in crops can be enhanced by modification of both activation and recognition phases, to both accentuate the positive and eliminate the negative aspects of disease resistance.
[Mh] Termos MeSH primário: Engenharia Genética/métodos
Imunidade Inata/genética
Proteínas de Plantas/genética
Proteínas/genética
Tabaco/imunologia
[Mh] Termos MeSH secundário: Agricultura/métodos
Agrobacterium tumefaciens
Substituição de Aminoácidos/genética
Western Blotting
Proteínas do Capsídeo/genética
Carlavirus/genética
Genes vpr/genética
Proteínas de Plantas/imunologia
Plantas Geneticamente Modificadas
Proteínas/imunologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Tabaco/genética
Tabaco/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Capsid Proteins); 0 (Plant Proteins); 0 (Proteins); 0 (leucine-rich repeat proteins)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131211
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1311134110


  6 / 163 MEDLINE  
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[PMID]:22936397
[Au] Autor:Zhu S; Duwal A; Su Q; Vossen JH; Visser RG; Jacobsen E
[Ad] Endereço:Wageningen UR Plant Breeding, Wageningen University and Research Center, 6708 PB, Wageningen, The Netherlands. suxian.zhu@wur.nl
[Ti] Título:Vector integration in triple R gene transformants and the clustered inheritance of resistance against potato late blight.
[So] Source:Transgenic Res;22(2):315-25, 2013 Apr.
[Is] ISSN:1573-9368
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Genetic transformation with resistance (R) genes is expected to enhance resistance durability against pathogens, especially for potato, a vegetatively propagated crop with tetrasomic inheritance and a long-term breeding program. In this study, 128 potato transformants were analysed for the presence of vector T-DNA genes, borders and backbone sequences. They were harvested after transformation using a construct containing neomycin phosphotransferase II (nptII) and three R genes against potato late blight (Phytophthora infestans). Our analysis revealed that 45 % of the R gene-containing transformants possessed a low T-DNA copy number, without the integration of vector backbone and borders. The integration of vector backbone sequences was characterized using eight genes, and backbone gene tetA was selected for the early prediction of plants with backbone sequence integration. Three transformants, two plants harbouring one T-DNA copy and one plant harbouring three T-DNA copies, were crossed with susceptible cv. Katahdin. Based on our results, we conclude that all four T-DNA genes were inherited as one cluster and segregated in a Mendelian fashion. The three T-DNA inserts from the transformant harbouring three T-DNA copies were statistically proven to be un-linked and inherited into the offspring plants independently. All of the R genes were functionally expressed in the offspring plants as in their parental transformants. This functional gene stacking has important implications towards achieving more durable resistance against potato late blight.
[Mh] Termos MeSH primário: Resistência à Doença/genética
Genes vpr
Plantas Geneticamente Modificadas
Solanum tuberosum/genética
[Mh] Termos MeSH secundário: DNA Bacteriano/genética
DNA Bacteriano/isolamento & purificação
Vetores Genéticos
Phytophthora infestans/genética
Phytophthora infestans/patogenicidade
Doenças das Plantas/genética
Solanum tuberosum/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Bacterial); 0 (T-DNA)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120901
[St] Status:MEDLINE
[do] DOI:10.1007/s11248-012-9644-9


  7 / 163 MEDLINE  
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[PMID]:23189821
[Au] Autor:Shimura H; Masuta C
[Ad] Endereço:Graduate School of Agriculture, Hokkaido University.
[Ti] Título:[RNA silencing and viral disease induction in plants].
[So] Source:Uirusu;62(1):19-26, 2012 Jun.
[Is] ISSN:0042-6857
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:RNA silencing plays an important role in plant resistance against viruses. As a counter-defense against RNA silencing, plant viruses have evolved RNA silencing suppressors (RSSs). RNA silencing is likely to play a major role in disease development. For example, RSSs have been found to disturb the gene expression controlled by miRNAs in plant tissue and organ development, resulting in plant malformation. Mosaic symptoms, which are typical in virus-infected plants, are actually a consequence of local arms race between host RNA silencing and viral RSSs. In addition, recent studies revealed that viral siRNAs could induce RNA silencing even against a certain host gene and thus a disease symptom through a complementary (homologous) sequence coincidentally found between virus and host gene. RNA silencing is the principal mediator of viral pathogenicity and disease induction and therefore should be exploited as a powerful tool for engineering virus resistance in plants as well as in animals.
[Mh] Termos MeSH primário: Doenças das Plantas/virologia
Vírus de Plantas/patogenicidade
Plantas/genética
Interferência de RNA/fisiologia
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica de Plantas
Genes vpr
MicroRNAs/fisiologia
Desenvolvimento Vegetal
Doenças das Plantas/genética
Vírus de Plantas/fisiologia
Plantas/embriologia
RNA Interferente Pequeno/fisiologia
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Small Interfering)
[Em] Mês de entrada:1304
[Cu] Atualização por classe:121129
[Lr] Data última revisão:
121129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121130
[St] Status:MEDLINE


  8 / 163 MEDLINE  
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[PMID]:22138483
[Au] Autor:Fourati S; Malet I; Guenzel CA; Soulie C; Maidou-Peindara P; Morand-Joubert L; Wirden M; Sayon S; Peytavin G; Simon A; Katlama C; Benichou S; Calvez V; Marcelin AG
[Ad] Endereço:Université Pierre et Marie Curie, Paris, France. slim.fourati@psl.aphp.fr
[Ti] Título:E17A mutation in HIV-1 Vpr confers resistance to didanosine in association with thymidine analog mutations.
[So] Source:Antiviral Res;93(1):167-74, 2012 Jan.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: HIV-1 accessory Vpr protein is involved in the reverse transcription process and has been shown to modulate the virus mutation rate. This process may play a role in the kinetics of appearance of drug resistance mutations under antiretroviral treatment. METHODS: Vpr sequences were analyzed from plasma viruses derived from 97 HIV-1-infected individuals failing antiretroviral treatment and 63 antiretroviral-naïve patients. Vpr genetic variability was analyzed for association with specific drug treatment and drug resistance mutations. Biological and virological experiments were employed to characterize a mutation in Vpr found to be associated with virological failure. RESULTS: E17A mutation located in the first α-helix of Vpr was more prevalent in HAART-treated individuals compared to untreated individuals. E17A was associated with thymidine analog mutations (TAMs) in reverse transcriptase M41L, L210W and T215Y and with the use of didanosine in the patients' treatment histories. E17A had no impact on the biochemical and functional properties of Vpr, and did not affect kinetics of replication of wild-type or TAMs-containing viruses. However, its association with TAMs and the use of didanosine was consistent with phenotypic susceptibility assays showing a significant 3-fold decrease in didanosine susceptibility of viruses harboring Vpr E17A combined with TAMs compared to viruses harboring TAMs alone. CONCLUSION: These findings highlight a novel role of Vpr in HIV-1 drug resistance. Vpr E17A confers resistance to didanosine when associated with TAMs. Whether Vpr E17A facilitates excision of didanosine is still to be determined.
[Mh] Termos MeSH primário: Fármacos Anti-HIV/farmacologia
Didanosina/farmacologia
HIV-1/efeitos dos fármacos
HIV-1/genética
Mutação
Produtos do Gene vpr do Vírus da Imunodeficiência Humana/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Fármacos Anti-HIV/uso terapêutico
Didanosina/uso terapêutico
Farmacorresistência Viral/genética
Feminino
Genes vpr
Células HEK293
Infecções por HIV/tratamento farmacológico
Infecções por HIV/virologia
Células HeLa
Seres Humanos
Masculino
Testes de Sensibilidade Microbiana
Meia-Idade
Dados de Sequência Molecular
Polimorfismo Genético
Transporte Proteico
Timidina/análogos & derivados
Timidina/genética
Replicação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (vpr Gene Products, Human Immunodeficiency Virus); 0 (vpr protein, Human immunodeficiency virus 1); K3GDH6OH08 (Didanosine); VC2W18DGKR (Thymidine)
[Em] Mês de entrada:1204
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111206
[St] Status:MEDLINE
[do] DOI:10.1016/j.antiviral.2011.11.008


  9 / 163 MEDLINE  
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[PMID]:22310812
[Au] Autor:Neogi U; Sood V; Ronsard L; Singh J; Lata S; Ramachandran VG; Das S; Wanchu A; Banerjea AC
[Ad] Endereço:Department of Virology, National Institute of Immunology, New Delhi, India.
[Ti] Título:Genetic architecture of HIV-1 genes circulating in north India & their functional implications.
[So] Source:Indian J Med Res;134(6):769-78, 2011 Dec.
[Is] ISSN:0971-5916
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:This review presents data on genetic and functional analysis of some of the HIV-1 genes derived from HIV-1 infected individuals from north India (Delhi, Punjab and Chandigarh). We found evidence of novel B/C recombinants in HIV-1 LTR region showing relatedness to China/Myanmar with 3 copies of Nfκb sites; B/C/D mosaic genomes for HIV-1 Vpr and novel B/C Tat. We reported appearance of a complex recombinant form CRF_02AG of HIV-1 envelope sequences which is predominantly found in Central/Western Africa. Also one Indian HIV-1 envelope subtype C sequence suggested exclusive CXCR4 co-receptor usage. This extensive recombination, which is observed in about 10 per cent HIV-1 infected individuals in the Vpr genes, resulted in remarkably altered functions when compared with prototype subtype B Vpr. The Vpu C was found to be more potent in causing apoptosis when compared with Vpu B when analyzed for subG1 DNA content. The functional implications of these changes as well as in other genes of HIV-1 are discussed in detail with possible implications for subtype-specific pathogenesis highlighted.
[Mh] Termos MeSH primário: Genes vpr/genética
Variação Genética
Infecções por HIV/epidemiologia
Infecções por HIV/virologia
Repetição Terminal Longa de HIV/genética
HIV-1/genética
Recombinação Genética/genética
Produtos do Gene env do Vírus da Imunodeficiência Humana/genética
[Mh] Termos MeSH secundário: Seres Humanos
Índia/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (env Gene Products, Human Immunodeficiency Virus)
[Em] Mês de entrada:1206
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120208
[St] Status:MEDLINE
[do] DOI:10.4103/0971-5916.92624


  10 / 163 MEDLINE  
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[PMID]:21871425
[Au] Autor:Kumar D; Salhan D; Magoon S; Torri DD; Sayeneni S; Sagar A; Bandhlish A; Malhotra A; Chander PN; Singhal PC
[Ad] Endereço:Department of Medicine, North Shore-Long Island Jewish Health System, New Hyde Park, New York, NY 11021, USA.
[Ti] Título:Adverse host factors exacerbate occult HIV-associated nephropathy.
[So] Source:Am J Pathol;179(4):1681-92, 2011 Oct.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the present study, we hypothesized that HIV-1-induced occult HIV-associated nephropathy (HIVAN) would become apparent in the presence of adverse host factors. To test our hypothesis, Vpr mice (which display doxycycline-dependent Vpr expression in podocytes) with two, three, and four copies of the angiotensinogen (Agt) gene (Vpr-Agt-2, Vpr-Agt-3, and Vpr-Agt-4) were administered doxycycline for 3 weeks (to develop clinically occult HIVAN) followed by doxycycline-free water during the next 3 weeks. Subsequently, renal biomarkers were measured, and kidneys were harvested for renal histology. Vpr-Agt-2 developed neither proteinuria nor elevated blood pressure, and displayed minimal glomerular and tubular lesions only, without any microcyst formation. Vpr-Agt-3 showed mild glomerular and tubular lesions and microcyst formation, whereas Vpr-Agt-4 showed moderate proteinuria, hypertension, glomerular sclerosis, tubular dilation, microcysts, and expression of epithelial mesenchymal transition markers. Vpr-Agt-4 not only displayed enhanced renal tissue expression of Agt, renin, and angiotensin-converting enzyme, but also had higher renal tissue concentrations of angiotensin II. Moreover, renal cells in Vpr-Agt-4 showed enhanced expression of transforming growth factor-ß, connective tissue growth factor, and vascular endothelial growth factor. These findings indicate that adverse host factors, such as the activation of the renin-angiotensin system, promote the progression of occult HIVAN to apparent HIVAN.
[Mh] Termos MeSH primário: Nefropatia Associada a AIDS/patologia
Interações Hospedeiro-Patógeno
[Mh] Termos MeSH secundário: Nefropatia Associada a AIDS/complicações
Nefropatia Associada a AIDS/fisiopatologia
Angiotensina II/metabolismo
Angiotensinogênio/genética
Angiotensinogênio/metabolismo
Animais
Biomarcadores/metabolismo
Pressão Sanguínea/efeitos dos fármacos
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Doxiciclina/farmacologia
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Feminino
Dosagem de Genes/genética
Genes vpr
Interações Hospedeiro-Patógeno/efeitos dos fármacos
Rim/efeitos dos fármacos
Rim/enzimologia
Rim/patologia
Masculino
Camundongos
Camundongos Transgênicos
Peptidil Dipeptidase A/metabolismo
Fenótipo
Proteinúria/complicações
Proteinúria/patologia
Proteinúria/fisiopatologia
Renina/metabolismo
Sistema Renina-Angiotensina/efeitos dos fármacos
Fator de Crescimento Transformador beta/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (Ctgf protein, mouse); 0 (Transforming Growth Factor beta); 0 (Vascular Endothelial Growth Factor A); 11002-13-4 (Angiotensinogen); 11128-99-7 (Angiotensin II); 139568-91-5 (Connective Tissue Growth Factor); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.23.15 (Renin); N12000U13O (Doxycycline)
[Em] Mês de entrada:1201
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:110830
[St] Status:MEDLINE
[do] DOI:10.1016/j.ajpath.2011.06.013



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