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  1 / 573 MEDLINE  
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[PMID]:27575477
[Au] Autor:Win NN; Ito T; Win YY; Ngwe H; Kodama T; Abe I; Morita H
[Ad] Endereço:Institute of Natural Medicine, University of Toyama, 2630-Sugitani, Toyama 930-0194, Japan; Department of Chemistry, University of Yangon, Yangon 11041, Myanmar. Electronic address: nwetwin2012@gmail.com.
[Ti] Título:Quassinoids: Viral protein R inhibitors from Picrasma javanica bark collected in Myanmar for HIV infection.
[So] Source:Bioorg Med Chem Lett;26(19):4620-4624, 2016 10 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Viral protein R (Vpr) is an accessory protein that plays important roles in the viral pathogenesis of Human Immunodeficiency Virus-1 (HIV-1). An assay for anti-Vpr activity, using TREx-HeLa-Vpr cells, is a promising strategy to discover Vpr inhibitors. The anti-Vpr assay revealed that the CHCl3-soluble extract of Picrasma javanica bark possesses potent anti-Vpr activity. Furthermore, studies of quassinoids (1-15) previously isolated from the extract demonstrated that all of the tested quassinoids exhibit anti-Vpr activity. Among the tested compounds, javanicin I (15) exhibited the most potent anti-Vpr activity ((***)p <0.001) in comparing with that of the positive control, damnacanthal. The structure-activity relationships of the active quassinoids suggested that the presence of a methyl group at C-13 in the 2,12,14-triene-1,11,16-trione-2,12-dimethoxy-18-norpicrasane quassinoids is the important factor for the potent inhibitory effect in TREx-HeLa-Vpr cells.
[Mh] Termos MeSH primário: Fármacos Anti-HIV/uso terapêutico
Produtos do Gene vpr/antagonistas & inibidores
Infecções por HIV/tratamento farmacológico
Picrasma/química
Casca de Planta/química
Quassinas/farmacologia
[Mh] Termos MeSH secundário: Fármacos Anti-HIV/química
Fármacos Anti-HIV/farmacologia
Células HeLa
Seres Humanos
Mianmar
Quassinas/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (Gene Products, vpr); 0 (Quassins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE


  2 / 573 MEDLINE  
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[PMID]:27181198
[Au] Autor:Miyatake H; Sanjoh A; Murakami T; Murakami H; Matsuda G; Hagiwara K; Yokoyama M; Sato H; Miyamoto Y; Dohmae N; Aida Y
[Ad] Endereço:Nano Medical Engineering Laboratory, RIKEN, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan. Electronic address: miyatake@riken.jp.
[Ti] Título:Molecular Mechanism of HIV-1 Vpr for Binding to Importin-α.
[So] Source:J Mol Biol;428(13):2744-57, 2016 Jul 03.
[Is] ISSN:1089-8638
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Viral protein R (Vpr) is an accessory gene product of human immunodeficiency virus type 1 (HIV-1) that plays multiple important roles associated with viral replication. Structural studies using NMR have revealed that Vpr consists of three α-helices and contains flexible N- and C-termini. However, the molecular mechanisms associated with Vpr function have not been elucidated. To investigate Vpr multifunctionality, we performed an X-ray crystallographic study of Vpr complexes containing importin-α, a known Vpr binding partner present in host cells. Elucidation of the crystal structure revealed that the flexible C-terminus changes its conformation to a twisted ß-turn via an induced-fit mechanism, enabling binding to a minor nuclear localization signal (NLS) site of importin-α. The Vpr C-terminus can also bind with major NLS sites of importin-α in an extended conformation in different ways. These results, which represent the first reported crystallographic analysis of Vpr, demonstrate the multifunctional aspects that enable Vpr interaction with a variety of cellular proteins.
[Mh] Termos MeSH primário: Produtos do Gene vpr/metabolismo
HIV-1/metabolismo
Ligação Proteica/fisiologia
alfa Carioferinas/metabolismo
Produtos do Gene vpr do Vírus da Imunodeficiência Humana/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Núcleo Celular/metabolismo
Seres Humanos
Sinais de Localização Nuclear/metabolismo
Replicação Viral/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, vpr); 0 (Nuclear Localization Signals); 0 (alpha Karyopherins); 0 (vpr Gene Products, Human Immunodeficiency Virus)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160517
[St] Status:MEDLINE


  3 / 573 MEDLINE  
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[PMID]:26916438
[Au] Autor:Win NN; Ito T; Matsui T; Aimaiti S; Kodama T; Ngwe H; Okamoto Y; Tanaka M; Asakawa Y; Abe I; Morita H
[Ad] Endereço:Institute of Natural Medicine, University of Toyama, 2630-Sugitani, Toyama 930-0194, Japan; Department of Chemistry, University of Yangon, Yangon 11041, Myanmar.
[Ti] Título:Isopimarane diterpenoids from Kaempferia pulchra rhizomes collected in Myanmar and their Vpr inhibitory activity.
[So] Source:Bioorg Med Chem Lett;26(7):1789-93, 2016 Apr 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Viral protein R (Vpr), an accessory gene of HIV-1, plays important roles in viral pathogenesis. Screening of Myanmar medicinal plants that are popular as primary treatments for HIV/AIDS and for HIV-related problems revealed the potent anti-Vpr activity of the CHCl3-soluble extract of Kaempferia pulchra rhizomes, in comparison with that of the positive control, damnacanthal. Fractionation of the active CHCl3-soluble extract led to the identification of 30 isopimarane diterpenoids, including kaempulchraols A-W (1-23). All isolates were assayed for anti-Vpr activity against TREx-HeLa-Vpr cells, in which Vpr expression is tightly regulated by tetracycline. Kaempulchraols B (2), D (4), G (7), Q (17), T (20), U (21), and W (23) exhibited potent anti-Vpr activity, at concentrations ranging from 1.56 to 6.25µM. The structure-activity relationships of the active kaempulchraols suggested that the presence of a hydroxy group at C-14 in an isopimara-8(9),15-diene skeleton and the presence of an acetoxy group at C-1 or C-7 in an isopimara-8(14),15-diene skeleton are the critical factors for the inhibitory effects against TREx-HeLa-Vpr cells.
[Mh] Termos MeSH primário: Fármacos Anti-HIV/química
Fármacos Anti-HIV/farmacologia
Diterpenos/química
Diterpenos/farmacologia
Produtos do Gene vpr/antagonistas & inibidores
HIV-1/efeitos dos fármacos
Zingiberaceae/química
[Mh] Termos MeSH secundário: Fármacos Anti-HIV/isolamento & purificação
Diterpenos/isolamento & purificação
Produtos do Gene vpr/metabolismo
Infecções por HIV/tratamento farmacológico
Infecções por HIV/virologia
HIV-1/metabolismo
Células HeLa
Seres Humanos
Rizoma/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (Diterpenes); 0 (Gene Products, vpr)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160227
[St] Status:MEDLINE


  4 / 573 MEDLINE  
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[PMID]:26270987
[Au] Autor:Gangwani MR; Kumar A
[Ad] Endereço:Division of Pharmacology and Toxicology, School of Pharmacy, University of Missouri, Kansas City, Missouri, United States of America.
[Ti] Título:Multiple Protein Kinases via Activation of Transcription Factors NF-κB, AP-1 and C/EBP-δ Regulate the IL-6/IL-8 Production by HIV-1 Vpr in Astrocytes.
[So] Source:PLoS One;10(8):e0135633, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neurocognitive impairments affect a substantial population of HIV-1 infected individuals despite the success of anti-retroviral therapy in controlling viral replication. Astrocytes are emerging as a crucial cell type that might be playing a very important role in the persistence of neuroinflammation seen in patients suffering from HIV-1 associated neurocognitive disorders. HIV-1 viral proteins including Vpr exert neurotoxicity through direct and indirect mechanisms. Induction of IL-8 in microglial cells has been shown as one of the indirect mechanism through which Vpr reduces neuronal survival. We show that HIV-1 Vpr induces IL-6 and IL-8 in astrocytes in a time-dependent manner. Additional experiments utilizing chemical inhibitors and siRNA revealed that HIV-1 Vpr activates transcription factors NF-κB, AP-1 and C/EBP-δ via upstream protein kinases PI3K/Akt, p38-MAPK and Jnk-MAPK leading to the induction of IL-6 and IL-8 in astrocytes. We demonstrate that one of the mechanism for neuroinflammation seen in HIV-1 infected individuals involves induction of IL-6 and IL-8 by Vpr in astrocytes. Understanding the molecular pathways involved in the HIV-1 neuroinflammation would be helpful in the design of adjunct therapy to ameliorate some of the symptoms associated with HIV-1 neuropathogenesis.
[Mh] Termos MeSH primário: Astrócitos/enzimologia
Regulação da Expressão Gênica/fisiologia
Produtos do Gene vpr/metabolismo
HIV-1/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Proteínas Estimuladoras de Ligação a CCAAT/genética
Proteínas Estimuladoras de Ligação a CCAAT/metabolismo
Linhagem Celular
Células Cultivadas
Produtos do Gene vpr/genética
Seres Humanos
Imuno-Histoquímica
Interleucina-6/genética
Interleucina-6/metabolismo
Interleucina-8/genética
Interleucina-8/metabolismo
NF-kappa B/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Transcrição AP-1/genética
Fator de Transcrição AP-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Proteins); 0 (Gene Products, vpr); 0 (Interleukin-6); 0 (Interleukin-8); 0 (NF-kappa B); 0 (Transcription Factor AP-1); 0 (Transcription Factors)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150814
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0135633


  5 / 573 MEDLINE  
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[PMID]:25618414
[Au] Autor:DePaula-Silva AB; Cassiday PA; Chumley J; Bosque A; Monteiro-Filho CM; Mahon CS; Cone KR; Krogan N; Elde NC; Planelles V
[Ad] Endereço:Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, 15 North Medical Drive East #2100, Salt Lake City, UT 84112, USA.
[Ti] Título:Determinants for degradation of SAMHD1, Mus81 and induction of G2 arrest in HIV-1 Vpr and SIVagm Vpr.
[So] Source:Virology;477:10-7, 2015 Mar.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vpr and Vpx are a group of highly related accessory proteins from primate lentiviruses. Despite the high degree of amino acid homology within this group, these proteins can be highly divergent in their functions. In this work, we constructed chimeric and mutant proteins between HIV-1 and SIVagm Vpr in order to better understand the structure-function relationships. We tested these constructs for their abilities to induce G2 arrest in human cells and to degrade agmSAMHD1 and Mus81. We found that the C-terminus of HIV-1 Vpr, when transferred onto SIVagm Vpr, provides the latter with the de novo ability to induce G2 arrest in human cells. We confirmed that HIV-1 Vpr induces degradation of Mus81 although, surprisingly, degradation is independent and genetically separable from Vpr׳s ability to induce G2 arrest.
[Mh] Termos MeSH primário: Ciclo Celular
Proteínas de Ligação a DNA/metabolismo
Endonucleases/metabolismo
Produtos do Gene vpr/metabolismo
HIV-1/fisiologia
Interações Hospedeiro-Patógeno
Proteínas Monoméricas de Ligação ao GTP/metabolismo
Vírus da Imunodeficiência Símia/fisiologia
[Mh] Termos MeSH secundário: Produtos do Gene vpr/genética
Células HeLa
Seres Humanos
Proteólise
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Proteína 1 com Domínio SAM e Domínio HD
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Gene Products, vpr); 0 (Recombinant Proteins); EC 3.1.- (Endonucleases); EC 3.1.- (MUS81 protein, human); EC 3.1.5.- (SAM Domain and HD Domain-Containing Protein 1); EC 3.1.5.- (SAMHD1 protein, human); EC 3.6.5.2 (Monomeric GTP-Binding Proteins)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150126
[St] Status:MEDLINE


  6 / 573 MEDLINE  
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[PMID]:25320300
[Au] Autor:Berger G; Lawrence M; Hué S; Neil SJ
[Ad] Endereço:Department of Infectious Diseases, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
[Ti] Título:G2/M cell cycle arrest correlates with primate lentiviral Vpr interaction with the SLX4 complex.
[So] Source:J Virol;89(1):230-40, 2015 Jan.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: The accessory gene vpr, common to all primate lentiviruses, induces potent G2/M arrest in cycling cells. A recent study showed that human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) mediates this through activation of the SLX4/MUS81/EME1 exonuclease complex that forms part of the Fanconi anemia DNA repair pathway. To confirm these observations, we have examined the G2/M arrest phenotypes of a panel of simian immunodeficiency virus (SIV) Vpr proteins. We show that SIV Vpr proteins differ in their ability to promote cell cycle arrest in human cells. While this is dependent on the DCAF1/DDB1/CUL4 ubiquitin ligase complex, interaction with human DCAF1 does not predict G2/M arrest activity of SIV Vpr in human cells. In all cases, SIV Vpr-mediated cell cycle arrest in human cells correlated with interaction with human SLX4 (huSLX4) and could be abolished by small interfering RNA (siRNA) depletion of any member of the SLX4 complex. In contrast, all but one of the HIV/SIV Vpr proteins tested, including those that lacked activity in human cells, were competent for G2/M arrest in grivet cells. Correspondingly, here cell cycle arrest correlated with interaction with the grivet orthologues of the SLX4 complex, suggesting a level of host adaptation in these interactions. Phylogenetic analyses strongly suggest that G2/M arrest/SLX4 interactions are ancestral activities of primate lentiviral Vpr proteins and that the ability to dysregulate the Fanconi anemia DNA repair pathway is an essential function of Vpr in vivo. IMPORTANCE: The Vpr protein of HIV-1 and related viruses is essential for the virus in vivo. The ability of Vpr to block the cell cycle at mitotic entry is well known, but the importance of this function for viral replication is unclear. Recent data have shown that HIV-1 Vpr targets the Fanconi anemia DNA repair pathway by interacting with and activating an endonuclease complex, SLX4/MUS81/EME1, that processes interstrand DNA cross-links. Here we show that the ability of a panel of SIV Vpr proteins to mediate cell cycle arrest correlates with species-specific interactions with the SLX4 complex in human and primate cells. The results of these studies suggest that the SLX4 complex is a conserved target of primate lentiviral Vpr proteins and that the ability to dysregulate members of the Fanconi anemia DNA repair pathway is essential for HIV/SIV replication in vivo.
[Mh] Termos MeSH primário: Pontos de Checagem do Ciclo Celular
Produtos do Gene vpr/metabolismo
Interações Hospedeiro-Patógeno
Recombinases/metabolismo
Vírus da Imunodeficiência Símia/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Cercopithecinae
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gene Products, vpr); 0 (Recombinases)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141017
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.02307-14


  7 / 573 MEDLINE  
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[PMID]:25169827
[Au] Autor:Widera M; Hillebrand F; Erkelenz S; Vasudevan AA; Münk C; Schaal H
[Ti] Título:A functional conserved intronic G run in HIV-1 intron 3 is critical to counteract APOBEC3G-mediated host restriction.
[So] Source:Retrovirology;11:72, 2014 Aug 29.
[Is] ISSN:1742-4690
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The HIV-1 accessory proteins, Viral Infectivity Factor (Vif) and the pleiotropic Viral Protein R (Vpr) are important for efficient virus replication. While in non-permissive cells an appropriate amount of Vif is critical to counteract APOBEC3G-mediated host restriction, the Vpr-induced G2 arrest sets the stage for highest transcriptional activity of the HIV-1 long terminal repeat. RESULTS: We identified a G run localized deep in the vpr AUG containing intron 3 (GI3-2), which was critical for balanced splicing of both vif and vpr non-coding leader exons. Inactivation of GI3-2 resulted in excessive exon 3 splicing as well as exon-definition mediated vpr mRNA formation. However, in an apparently mutually exclusive manner this was incompatible with recognition of upstream exon 2 and vif mRNA processing. As a consequence, inactivation of GI3-2 led to accumulation of Vpr protein with a concomitant reduction in Vif protein. We further demonstrate that preventing hnRNP binding to intron 3 by GI3-2 mutation diminished levels of vif mRNA. In APOBEC3G-expressing but not in APOBEC3G-deficient T cell lines, mutation of GI3-2 led to a considerable replication defect. Moreover, in HIV-1 isolates carrying an inactivating mutation in GI3-2, we identified an adjacent G-rich sequence (GI3-1), which was able to substitute for the inactivated GI3-2. CONCLUSIONS: The functionally conserved intronic G run in HIV-1 intron 3 plays a major role in the apparently mutually exclusive exon selection of vif and vpr leader exons and hence in vif and vpr mRNA formation. The competition between these exons determines the ability to evade APOBEC3G-mediated antiviral effects due to optimal vif expression.
[Mh] Termos MeSH primário: Citidina Desaminase/metabolismo
Infecções por HIV/virologia
HIV-1/genética
Especificidade de Hospedeiro/genética
Íntrons
[Mh] Termos MeSH secundário: Desaminase APOBEC-3G
Linhagem Celular
Linhagem Celular Tumoral
Citidina Desaminase/genética
Produtos do Gene vpr/genética
Células HEK293
Infecções por HIV/metabolismo
Células HeLa
Seres Humanos
Mutação/genética
Processamento de RNA/genética
RNA Mensageiro/genética
Linfócitos T/metabolismo
Linfócitos T/virologia
Replicação Viral/genética
Produtos do Gene vif do Vírus da Imunodeficiência Humana/genética
Produtos do Gene vpr do Vírus da Imunodeficiência Humana/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, vpr); 0 (RNA, Messenger); 0 (vif Gene Products, Human Immunodeficiency Virus); 0 (vpr Gene Products, Human Immunodeficiency Virus); EC 3.5.4.5 (APOBEC-3G Deaminase); EC 3.5.4.5 (APOBEC3G protein, human); EC 3.5.4.5 (Cytidine Deaminase)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140830
[St] Status:MEDLINE
[do] DOI:10.1186/s12977-014-0072-1


  8 / 573 MEDLINE  
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[PMID]:24912525
[Au] Autor:Liu R; Lin Y; Jia R; Geng Y; Liang C; Tan J; Qiao W
[Ti] Título:HIV-1 Vpr stimulates NF-κB and AP-1 signaling by activating TAK1.
[So] Source:Retrovirology;11:45, 2014 Jun 09.
[Is] ISSN:1742-4690
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The Vpr protein of human immunodeficiency virus type 1 (HIV-1) plays an important role in viral replication. It has been reported that Vpr stimulates the nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) signaling pathways, and thereby regulates viral and host cell gene expression. However, the molecular mechanism behind this function of Vpr is not fully understood. RESULTS: Here, we have identified transforming growth factor-ß-activated kinase 1 (TAK1) as the important upstream signaling molecule that Vpr associates with in order to activate NF-κB and AP-1 signaling. HIV-1 virion-associated Vpr is able to stimulate phosphorylation of TAK1. This activity of Vpr depends on its association with TAK1, since the S79A Vpr mutant lost interaction with TAK1 and was unable to activate TAK1. This association allows Vpr to promote the interaction of TAB3 with TAK1 and increase the polyubiquitination of TAK1, which renders TAK1 phosphorylation. In further support of the key role of TAK1 in this function of Vpr, knockdown of endogenous TAK1 significantly attenuated the ability of Vpr to activate NF-κB and AP-1 as well as the ability to stimulate HIV-1 LTR promoter. CONCLUSIONS: HIV-1 Vpr enhances the phosphorylation and polyubiquitination of TAK1, and as a result, activates NF-κB and AP-1 signaling pathways and stimulates HIV-1 LTR promoter.
[Mh] Termos MeSH primário: Produtos do Gene vpr/metabolismo
HIV-1/fisiologia
MAP Quinase Quinase Quinases/genética
NF-kappa B/metabolismo
Fator de Transcrição AP-1/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal
Linhagem Celular
Linhagem Celular Tumoral
Produtos do Gene vpr/genética
Células HEK293
HIV-1/genética
HIV-1/metabolismo
Células HeLa
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Células Jurkat
MAP Quinase Quinase Quinases/metabolismo
NF-kappa B/genética
Fosforilação
Regiões Promotoras Genéticas
Transdução de Sinais
Fator de Transcrição AP-1/genética
Ubiquitinação
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Gene Products, vpr); 0 (Intracellular Signaling Peptides and Proteins); 0 (NF-kappa B); 0 (TAB3 protein, human); 0 (Transcription Factor AP-1); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (MAP kinase kinase kinase 7)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140611
[St] Status:MEDLINE
[do] DOI:10.1186/1742-4690-11-45


  9 / 573 MEDLINE  
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[PMID]:24367500
[Au] Autor:Lata S; Ronsard L; Sood V; Dar SA; Ramachandran VG; Das S; Banerjea AC
[Ad] Endereço:Department of Microbiology, University College of Medical Sciences and Guru Teg Bahadur Hospital, Delhi, India.
[Ti] Título:Effect on HIV-1 gene expression, Tat-Vpr interaction and cell apoptosis by natural variants of HIV-1 Tat exon 1 and Vpr from Northern India.
[So] Source:PLoS One;8(12):e82128, 2013.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Since HIV-1 Tat and Vpr genes are involved in promoter transactivation, apoptosis, etc, we carried out studies to find out nature and extent of natural variation in the two genes from seropositive patients from Northern India and determined their functional implications. METHODS: HIV-1 tat exon 1 and vpr were amplified from the genomic DNA isolated from the blood of HIV-1 infected individuals using specific primers by Polymerase Chain reaction (PCR) and subjected to extensive genetic analysis (CLUSTAL W, Simplot etc). Their expression was monitored by generating myc fusion clones. Tat exon 1 and Vpr variants were co-transfected with the reporter gene construct (LTR-luc) and their transactivation potential was monitored by measuring luciferase activity. Apoptosis and cell cycle analysis was done by Propidium Iodide (PI) staining followed by FACS. RESULTS: Exon 1 of tat was amplified from 21 samples and vpr was amplified from 16 samples. One of the Tat exon 1 variants showed phylogenetic relatedness to subtype B & C and turned out to be a unique recombinant. Two of the Vpr variants were B/C/D recombinants. These natural variations were found to have no impact on the stability of Tat and Vpr. These variants differed in their ability to transactivate B LTR and C LTR promoters. B/C recombinant Tat showed better co-operative interaction with Vpr. B/C/D recombination in Vpr was found to have no effect on its co-operativity with Tat. Recombinant Tat (B/C) induced more apoptosis than wild type B and C Tat. The B/C/D recombination in Vpr did not affect its G2 arrest induction potential but reduced its apoptosis induction ability. CONCLUSIONS: Extensive sequence and region-specific variations were observed in Tat and Vpr genes from HIV-1 infected individuals from Northern India. These variations have functional implications & therefore important for the pathogenicity of virus.
[Mh] Termos MeSH primário: Apoptose/genética
Regulação Viral da Expressão Gênica/genética
Produtos do Gene vpr/genética
HIV-1/genética
Produtos do Gene tat do Vírus da Imunodeficiência Humana/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Western Blotting
Eletroforese em Gel de Poliacrilamida
Éxons/genética
Feminino
Citometria de Fluxo
Células HeLa
Seres Humanos
Índia
Masculino
Meia-Idade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gene Products, vpr); 0 (tat Gene Products, Human Immunodeficiency Virus)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131225
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0082128


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[PMID]:24285483
[Au] Autor:Agarwal N; Iyer D; Patel SG; Sekhar RV; Phillips TM; Schubert U; Oplt T; Buras ED; Samson SL; Couturier J; Lewis DE; Rodriguez-Barradas MC; Jahoor F; Kino T; Kopp JB; Balasubramanyam A
[Ad] Endereço:Translational Metabolism Unit, Diabetes Research Center, Division of Diabetes, Endocrinology and Metabolism, Baylor College of Medicine, Houston, TX 77030, USA.
[Ti] Título:HIV-1 Vpr induces adipose dysfunction in vivo through reciprocal effects on PPAR/GR co-regulation.
[So] Source:Sci Transl Med;5(213):213ra164, 2013 Nov 27.
[Is] ISSN:1946-6242
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viral infections, such as HIV, have been linked to obesity, but mechanistic evidence that they cause adipose dysfunction in vivo is lacking. We investigated a pathogenic role for the HIV-1 accessory protein viral protein R (Vpr), which can coactivate the glucocorticoid receptor (GR) and co-repress peroxisome proliferator-activated receptor γ (PPARγ) in vitro, in HIV-associated adipose dysfunction. Vpr circulated in the blood of most HIV-infected patients tested, including those on antiretroviral therapy (ART) with undetectable viral load. Vpr-mediated mechanisms were dissected in vivo using mouse models expressing the Vpr transgene in adipose tissues and liver (Vpr-Tg) or infused with synthetic Vpr. Both models demonstrated accelerated whole-body lipolysis, hyperglycemia and hypertriglyceridemia, and tissue-specific findings. Fat depots in these mice had diminished mass, macrophage infiltration, and blunted PPARγ target gene expression but increased GR target gene expression. In liver, we observed blunted PPARα target gene expression, steatosis with decreased adenosine monophosphate-activated protein kinase activity, and insulin resistance. Similar to human HIV-infected patients, Vpr circulated in the serum of Vpr-Tg mice. Vpr blocked differentiation in preadipocytes through cell cycle arrest, whereas in mature adipocytes, it increased lipolysis with reciprocally altered association of PPARγ and GR with their target promoters. These results delineate a distinct pathogenic sequence: Vpr, released from HIV-1 in tissue reservoirs after ART, can disrupt PPAR/GR co-regulation and cell cycle control to produce adipose dysfunction and hepatosteatosis. Confirmation of these mechanisms in HIV patients could lead to targeted treatment of the metabolic complications with Vpr inhibitors, GR antagonists, or PPARγ/PPARα agonists.
[Mh] Termos MeSH primário: Produtos do Gene vpr/metabolismo
HIV-1/metabolismo
Receptores de Glucocorticoides/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Animais
Cromatografia em Camada Delgada
Ensaio de Imunoadsorção Enzimática
Produtos do Gene vpr/genética
HIV-1/genética
Seres Humanos
Immunoblotting
Masculino
Camundongos
Camundongos Transgênicos
PPAR alfa/agonistas
PPAR alfa/metabolismo
PPAR gama/metabolismo
Receptores de Glucocorticoides/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gene Products, vpr); 0 (PPAR alpha); 0 (PPAR gamma); 0 (Receptors, Glucocorticoid)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131129
[St] Status:MEDLINE
[do] DOI:10.1126/scitranslmed.3007148



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