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Pesquisa : B04.280.210.400.700.400 [Categoria DeCS]
Referências encontradas : 506 [refinar]
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[PMID]:27751885
[Au] Autor:Kwon EK; Min CK; Kim Y; Lee JW; Aigerim A; Schmidt S; Nam HJ; Han SK; Kim K; Cha JS; Kim H; Kim S; Cho HS; Choi MS; Cho NH
[Ad] Endereço:Department of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.
[Ti] Título:Constitutive activation of T cells by γ2-herpesviral GPCR through the interaction with cellular CXCR4.
[So] Source:Biochim Biophys Acta;1864(1):1-11, 2017 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Members of the herpesviral family use multiple strategies to hijack infected host cells and exploit cellular signaling for their pathogenesis and latent infection. Among the most intriguing weapons in the arsenal of pathogenic herpesviruses are the constitutively active virally-encoded G protein-coupled receptors (vGPCRs). Even though vGPCRs contribute to viral pathogenesis such as immune evasion and proliferative disorders, the molecular details of how vGPCRs continuously activate cellular signaling are largely unknown. Here, we report that the vGPCR of Herpesvirus saimiri (HVS), an oncogenic γ2-herpesvirus, constitutively activates T cells via a heteromeric interaction with cellular CXCR4. Constitutive T cell activation also occurs with expression of the vGPCR of Kaposi's sarcoma-associated herpesvirus (KSHV), but not the vGPCR of Epstein-Barr virus. Expression of HVS vGPCR down-regulated the surface expression of CXCR4 but did not induce the degradation of the chemokine receptor, suggesting that vGPCR/CXCR4 signaling continues in cytosolic compartments. The physical association of vGPCR with CXCR4 was demonstrated by proximity ligation assay as well as immunoprecipitation. Interestingly, the constitutive activation of T cells by HVS vGPCR is independent of proximal T cell receptor (TCR) signaling molecules, such as TCRß, Lck, and ZAP70, whereas CXCR4 silencing by shRNA abolished T cell activation by vGPCRs of HVS and KSHV. Furthermore, previously identified inactive vGPCR mutants failed to interact with CXCR4. These findings on the positive cooperativity of vGPCR with cellular CXCR4 in T cell activation extend our current understanding of the molecular mechanisms of vGPCR function and highlight the importance of heteromerization for GPCR activity.
[Mh] Termos MeSH primário: Herpesvirus Saimiriíneo 2/metabolismo
Herpesvirus Humano 8/metabolismo
Receptores CXCR4/genética
Receptores de Quimiocinas/genética
Linfócitos T/virologia
[Mh] Termos MeSH secundário: Regulação da Expressão Gênica
Células HEK293
Herpesvirus Saimiriíneo 2/genética
Herpesvirus Saimiriíneo 2/crescimento & desenvolvimento
Herpesvirus Humano 4/genética
Herpesvirus Humano 4/crescimento & desenvolvimento
Herpesvirus Humano 4/metabolismo
Herpesvirus Humano 8/genética
Herpesvirus Humano 8/crescimento & desenvolvimento
Interações Hospedeiro-Patógeno
Seres Humanos
Ativação Linfocitária
Proteína Tirosina Quinase p56(lck) Linfócito-Específica/genética
Proteína Tirosina Quinase p56(lck) Linfócito-Específica/imunologia
Proteína Tirosina Quinase p56(lck) Linfócito-Específica/metabolismo
Cultura Primária de Células
Ligação Proteica
Multimerização Proteica
Receptores de Antígenos de Linfócitos T alfa-beta/genética
Receptores de Antígenos de Linfócitos T alfa-beta/imunologia
Receptores de Antígenos de Linfócitos T alfa-beta/metabolismo
Receptores CXCR4/imunologia
Receptores CXCR4/metabolismo
Receptores de Quimiocinas/imunologia
Receptores de Quimiocinas/metabolismo
Transdução de Sinais
Linfócitos T/imunologia
Linfócitos T/metabolismo
Proteína-Tirosina Quinase ZAP-70/genética
Proteína-Tirosina Quinase ZAP-70/imunologia
Proteína-Tirosina Quinase ZAP-70/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCR4 protein, human); 0 (G protein-coupled receptor, Human herpesvirus 8); 0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (Receptors, CXCR4); 0 (Receptors, Chemokine); EC 2.7.10.2 (Lymphocyte Specific Protein Tyrosine Kinase p56(lck)); EC 2.7.10.2 (ZAP-70 Protein-Tyrosine Kinase); EC 2.7.10.2 (ZAP70 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


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[PMID]:27335146
[Au] Autor:Pawlica P; Moss WN; Steitz JA
[Ad] Endereço:Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06536, USA.
[Ti] Título:Host miRNA degradation by Herpesvirus saimiri small nuclear RNA requires an unstructured interacting region.
[So] Source:RNA;22(8):1181-9, 2016 Aug.
[Is] ISSN:1469-9001
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Herpesvirus saimiri, an oncogenic herpesvirus, during latency produces seven small nuclear RNAs, called the Herpesvirus saimiri U RNAs (HSUR1-7). HSUR1 mediates degradation of the host microRNA, miR-27, via a process that requires imperfect base-pairing. The decreased levels of miR-27 lead to prolonged T-cell activation and likely contribute to oncogenesis. To gain insight into HSUR1-mediated degradation of miR-27, we probed the in vivo secondary structure of HSUR1 and coupled this with bioinformatic structural analyses. The results suggest that HSUR1 adopts a conformation different than previously believed and that the region complementary to miR-27 lacks stable structure. To determine whether HSUR1 structural flexibility is important for its ability to mediate miR-27 degradation, we performed structurally informative mutagenic analyses of HSUR1. HSUR1 mutants in which the miR-27 binding site sequence is preserved, but sequestered in predicted helices, lose their ability to decrease miR-27 levels. These results indicate that the HSUR1 miR27-binding region must be available in a conformationally flexible segment for noncoding RNA function.
[Mh] Termos MeSH primário: Genes Virais
Herpesvirus Saimiriíneo 2/metabolismo
MicroRNAs/metabolismo
RNA Nuclear Pequeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Callithrix
Herpesvirus Saimiriíneo 2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Small Nuclear)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160624
[St] Status:MEDLINE
[do] DOI:10.1261/rna.054817.115


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[PMID]:26539553
[Au] Autor:Vernot JP; Perdomo-Arciniegas AM; Pérez-Quintero LA; Martínez DF
[Ad] Endereço:Fisiología Celular y Molecular, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá 11001, Colombia ; Instituto de Investigaciones Biomédicas, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá 11001, Colombia.
[Ti] Título:Modulating p56Lck in T-Cells by a Chimeric Peptide Comprising Two Functionally Different Motifs of Tip from Herpesvirus saimiri.
[So] Source:J Immunol Res;2015:395371, 2015.
[Is] ISSN:2314-7156
[Cp] País de publicação:Egypt
[La] Idioma:eng
[Ab] Resumo:The Lck interacting protein Tip of Herpesvirus saimiri is responsible for T-cell transformation both in vitro and in vivo. Here we designed the chimeric peptide hTip-CSKH, comprising the Lck specific interacting motif CSKH of Tip and its hydrophobic transmembrane sequence (hTip), the latter as a vector targeting lipid rafts. We found that hTip-CSKH can induce a fivefold increase in proliferation of human and Aotus sp. T-cells. Costimulation with PMA did not enhance this proliferation rate, suggesting that hTip-CSKH is sufficient and independent of further PKC stimulation. We also found that human Lck phosphorylation was increased earlier after stimulation when T-cells were incubated previously with hTip-CSKH, supporting a strong signalling and proliferative effect of the chimeric peptide. Additionally, Lck downstream signalling was evident with hTip-CSKH but not with control peptides. Importantly, hTip-CSKH could be identified in heavy lipid rafts membrane fractions, a compartment where important T-cell signalling molecules (LAT, Ras, and Lck) are present during T-cell activation. Interestingly, hTip-CSKH was inhibitory to Jurkat cells, in total agreement with the different signalling pathways and activation requirements of this leukemic cell line. These results provide the basis for the development of new compounds capable of modulating therapeutic targets present in lipid rafts.
[Mh] Termos MeSH primário: Herpesvirus Saimiriíneo 2/química
Ativação Linfocitária
Proteína Tirosina Quinase p56(lck) Linfócito-Específica/metabolismo
Peptídeos/genética
Fosfoproteínas/química
Fosfoproteínas/metabolismo
Linfócitos T/imunologia
Proteínas Virais/química
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Animais
Aotidae
Herpesvirus Saimiriíneo 2/genética
Seres Humanos
Células Jurkat
Proteína Tirosina Quinase p56(lck) Linfócito-Específica/genética
Microdomínios da Membrana/metabolismo
Peptídeos/química
Fosfoproteínas/imunologia
Fosforilação
Fito-Hemaglutininas/imunologia
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/imunologia
Transdução de Sinais
Linfócitos T/metabolismo
Proteínas Virais/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Peptides); 0 (Phosphoproteins); 0 (Phytohemagglutinins); 0 (Recombinant Fusion Proteins); 0 (Viral Proteins); 0 (tyrosine kinase interacting protein, Saimiriine herpesvirus 2); EC 2.7.10.2 (Lymphocyte Specific Protein Tyrosine Kinase p56(lck))
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151106
[St] Status:MEDLINE
[do] DOI:10.1155/2015/395371


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[PMID]:26400439
[Au] Autor:Aswad A; Katzourakis A
[Ad] Endereço:Department of Zoology, University of Oxford, Oxford OX1 3PS, UK.
[Ti] Título:Convergent capture of retroviral superantigens by mammalian herpesviruses.
[So] Source:Nat Commun;6:8299, 2015 Sep 24.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Horizontal gene transfer from retroviruses to mammals is well documented and extensive, but is rare between unrelated viruses with distinct genome types. Three herpesviruses encode a gene with similarity to a retroviral superantigen gene (sag) of the unrelated mouse mammary tumour virus (MMTV). We uncover ancient retroviral sags in over 20 mammals to reconstruct their shared history with herpesviral sags, revealing that the acquisition is a convergent evolutionary event. A retrovirus circulating in South American primates over 10 million years ago was the source of sag in two monkey herpesviruses, and a different retrovirus was the source of sag in a Peruvian rodent herpesvirus. We further show through a timescaled phylogenetic analysis that a cross-species transmission of monkey herpesviruses occurred after the acquisition of sag. These results reveal that a diverse range of ancient sag-containing retroviruses independently donated sag twice from two separate lineages that are distinct from MMTV.
[Mh] Termos MeSH primário: Antígenos Virais/genética
Genes Virais/genética
Herpesviridae/genética
Retroviridae/genética
Superantígenos/genética
[Mh] Termos MeSH secundário: Animais
Aotidae
Quirópteros
Evolução Molecular
Transferência Genética Horizontal/genética
Herpesvirus Saimiriíneo 2
Hylobates
Vírus do Tumor Mamário do Camundongo/genética
Camundongos
Filogenia
Ratos
Rhadinovirus/genética
Ovinos
América do Sul
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Viral); 0 (Superantigens)
[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:150925
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms9299


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[PMID]:26292323
[Au] Autor:Guo YE; Oei T; Steitz JA
[Ad] Endereço:Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale School of Medicine, New Haven, Connecticut, USA.
[Ti] Título:Herpesvirus saimiri MicroRNAs Preferentially Target Host Cell Cycle Regulators.
[So] Source:J Virol;89(21):10901-11, 2015 Nov.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: In latently infected marmoset T cells, Herpesvirus saimiri (HVS) expresses six microRNAs (known as miR-HSURs [H. saimiri U-rich RNAs]). The viral miR-HSURs are processed from chimeric primary transcripts, each containing a noncoding U-rich RNA (HSUR) and a pre-miRNA hairpin. To uncover the functions of miR-HSURs, we identified mRNA targets in infected cells using high-throughput sequencing of RNA isolated by cross-linking immunoprecipitation (HITS-CLIP). HITS-CLIP revealed hundreds of robust Argonaute (Ago) binding sites mediated by miR-HSURs that map to the host genome but few in the HVS genome. Gene ontology analysis showed that several pathways regulating the cell cycle are enriched among cellular targets of miR-HSURs. Interestingly, miR-HSUR4-3p represses expression of the p300 transcriptional coactivator by binding the open reading frame of its mRNA. miR-HSUR5-3p directly regulates BiP, an endoplasmic reticulum (ER)-localized chaperone facilitating maturation of major histocompatibility complex class I (MHC-I) and the antiviral response. miR-HSUR5-3p also robustly downregulates WEE1, a key negative regulator of cell cycle progression, leading to reduced phosphorylation of its substrate, cyclin-dependent kinase (Cdk1). Consistently, inhibition of miR-HSUR5-3p in HVS-infected cells decreases their proliferation. Together, our results shed light on the roles of viral miRNAs in cellular transformation and viral latency. IMPORTANCE: Viruses express miRNAs during various stages of infection, suggesting that viral miRNAs play critical roles in the viral life cycle. Compared to protein-coding genes, the functions of viral miRNAs are not well understood. This is because it has been challenging to identify their mRNA targets. Here, we focused on the functions of the recently discovered HVS miRNAs, called miR-HSURs. HVS is an oncogenic gammaherpesvirus that causes acute T-cell lymphomas and leukemias in New World primates and transforms human T cells. A better understanding of HVS biology will help advance our knowledge of virus-induced oncogenesis. Because numerous cellular miRNAs play crucial roles in cancer, viral miRNAs from the highly oncogenic HVS might also be important for transformation. Here, we found that the miR-HSURs preferentially modulate expression of host cell cycle regulators, as well as antiviral response factors. Our work provides further insight into the functions of herpesviral miRNAs in virus-induced oncogenesis and latency.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Herpesvirus Saimiriíneo 2/genética
MicroRNAs/metabolismo
RNA Mensageiro/metabolismo
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação/genética
Western Blotting
Proteína Quinase CDC2/metabolismo
Callithrix
Células HEK293
Proteínas de Choque Térmico/metabolismo
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Imunoprecipitação
Luciferases
MicroRNAs/genética
Fosforilação
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Heat-Shock Proteins); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (molecular chaperone GRP78); EC 1.13.12.- (Luciferases); EC 2.7.11.22 (CDC2 Protein Kinase)
[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:150821
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.01884-15


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[PMID]:26220997
[Au] Autor:Xie M; Zhang W; Shu MD; Xu A; Lenis DA; DiMaio D; Steitz JA
[Ad] Endereço:Howard Hughes Medical Institute, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536, USA; Department of Molecular Biophysics and Biochemistry, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536, USA
[Ti] Título:The host Integrator complex acts in transcription-independent maturation of herpesvirus microRNA 3' ends.
[So] Source:Genes Dev;29(14):1552-64, 2015 Jul 15.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Herpesvirus saimiri (HVS) is an oncogenic γ-herpesvirus that produces microRNAs (miRNAs) by cotranscription of precursor miRNA (pre-miRNA) hairpins immediately downstream from viral small nuclear RNAs (snRNA). The host cell Integrator complex, which recognizes the snRNA 3' end processing signal (3' box), generates the 5' ends of HVS pre-miRNA hairpins. Here, we identify a novel 3' box-like sequence (miRNA 3' box) downstream from HVS pre-miRNAs that is essential for miRNA biogenesis. In vivo knockdown and rescue experiments confirmed that the 3' end processing of HVS pre-miRNAs also depends on Integrator activity. Interaction between Integrator and HVS primary miRNA (pri-miRNA) substrates that contain only the miRNA 3' box was confirmed by coimmunoprecipitation and an in situ proximity ligation assay (PLA) that we developed to localize specific transient RNA-protein interactions inside cells. Surprisingly, in contrast to snRNA 3' end processing, HVS pre-miRNA 3' end processing by Integrator can be uncoupled from transcription, enabling new approaches to study Integrator enzymology.
[Mh] Termos MeSH primário: Herpesvirus Saimiriíneo 2/genética
MicroRNAs/metabolismo
Processamento de Terminações 3´ de RNA/fisiologia
[Mh] Termos MeSH secundário: Técnicas de Silenciamento de Genes
Células HEK293
Células HeLa
Herpesvirus Saimiriíneo 2/metabolismo
Interações Hospedeiro-Patógeno/genética
Seres Humanos
Imunoprecipitação
MicroRNAs/química
MicroRNAs/genética
Complexos Multiproteicos/genética
Complexos Multiproteicos/metabolismo
Processamento de Terminações 3' de RNA/genética
Precursores de RNA/genética
Precursores de RNA/metabolismo
RNA Nuclear Pequeno/metabolismo
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Multiprotein Complexes); 0 (RNA Precursors); 0 (RNA, Small Nuclear)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150730
[St] Status:MEDLINE
[do] DOI:10.1101/gad.266973.115


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[PMID]:24725595
[Au] Autor:Guo YE; Riley KJ; Iwasaki A; Steitz JA
[Ad] Endereço:Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06536, USA.
[Ti] Título:Alternative capture of noncoding RNAs or protein-coding genes by herpesviruses to alter host T cell function.
[So] Source:Mol Cell;54(1):67-79, 2014 Apr 10.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In marmoset T cells transformed by Herpesvirus saimiri (HVS), a viral U-rich noncoding (nc) RNA, HSUR 1, specifically mediates degradation of host microRNA-27 (miR-27). High-throughput sequencing of RNA after crosslinking immunoprecipitation (HITS-CLIP) identified mRNAs targeted by miR-27 as enriched in the T cell receptor (TCR) signaling pathway, including GRB2. Accordingly, transfection of miR-27 into human T cells attenuates TCR-induced activation of mitogen-activated protein kinases (MAPKs) and induction of CD69. MiR-27 also robustly regulates SEMA7A and IFN-γ, key modulators and effectors of T cell function. Knockdown or ectopic expression of HSUR 1 alters levels of these proteins in virally transformed cells. Two other T-lymphotropic γ-herpesviruses, AlHV-1 and OvHV-2, do not produce a noncoding RNA to downregulate miR-27 but instead encode homologs of miR-27 target genes. Thus, oncogenic γ-herpesviruses have evolved diverse strategies to converge on common targets in host T cells.
[Mh] Termos MeSH primário: Herpesvirus Saimiriíneo 2/metabolismo
Ativação Linfocitária
MicroRNAs/metabolismo
RNA não Traduzido/metabolismo
RNA Viral/metabolismo
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Antígenos CD/metabolismo
Antígenos de Diferenciação de Linfócitos T/metabolismo
Sequência de Bases
Callithrix
Ativação Enzimática
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Proteína Adaptadora GRB2/genética
Proteína Adaptadora GRB2/metabolismo
Regulação da Expressão Gênica
Células HEK293
Herpesvirus Saimiriíneo 2/genética
Herpesvirus Saimiriíneo 2/patogenicidade
Sequenciamento de Nucleotídeos em Larga Escala
Interações Hospedeiro-Patógeno
Seres Humanos
Imunoprecipitação
Interferon gama/genética
Interferon gama/metabolismo
Células Jurkat
Lectinas Tipo C/metabolismo
MicroRNAs/genética
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Dados de Sequência Molecular
Estabilidade de RNA
RNA não Traduzido/genética
RNA Viral/genética
Receptores de Antígenos de Linfócitos T/genética
Receptores de Antígenos de Linfócitos T/metabolismo
Semaforinas/genética
Semaforinas/metabolismo
Análise de Sequência de RNA
Transdução de Sinais
Linfócitos T/imunologia
Linfócitos T/virologia
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, T-Lymphocyte); 0 (CD69 antigen); 0 (GPI-Linked Proteins); 0 (GRB2 Adaptor Protein); 0 (GRB2 protein, human); 0 (IFNG protein, human); 0 (Lectins, C-Type); 0 (MIRN27 microRNA, human); 0 (MicroRNAs); 0 (RNA, Untranslated); 0 (RNA, Viral); 0 (Receptors, Antigen, T-Cell); 0 (SEMA7A protein, human); 0 (Semaphorins); 82115-62-6 (Interferon-gamma); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1405
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140415
[St] Status:MEDLINE


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[PMID]:24550725
[Au] Autor:Tunnicliffe RB; Hautbergue GM; Wilson SA; Kalra P; Golovanov AP
[Ad] Endereço:Manchester Institute of Biotechnology and Faculty of Life Sciences, The University of Manchester, Manchester, United Kingdom.
[Ti] Título:Competitive and cooperative interactions mediate RNA transfer from herpesvirus saimiri ORF57 to the mammalian export adaptor ALYREF.
[So] Source:PLoS Pathog;10(2):e1003907, 2014 Feb.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The essential herpesvirus adaptor protein HVS ORF57, which has homologs in all other herpesviruses, promotes viral mRNA export by utilizing the cellular mRNA export machinery. ORF57 protein specifically recognizes viral mRNA transcripts, and binds to proteins of the cellular transcription-export (TREX) complex, in particular ALYREF. This interaction introduces viral mRNA to the NXF1 pathway, subsequently directing it to the nuclear pore for export to the cytoplasm. Here we have used a range of techniques to reveal the sites for direct contact between RNA and ORF57 in the absence and presence of ALYREF. A binding site within ORF57 was characterized which recognizes specific viral mRNA motifs. When ALYREF is present, part of this ORF57 RNA binding site, composed of an α-helix, binds preferentially to ALYREF. This competitively displaces viral RNA from the α-helix, but contact with RNA is still maintained by a flanking region. At the same time, the flexible N-terminal domain of ALYREF comes into contact with the viral RNA, which becomes engaged in an extensive network of synergistic interactions with both ALYREF and ORF57. Transfer of RNA to ALYREF in the ternary complex, and involvement of individual ORF57 residues in RNA recognition, were confirmed by UV cross-linking and mutagenesis. The atomic-resolution structure of the ORF57-ALYREF interface was determined, which noticeably differed from the homologous ICP27-ALYREF structure. Together, the data provides the first site-specific description of how viral mRNA is locked by a herpes viral adaptor protein in complex with cellular ALYREF, giving herpesvirus access to the cellular mRNA export machinery. The NMR strategy used may be more generally applicable to the study of fuzzy protein-protein-RNA complexes which involve flexible polypeptide regions.
[Mh] Termos MeSH primário: Infecções por Herpesviridae/metabolismo
Interações Hospedeiro-Parasita/fisiologia
Proteínas Nucleares/metabolismo
RNA Viral/metabolismo
Proteínas de Ligação a RNA/metabolismo
Proteínas Repressoras/metabolismo
Transativadores/metabolismo
Fatores de Transcrição/metabolismo
Infecções Tumorais por Vírus/metabolismo
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/fisiologia
Herpesvirus Saimiriíneo 2/química
Herpesvirus Saimiriíneo 2/metabolismo
Herpesvirus Saimiriíneo 2/patogenicidade
Seres Humanos
Proteínas Nucleares/química
Estrutura Quaternária de Proteína
Transporte de RNA/fisiologia
RNA Viral/análise
Proteínas de Ligação a RNA/química
Proteínas Repressoras/química
Transativadores/química
Fatores de Transcrição/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ALYREF protein, human); 0 (Nuclear Proteins); 0 (ORF57 protein, Herpesvirus saimiri); 0 (RNA, Viral); 0 (RNA-Binding Proteins); 0 (Repressor Proteins); 0 (Trans-Activators); 0 (Transcription Factors)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140220
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1003907


  9 / 506 MEDLINE  
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[PMID]:24232864
[Au] Autor:Folcik VA; Garofalo M; Coleman J; Donegan JJ; Rabbani E; Suster S; Nuovo A; Magro CM; Di Leva G; Nuovo GJ
[Ad] Endereço:1] The Ohio State University (OSU) at Marion, Marion, OH, USA [2] OSU Computer Science and Engineering, Marion, OH, USA [3] OSU Innovation Group for the Study of Complexity in Human, Natural, and Engineered Systems, Marion, OH, USA.
[Ti] Título:Idiopathic pulmonary fibrosis is strongly associated with productive infection by herpesvirus saimiri.
[So] Source:Mod Pathol;27(6):851-62, 2014 Jun.
[Is] ISSN:1530-0285
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Idiopathic pulmonary fibrosis is a fatal disease without effective therapy or diagnostic test. To investigate a potential role for γ-herpesviruses in this disease, 21 paraffin-embedded lung biopsies from patients diagnosed with idiopathic pulmonary fibrosis and 21 lung biopsies from age-matched controls with pulmonary fibrosis of known etiology were examined for a series of γ-herpesviruses' DNA/RNA and related proteins using in situ hybridization and reverse transcriptase-polymerase chain reaction (RT-PCR)-based methods. We detected four proteins known to be in the genome of several γ-herpesviruses (cyclin D, thymidylate synthase, dihydrofolate reductase, and interleukin-17) that were strongly co-expressed in the regenerating epithelial cells of each of the 21 idiopathic pulmonary fibrosis cases and not in the benign epithelia of the controls. Among the γ-herpesviruses, only herpesvirus saimiri expresses all four of these 'pirated' mammalian proteins. We found herpesvirus saimiri DNA in the regenerating epithelial cells of 21/21 idiopathic pulmonary fibrosis cases using four separate probe sets but not in the 21 controls. RT-PCR showed that the source of the cyclin D RNA in active idiopathic pulmonary fibrosis was herpesvirus saimiri and not human. We cloned and sequenced part of genome corresponding to the DNA polymerase herpesvirus saimiri gene from an idiopathic pulmonary fibrosis sample and it matched 100% with the published viral sequence. These data are consistent with idiopathic pulmonary fibrosis representing herpesvirus saimiri-induced pulmonary fibrosis. Thus, treatment directed against viral proliferation and/or viral-associated proteins may halt disease progression. Further, demonstration of the viral nucleic acids or proteins may help diagnose the disease.
[Mh] Termos MeSH primário: Infecções por Herpesviridae/complicações
Fibrose Pulmonar Idiopática/virologia
[Mh] Termos MeSH secundário: Idoso
DNA Viral/isolamento & purificação
Feminino
Herpesvirus Saimiriíneo 2
Seres Humanos
Hibridização In Situ
Masculino
Meia-Idade
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Viral)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:150422
[Lr] Data última revisão:
150422
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131116
[St] Status:MEDLINE
[do] DOI:10.1038/modpathol.2013.198


  10 / 506 MEDLINE  
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[PMID]:24219244
[Au] Autor:Ingram N; Macnab SA; Marston G; Scott N; Carr IM; Markham AF; Whitehouse A; Coletta PL
[Ad] Endereço:School of Medicine, University of Leeds Brenner Building, St James's University Hospital, Leeds LS9 7TF, UK. n.ingram@leeds.ac.uk.
[Ti] Título:The use of high-frequency ultrasound imaging and biofluorescence for in vivo evaluation of gene therapy vectors.
[So] Source:BMC Med Imaging;13:35, 2013 Nov 12.
[Is] ISSN:1471-2342
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Non-invasive imaging of the biodistribution of novel therapeutics including gene therapy vectors in animal models is essential. METHODS: This study assessed the utility of high-frequency ultrasound (HF-US) combined with biofluoresence imaging (BFI) to determine the longitudinal impact of a Herpesvirus saimiri amplicon on human colorectal cancer xenograft growth. RESULTS: HF-US imaging of xenografts resulted in an accurate and informative xenograft volume in a longitudinal study. The volumes correlated better with final ex vivo volume than mechanical callipers (R2 = 0.7993, p = 0.0002 vs. R2 = 0.7867, p = 0.0014). HF-US showed that the amplicon caused lobe formation. BFI demonstrated retention and expression of the amplicon in the xenografts and quantitation of the fluorescence levels also correlated with tumour volumes. CONCLUSIONS: The use of multi-modal imaging provided useful and enhanced insights into the behaviour of gene therapy vectors in vivo in real-time. These relatively inexpensive technologies are easy to incorporate into pre-clinical studies.
[Mh] Termos MeSH primário: Neoplasias Colorretais/patologia
Neoplasias Colorretais/terapia
Terapia Genética
Vetores Genéticos
Herpesvirus Saimiriíneo 2/genética
Imagem Óptica/métodos
Ultrassonografia/métodos
[Mh] Termos MeSH secundário: Animais
Proteínas de Fluorescência Verde
Células HCT116
Seres Humanos
Estudos Longitudinais
Camundongos
Camundongos Nus
Imagem Multimodal
Carga Tumoral
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:150422
[Lr] Data última revisão:
150422
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131114
[St] Status:MEDLINE
[do] DOI:10.1186/1471-2342-13-35



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