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  1 / 2134 MEDLINE  
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[PMID]:29054407
[Au] Autor:Wang Z; Hou X; Wang Y; Xu A; Cao W; Liao M; Zhang R; Tang J
[Ad] Endereço:College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing 100193, China.
[Ti] Título:Ubiquitination of non-lysine residues in the retroviral integrase.
[So] Source:Biochem Biophys Res Commun;494(1-2):57-62, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Retroviral integrase catalyzes the integration of retroviral genome into host chromosomal DNA, which is a prerequisite of effective viral replication and infection. The human immunodeficiency virus type 1 (HIV-1) integrase has previously been reported to be regulated by the ubiquitination, but the molecular characterization of integrase ubiquitination is still unclear. In this study, we analyzed the ubiquitination of avian leukosis virus (ALV) integrase in detail. The ubiquitination assay showed that, like HIV-1, ALV integrase could also be modified by ubiquitination when expressed in 293 T and DF-1 cells. Domain mapping analysis revealed that the ubiquitination of ALV integrase might mainly occurred in the catalytic core and the N-terminal zinc-binding domains. Both lysine and non-lysine residues within integrase of ALV and HIV-1 were responsible for the ubiquitin conjugation, and the N-terminal HHCC zinc-binding motif might play an important role in mediating integrase ubiquitination. Interestingly, mass spectrometry analysis identified the Thr10 and Cys37 residues in the HHCC zinc-binding motif as the ubiquitination sites, indicating that ubiquitin may be conjugated to ALV integrase through direct interaction with the non-lysine residues. These findings revealed the detailed features of retroviral integrase ubiquitination and found a novel mechanism of ubiquitination mediated by the non-lysine residues within the N-terminal zinc-binding domain of integrase.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/enzimologia
Integrase de HIV/química
Integrase de HIV/metabolismo
Integrases/química
Integrases/metabolismo
Proteínas dos Retroviridae/química
Proteínas dos Retroviridae/metabolismo
Retroviridae/enzimologia
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Sequência de Aminoácidos
Animais
Vírus da Leucose Aviária/genética
Vírus da Leucose Aviária/fisiologia
Linhagem Celular
Galinhas
Células HEK293
Integrase de HIV/genética
HIV-1/enzimologia
HIV-1/genética
HIV-1/fisiologia
Seres Humanos
Integrases/genética
Lisina/química
Mutagênese Sítio-Dirigida
Retroviridae/genética
Retroviridae/fisiologia
Proteínas dos Retroviridae/genética
Ubiquitinação
Zinco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Retroviridae Proteins); 0 (p31 integrase protein, Human immunodeficiency virus 1); EC 2.7.7.- (HIV Integrase); EC 2.7.7.- (Integrases); J41CSQ7QDS (Zinc); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171022
[St] Status:MEDLINE


  2 / 2134 MEDLINE  
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[PMID]:28768861
[Au] Autor:Narulla MS; Alsairi A; Charmier L; Noonan S; Conroy D; Hall WW; Sheehy N
[Ad] Endereço:Centre for Research in Infectious Diseases, School of Medicine and Medical Science, University College Dublin, Belfield, Dublin, Ireland.
[Ti] Título:Positive and Negative Regulation of Type I Interferons by the Human T Cell Leukemia Virus Antisense Protein HBZ.
[So] Source:J Virol;91(20), 2017 Oct 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pathogenesis of human T cell leukemia virus type 1 (HTLV-1) is strongly linked to the viral regulatory proteins Tax1 and HBZ, whose opposing functions contribute to the clinical outcome of infection. Type I interferons alpha and beta (IFN-α and IFN-ß) are key cytokines involved in innate immunity, and IFN-α, in combination with other antivirals, is extensively used in the treatment of HTLV-1 infection. The relationship between HTLV-1 and IFN signaling is unclear, and to date the effect of HBZ on this pathway has not been examined. Here we report that HBZ significantly enhances interferon regulatory factor 7 (IRF7)-induced IFN-α- and IFN-stimulated response element (ISRE) promoter activities and IFN-α production and can counteract the inhibitory effect of Tax1. In contrast to this, we show that HBZ and Tax1 cooperate to inhibit the induction of IFN-ß and ISRE promoters by IRF3 and IFN-ß production. In addition, we reveal that HBZ enhances ISRE activation by IFN-α. We further show that HBZ enhances IRF7 and suppresses IRF3 activation by TBK1 and IKKε. We demonstrate that HBZ has no effect on virus-induced nuclear accumulation of IRF3, suggesting that it may inhibit IRF3 activity at a transcriptional level. We show that HBZ physically interacts with IRF7 and IKKε but not with IRF3 or TBK1. Overall, our findings suggest that both HBZ and Tax1 are negative regulators of immediate early IFN-ß innate immune responses, while HBZ but not Tax1 positively regulates the induction of IFN-α and downstream IFN-α signaling. Type I interferons are powerful antiviral cytokines and are used extensively in the treatment of HTLV-1-induced adult T cell leukemia (ATL). To date, the relationship between HTLV-1 and the IFN pathway is poorly understood, and studies so far have focused on Tax1. Our study is unique in that it examined the effect of HBZ, alone or in combination with Tax1, on type I IFN signaling. This is important because HBZ is frequently the only viral protein expressed in infected cells, particularly at later stages of infection. A better understanding of the how HBZ regulates IFN signaling may lead to the development of therapeutics that can modify such responses and improve the clinical outcome for infected individuals.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Interações Hospedeiro-Patógeno
Vírus 1 Linfotrópico T Humano/metabolismo
Interferon-alfa/metabolismo
Interferon beta/metabolismo
Proteínas dos Retroviridae/metabolismo
[Mh] Termos MeSH secundário: Antivirais/imunologia
Antivirais/metabolismo
Linhagem Celular
Seres Humanos
Quinase I-kappa B/metabolismo
Imunidade Inata
Fator Regulador 3 de Interferon/metabolismo
Fator Regulador 7 de Interferon/metabolismo
Interferon-alfa/imunologia
Interferon beta/imunologia
Regiões Promotoras Genéticas
Proteínas Serina-Treonina Quinases/metabolismo
Elementos de Resposta
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Basic-Leucine Zipper Transcription Factors); 0 (HBZ protein, human T-cell leukemia virus type I); 0 (IRF3 protein, human); 0 (Interferon Regulatory Factor-3); 0 (Interferon Regulatory Factor-7); 0 (Interferon-alpha); 0 (Retroviridae Proteins); 77238-31-4 (Interferon-beta); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (TBK1 protein, human); EC 2.7.11.10 (I-kappa B Kinase)
[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:170804
[St] Status:MEDLINE


  3 / 2134 MEDLINE  
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[PMID]:28260789
[Au] Autor:Terol M; Gazon H; Lemasson I; Duc-Dodon M; Barbeau B; Césaire R; Mesnard JM; Péloponèse JM
[Ad] Endereço:IRIM (ex-CPBS)-UMR 9004, Research Institute in Infectiology of Montpellier, University of Montpellier, CNRS, Montpellier, France.
[Ti] Título:HBZ-mediated shift of JunD from growth suppressor to tumor promoter in leukemic cells by inhibition of ribosomal protein S25 expression.
[So] Source:Leukemia;31(10):2235-2243, 2017 Oct.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human T-cell leukemia virus type 1 (HTLV-1) basic-leucine zipper (bZIP) factor (HBZ) is a key player in proliferation and transformation of HTLV-1-infected cells, thus contributing to adult T-cell leukemia (ATL) development. HBZ deregulates gene expression within the host cell by interacting with several cellular partners. Through its C-terminal ZIP domain, HBZ is able to contact and activate JunD, a transcription factor of the AP-1 family. JunD mRNA is intronless but can generate two protein isoforms by alternative translation initiation: JunD full-length and Δ JunD, an N-terminal truncated form unresponsive to the tumor suppressor menin. Using various cell lines and primary T-lymphocytes, we show that after serum deprivation HBZ induces the expression of Δ JunD isoform. We demonstrate that, unlike JunD, Δ JunD induces proliferation and transformation of cells. To decipher the mechanisms for Δ JunD production, we looked into the translational machinery and observed that HBZ induces nuclear retention of RPS25 mRNA and loss of RPS25 protein expression, a component of the small ribosomal subunit. Therefore, HBZ bypasses translational control of JunD uORF and favors the expression of Δ JunD. In conclusion, we provide strong evidences that HBZ induces Δ JunD expression through alteration of the cellular translational machinery and that the truncated isoform Δ JunD has a central role in the oncogenic process leading to ATL.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/fisiologia
Transformação Celular Viral/genética
Regulação Leucêmica da Expressão Gênica/genética
Regulação Viral da Expressão Gênica/genética
Biossíntese de Proteínas/genética
Proteínas Proto-Oncogênicas c-jun/fisiologia
Proteínas dos Retroviridae/fisiologia
Proteínas Ribossômicas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Transporte Biológico
Linhagem Celular
Núcleo Celular/metabolismo
Meios de Cultura Livres de Soro
Células HEK293
Infecções por HTLV-I/sangue
Seres Humanos
Isoformas de Proteínas/genética
Isoformas de Proteínas/fisiologia
Proteínas Proto-Oncogênicas/fisiologia
Proteínas Proto-Oncogênicas c-jun/genética
RNA Mensageiro/metabolismo
Proteínas Ribossômicas/genética
Ribossomos/metabolismo
Linfócitos T/patologia
Linfócitos T/virologia
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic-Leucine Zipper Transcription Factors); 0 (Culture Media, Serum-Free); 0 (HBZ protein, human T-cell leukemia virus type I); 0 (JunD protein, human); 0 (MEN1 protein, human); 0 (Protein Isoforms); 0 (Proto-Oncogene Proteins); 0 (Proto-Oncogene Proteins c-jun); 0 (RNA, Messenger); 0 (RPS25 protein, human); 0 (Retroviridae Proteins); 0 (Ribosomal Proteins)
[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:170307
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2017.74


  4 / 2134 MEDLINE  
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[PMID]:28204810
[Au] Autor:Ma Y; Zhang B; Wang D; Qian L; Song X; Wang X; Yang C; Zhao G
[Ad] Endereço:Henan Medical College, Zhengzhou, Henan 451191, P.R. China.
[Ti] Título:HTLV-1 basic leucine zipper factor downregulates cyclin D1 expression via interactions with NF-κB.
[So] Source:Int J Mol Med;39(3):764-770, 2017 Mar.
[Is] ISSN:1791-244X
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Human T cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus. It can cause adult T cell leukemia (ATL) and other diseases. The HTLV-1 basic leucine zipper (bZIP) factor (HBZ), which is encoded by the minus-strand of the provirus, is expressed in all cases of ATL and involved in T cell proliferation. However, the exact mechanism underlying its growth-promoting activity is poorly understood. Herein, we demonstrated that HBZ suppressed cyclin D1 expression by inhibiting the nuclear factor (NF)-κB signaling pathway. Among the potential mechanisms of cyclin D1 inhibition mediated by HBZ, we found that HBZ suppressed cyclin D1 promoter activity. Luciferase assay analysis revealed that HBZ repressed cyclin D1 promoter activity by suppressing NF-κB­driven transcription mediated by the p65 subunit. Using an immunoprecipitation assay, we found that HBZ could bind to p65, but not p50. Finally, we showed that HBZ selectively interacted with p65 via its AD+bZIP domains. By suppressing cyclin D1 expression, HBZ can alter cell cycle progression of HTLV-1-infected cells, which may be critical for oncogenesis.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Ciclina D1/genética
Regulação da Expressão Gênica
Vírus 1 Linfotrópico T Humano/fisiologia
NF-kappa B/metabolismo
Proteínas dos Retroviridae/metabolismo
[Mh] Termos MeSH secundário: Fatores de Transcrição de Zíper de Leucina Básica/química
Linhagem Celular
Ordem dos Genes
Vetores Genéticos/genética
Seres Humanos
Zíper de Leucina
Regiões Promotoras Genéticas
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Proteínas dos Retroviridae/química
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic-Leucine Zipper Transcription Factors); 0 (HBZ protein, human T-cell leukemia virus type I); 0 (NF-kappa B); 0 (Retroviridae Proteins); 136601-57-5 (Cyclin D1)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170315
[Lr] Data última revisão:
170315
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE
[do] DOI:10.3892/ijmm.2017.2868


  5 / 2134 MEDLINE  
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[PMID]:28095504
[Au] Autor:Baratella M; Forlani G; Raval GU; Tedeschi A; Gout O; Gessain A; Tosi G; Accolla RS
[Ad] Endereço:Department of Surgical and Morphological Sciences, School of Medicine, University of Insubria, Varese, Italy.
[Ti] Título:Cytoplasmic Localization of HTLV-1 HBZ Protein: A Biomarker of HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP).
[So] Source:PLoS Negl Trop Dis;11(1):e0005285, 2017 Jan.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HTLV-1 is the causative agent of a severe form of adult T cell leukemia/Lymphoma (ATL), and of a chronic progressive neuromyelopathy designated HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). Two important HTLV-1-encoded proteins, Tax-1 and HBZ, play crucial roles in the generation and maintenance of the oncogenic process. Less information is instead available on the molecular and cellular mechanisms leading to HAM/TSP. More importantly, no single specific biomarker has been described that unambiguously define the status of HAM/TSP. Here we report for the first time the finding that HBZ, described until now as an exclusive nuclear protein both in chronically infected and in ATL cells, is instead exclusively localized in the cytoplasm of peripheral blood mononuclear cells (PBMC) from patients suffering of HAM/TSP. Interestingly, at the single cell level, HBZ and Tax-1 proteins are never found co-expressed in the same cell, suggesting the existence of mechanisms of expression uncoupling of these two important HTLV-1 viral products in HAM/TSP patients. Cells expressing cytoplasmic HBZ were almost exclusively found in the CD4+ T cell compartment that was not, at least in a representative HAM/TSP patient, expressing the CD25 marker. Less than 1 percent CD8+ T cells were fond positive for HBZ, while B cells and NK cells were found negative for HBZ in HAM/TSP patients. Our results identify the cytoplasmic localization of HBZ in HAM/TSP patient as a possible biomarker of this rather neglected tropical disease, and raise important hypotheses on the role of HBZ in the pathogenesis of the neuromyelopathy associated to HTLV-1 infection.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Citoplasma/virologia
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/fisiologia
Leucemia-Linfoma de Células T do Adulto/virologia
Proteínas dos Retroviridae/metabolismo
[Mh] Termos MeSH secundário: Fatores de Transcrição de Zíper de Leucina Básica/genética
Biomarcadores/metabolismo
Linfócitos T CD4-Positivos/virologia
Seres Humanos
Leucócitos Mononucleares/virologia
Paraparesia Espástica Tropical
Transporte Proteico
Proteínas dos Retroviridae/genética
Doenças da Medula Espinal
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic-Leucine Zipper Transcription Factors); 0 (Biomarkers); 0 (HBZ protein, human T-cell leukemia virus type I); 0 (Retroviridae Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170118
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0005285


  6 / 2134 MEDLINE  
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[PMID]:28046066
[Au] Autor:Kinosada H; Yasunaga JI; Shimura K; Miyazato P; Onishi C; Iyoda T; Inaba K; Matsuoka M
[Ad] Endereço:Laboratory of Virus Control, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto, Japan.
[Ti] Título:HTLV-1 bZIP Factor Enhances T-Cell Proliferation by Impeding the Suppressive Signaling of Co-inhibitory Receptors.
[So] Source:PLoS Pathog;13(1):e1006120, 2017 Jan.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia-lymphoma (ATL) and inflammatory diseases. To enhance cell-to-cell transmission of HTLV-1, the virus increases the number of infected cells in vivo. HTLV-1 bZIP factor (HBZ) is constitutively expressed in HTLV-1 infected cells and ATL cells and promotes T-cell proliferation. However, the detailed mechanism by which it does so remains unknown. Here, we show that HBZ enhances the proliferation of expressing T cells after stimulation via the T-cell receptor. HBZ promotes this proliferation by influencing the expression and function of multiple co-inhibitory receptors. HBZ suppresses the expression of BTLA and LAIR-1 in HBZ expressing T cells and ATL cells. Expression of T cell immunoglobulin and ITIM domain (TIGIT) and Programmed cell death 1 (PD-1) was enhanced, but their suppressive effect on T-cell proliferation was functionally impaired. HBZ inhibits the co-localization of SHP-2 and PD-1 in T cells, thereby leading to impaired inhibition of T-cell proliferation and suppressed dephosphorylation of ZAP-70 and CD3ζ. HBZ does this by interacting with THEMIS, which associates with Grb2 and SHP-2. Thus, HBZ interacts with the SHP containing complex, impedes the suppressive signal from PD-1 and TIGIT, and enhances the proliferation of T cells. Although HBZ was present in both the nucleus and the cytoplasm of T cells, HBZ was localized largely in the nucleus by suppressed expression of THEMIS by shRNA. This indicates that THEMIS is responsible for cytoplasmic localization of HBZ in T cells. Since THEMIS is expressed only in T-lineage cells, HBZ mediated inhibition of the suppressive effects of co-inhibitory receptors accounts for how HTLV-1 induces proliferation only of T cells in vivo. This study reveals that HBZ targets co-inhibitory receptors to cause the proliferation of infected cells.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Proliferação Celular/fisiologia
Infecções por HTLV-I/transmissão
Vírus 1 Linfotrópico T Humano/patogenicidade
Proteínas/metabolismo
Proteínas dos Retroviridae/metabolismo
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição de Zíper de Leucina Básica/genética
Complexo CD3/metabolismo
Linhagem Celular Tumoral
Encefalomielite Autoimune Experimental/virologia
Proteína Adaptadora GRB2/metabolismo
Infecções por HTLV-I/virologia
Seres Humanos
Células Jurkat
Ativação Linfocitária/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Receptor de Morte Celular Programada 1/biossíntese
Receptor de Morte Celular Programada 1/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 11/metabolismo
Receptores Imunológicos/biossíntese
Receptores Imunológicos/metabolismo
Proteínas dos Retroviridae/genética
Proteína-Tirosina Quinase ZAP-70/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BTLA protein, mouse); 0 (Basic-Leucine Zipper Transcription Factors); 0 (CD3 Complex); 0 (CD3 antigen, zeta chain); 0 (GRB2 Adaptor Protein); 0 (Grb2 protein, mouse); 0 (HBZ protein, human T-cell leukemia virus type I); 0 (Pdcd1 protein, mouse); 0 (Programmed Cell Death 1 Receptor); 0 (Proteins); 0 (Receptors, Immunologic); 0 (Retroviridae Proteins); 0 (T cell Ig and ITIM domain protein, mouse); 0 (leukocyte-associated immunoglobulin-like receptor 1); 0 (themis protein, mouse); EC 2.7.10.2 (ZAP-70 Protein-Tyrosine Kinase); EC 2.7.10.2 (Zap70 protein, mouse); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11); EC 3.1.3.48 (Ptpn11 protein, mouse)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006120


  7 / 2134 MEDLINE  
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[PMID]:28039384
[Au] Autor:Henzy JE; Gifford RJ; Kenaley CP; Johnson WE
[Ad] Endereço:Biology Department, Boston College, Chestnut Hill, MA.
[Ti] Título:An Intact Retroviral Gene Conserved in Spiny-Rayed Fishes for over 100 My.
[So] Source:Mol Biol Evol;34(3):634-639, 2017 Mar 01.
[Is] ISSN:1537-1719
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have identified a retroviral envelope gene with a complete, intact open reading frame (ORF) in 20 species of spiny-rayed fishes (Acanthomorpha). The taxonomic distribution of the gene, "percomORF", indicates insertion into the ancestral lineage >110 Ma, making it the oldest known conserved gene of viral origin in a vertebrate genome. Underscoring its ancient provenence, percomORF exists as an isolated ORF within the intron of a widely conserved host gene, with no discernible proviral sequence nearby. Despite its remarkable age, percomORF retains canonical features of a retroviral glycoprotein, and tests for selection strongly suggest cooption for a host function. Retroviral envelope genes have been coopted for a role in placentogenesis by numerous lineages of mammals, including eutherians and marsupials, representing a variety of placental structures. Therefore percomORF's presence within the group Percomorpha-unique among spiny-finned fishes in having evolved placentation and live birth-is especially intriguing.
[Mh] Termos MeSH primário: Retrovirus Endógenos/genética
Peixes/genética
Peixes/virologia
Produtos do Gene env/genética
[Mh] Termos MeSH secundário: Animais
Evolução Biológica
Sequência Conservada
Evolução Molecular
Fases de Leitura Aberta
Filogenia
Provírus/genética
Proteínas dos Retroviridae/genética
Análise de Sequência de DNA/métodos
Proteínas do Envelope Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, env); 0 (Retroviridae Proteins); 0 (Viral Envelope Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170101
[St] Status:MEDLINE
[do] DOI:10.1093/molbev/msw262


  8 / 2134 MEDLINE  
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[PMID]:27887847
[Au] Autor:Karimi M; Mohammadi H; Hemmatzadeh M; Mohammadi A; Rafatpanah H; Baradaran B
[Ad] Endereço:Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; Tabriz University of Medical Sciences, International Branch (Aras), Tabriz, Iran.
[Ti] Título:Role of the HTLV-1 viral factors in the induction of apoptosis.
[So] Source:Biomed Pharmacother;85:334-347, 2017 Jan.
[Is] ISSN:1950-6007
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Adult T-cell leukemia (ATL) and HTLV-1-associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) are the two main diseases that are caused by the HTLV-1 virus. One of the features of HTLV-1 infection is its resistance against programmed cell death, which maintains the survival of cells to oncogenic transformation and underlies the viruses' therapeutic resistance. Two main genes by which the virus develops cancer are Tax and HBZ; playing an essential role in angiogenesis in regulating viral transcription and modulating multiple host factors as well as apoptosis pathways. Here we have reviewed by prior research how the apoptosis pathways are suppressed by the Tax and HBZ and new drugs which have been designed to deal with this suppression.
[Mh] Termos MeSH primário: Apoptose
Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Produtos do Gene tax/metabolismo
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/metabolismo
Leucemia-Linfoma de Células T do Adulto/virologia
Paraparesia Espástica Tropical/virologia
Proteínas dos Retroviridae/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Antivirais/uso terapêutico
Proteínas Reguladoras de Apoptose/metabolismo
Fatores de Transcrição de Zíper de Leucina Básica/genética
Transformação Celular Viral
Produtos do Gene tax/genética
Genoma Viral
Infecções por HTLV-I/tratamento farmacológico
Infecções por HTLV-I/metabolismo
Infecções por HTLV-I/patologia
Interações Hospedeiro-Patógeno
Vírus 1 Linfotrópico T Humano/efeitos dos fármacos
Vírus 1 Linfotrópico T Humano/genética
Vírus 1 Linfotrópico T Humano/patogenicidade
Seres Humanos
Leucemia-Linfoma de Células T do Adulto/tratamento farmacológico
Leucemia-Linfoma de Células T do Adulto/metabolismo
Leucemia-Linfoma de Células T do Adulto/patologia
Paraparesia Espástica Tropical/tratamento farmacológico
Paraparesia Espástica Tropical/metabolismo
Paraparesia Espástica Tropical/patologia
Proteínas dos Retroviridae/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Antiviral Agents); 0 (Apoptosis Regulatory Proteins); 0 (Basic-Leucine Zipper Transcription Factors); 0 (Gene Products, tax); 0 (HBZ protein, human T-cell leukemia virus type I); 0 (Retroviridae Proteins); 0 (tax protein, Human T-lymphotrophic virus 1)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170213
[Lr] Data última revisão:
170213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161127
[St] Status:MEDLINE


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[PMID]:27787900
[Au] Autor:Mozhgani SH; Jaberi N; Rezaee SA; Bustani R; Jazayeri SM; Akbarin MM; Milani S; Tarokhian H; Norouzi M
[Ad] Endereço:Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Título:Evaluation of HTLV-1 HBZ and proviral load, together with host IFN λ3, in pathogenesis of HAM/TSP.
[So] Source:J Med Virol;89(6):1102-1107, 2017 Jun.
[Is] ISSN:1096-9071
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human T-cell lymphotropic virus 1 (HTLV-1) is associated with two progressive diseases: HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and adult T-cell leukemia/lymphoma (ATLL). Although HTLV-1 proviral load (PVL) has been introduced as a risk factor for these diseases' progression, it is not sufficient on its own to yield an accurate estimation of the outcome of the infection. In the present study, PVL and HTLV-1 basic leucine zipper factor (HBZ) expression level as viral factors, and IFN λ3 as a host factor, were evaluated in HAM/TSP patients and HTLV-1 asymptomatic carriers (ACs). During 2014-2015, 12 HAM/TSP patients and 18 ACs who had been referred to the HTLV-1 Clinic, Ghaem Hospital, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran, were enrolled in this study. Peripheral blood mononuclear cells (PBMCs) were isolated and the DNA and mRNA were extracted for quantification of HBZ, IFN λ3 expression, and PVL using real-time PCR (TaqMan method). Although the PVL was higher in the HAM/TSP group, with a 94% confidence interval, there were no considerable differences in terms of HBZ mRNA and PVL between ACs and HAM patients. IFN λ3 expression in the HAM/TSP group was significantly higher than in the ACs (P = 0.02). To the best of our knowledge, no study has evaluated the expression level of IFN λ3 in HTLV-1 positive patients. The immune response against HTLV-1 viral antigens and virulent factors will therefore further refine our knowledge of interactions between the virus and host in the pathogenesis of HTLV-1-related disorders. The virus PVL and the host IFN λ3 can be used as pathogenic factors of HTLV-1 infected patients at risk of HAM/TSP manifestation. J. Med. Virol. 89:1102-1107, 2017. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/biossíntese
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/patogenicidade
Interleucinas/biossíntese
Provírus/patogenicidade
Proteínas dos Retroviridae/biossíntese
Carga Viral
[Mh] Termos MeSH secundário: Adulto
Fatores de Transcrição de Zíper de Leucina Básica/genética
DNA Viral/análise
Feminino
Perfilação da Expressão Gênica
Infecções por HTLV-I/patologia
Interações Hospedeiro-Patógeno
Vírus 1 Linfotrópico T Humano/isolamento & purificação
Seres Humanos
Interleucinas/genética
Irã (Geográfico)
Leucócitos Mononucleares/virologia
Masculino
Meia-Idade
Provírus/isolamento & purificação
RNA Mensageiro/análise
Reação em Cadeia da Polimerase em Tempo Real
Proteínas dos Retroviridae/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic-Leucine Zipper Transcription Factors); 0 (DNA, Viral); 0 (HBZ protein, human T-cell leukemia virus type I); 0 (IL29 protein, human); 0 (Interleukins); 0 (RNA, Messenger); 0 (Retroviridae Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161028
[St] Status:MEDLINE
[do] DOI:10.1002/jmv.24721


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Fotocópia
[PMID]:27697867
[Au] Autor:Mukai R; Ohshima T
[Ad] Endereço:Faculty of Pharmaceutical Science at Kagawa Campus, Tokushima Bunri University, Sanuki, Kagawa, Japan.
[Ti] Título:Enhanced Stabilization of MCL1 by the Human T-Cell Leukemia Virus Type 1 bZIP Factor Is Modulated by Blocking the Recruitment of Cullin 1 to the SCF Complex.
[So] Source:Mol Cell Biol;36(24):3075-3085, 2016 Dec 15.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus that is the etiological agent of adult T-cell leukemia (ATL). The HTLV-1 basic leucine zipper factor (HBZ), which is encoded by the minus strand of the provirus, is constitutively expressed in all ATL patient cells and likely contributes to the development and maintenance of ATL. Furthermore, the overexpression of the myeloid cell leukemia 1 (MCL1) protein is frequently observed in hematological cancers as well as several other types of cancers. Here, we found that the expression of HBZ in cells stabilized MCL1 protein expression and suppressed the MCL1-mediated release of cytochrome c from the mitochondria. This effect was mediated by inhibition of the ubiquitin-dependent degradation of MCL1. In a serial binding assay, HBZ interacted with cullin 1 (CUL1) through a head-to-tail interaction. The association between CUL1 and Skp1, which serves as the molecular scaffold for the components of SCF ubiquitin ligase complexes, was markedly repressed in the presence of HBZ. Mechanistic analysis indicated that HBZ abrogated the CUL1 association with Skp1, which in turn promoted the cellular expression of MCL1. This novel function of HBZ likely plays a role in the viral pathogenesis of HTLV-1 and provides important insights into our understanding of the development of ATL.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Proteínas Culina/metabolismo
Infecções por HTLV-I/metabolismo
Proteína de Sequência 1 de Leucemia de Células Mieloides/metabolismo
Proteínas dos Retroviridae/metabolismo
Proteínas Ligases SKP Culina F-Box/metabolismo
[Mh] Termos MeSH secundário: Animais
Citocromos c/metabolismo
Células HEK293
Células HeLa
Vírus 1 Linfotrópico T Humano/metabolismo
Seres Humanos
Camundongos
Proteína de Sequência 1 de Leucemia de Células Mieloides/química
Células NIH 3T3
Estabilidade Proteica
Proteínas Quinases Associadas a Fase S/metabolismo
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic-Leucine Zipper Transcription Factors); 0 (Cullin 1); 0 (Cullin Proteins); 0 (HBZ protein, human T-cell leukemia virus type I); 0 (MCL1 protein, human); 0 (Myeloid Cell Leukemia Sequence 1 Protein); 0 (Retroviridae Proteins); 0 (S-Phase Kinase-Associated Proteins); 0 (SKP1 protein, human); 9007-43-6 (Cytochromes c); EC 2.3.2.27 (SKP Cullin F-Box Protein Ligases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161005
[St] Status:MEDLINE



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