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[PMID]:29186194
[Au] Autor:Furuta R; Yasunaga JI; Miura M; Sugata K; Saito A; Akari H; Ueno T; Takenouchi N; Fujisawa JI; Koh KR; Higuchi Y; Mahgoub M; Shimizu M; Matsuda F; Melamed A; Bangham CR; Matsuoka M
[Ad] Endereço:Laboratory of Virus Control, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan.
[Ti] Título:Human T-cell leukemia virus type 1 infects multiple lineage hematopoietic cells in vivo.
[So] Source:PLoS Pathog;13(11):e1006722, 2017 Nov.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human T-cell leukemia virus type 1 (HTLV-1) infects mainly CD4+CCR4+ effector/memory T cells in vivo. However, it remains unknown whether HTLV-1 preferentially infects these T cells or this virus converts infected precursor cells to specialized T cells. Expression of viral genes in vivo is critical to study viral replication and proliferation of infected cells. Therefore, we first analyzed viral gene expression in non-human primates naturally infected with simian T-cell leukemia virus type 1 (STLV-1), whose virological attributes closely resemble those of HTLV-1. Although the tax transcript was detected only in certain tissues, Tax expression was much higher in the bone marrow, indicating the possibility of de novo infection. Furthermore, Tax expression of non-T cells was suspected in bone marrow. These data suggest that HTLV-1 infects hematopoietic cells in the bone marrow. To explore the possibility that HTLV-1 infects hematopoietic stem cells (HSCs), we analyzed integration sites of HTLV-1 provirus in various lineages of hematopoietic cells in patients with HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) and a HTLV-1 carrier using the high-throughput sequencing method. Identical integration sites were detected in neutrophils, monocytes, B cells, CD8+ T cells and CD4+ T cells, indicating that HTLV-1 infects HSCs in vivo. We also detected Tax protein in myeloperoxidase positive neutrophils. Furthermore, dendritic cells differentiated from HTLV-1 infected monocytes caused de novo infection to T cells, indicating that infected monocytes are implicated in viral spreading in vivo. Certain integration sites were re-detected in neutrophils from HAM/TSP patients at different time points, indicating that infected HSCs persist and differentiate in vivo. This study demonstrates that HTLV-1 infects HSCs, and infected stem cells differentiate into diverse cell lineages. These data indicate that infection of HSCs can contribute to the persistence and spread of HTLV-1 in vivo.
[Mh] Termos MeSH primário: Infecções por HTLV-I/virologia
Células-Tronco Hematopoéticas/virologia
Vírus 1 Linfotrópico T Humano/fisiologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD8-Positivos/virologia
Células Cultivadas
Produtos do Gene tax/genética
Produtos do Gene tax/metabolismo
Infecções por HTLV-I/imunologia
Vírus 1 Linfotrópico T Humano/genética
Seres Humanos
Macaca mulatta
Neutrófilos/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, tax)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006722


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[PMID]:28742148
[Au] Autor:Groussaud D; Khair M; Tollenaere AI; Waast L; Kuo MS; Mangeney M; Martella C; Fardini Y; Coste S; Souidi M; Benit L; Pique C; Issad T
[Ad] Endereço:INSERM, U1016, Institut Cochin, Paris, France.
[Ti] Título:Hijacking of the O-GlcNAcZYME complex by the HTLV-1 Tax oncoprotein facilitates viral transcription.
[So] Source:PLoS Pathog;13(7):e1006518, 2017 Jul.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The viral Tax oncoprotein plays a key role in both Human T-cell lymphotropic virus type 1 (HTLV-1)-replication and HTLV-1-associated pathologies, notably adult T-cell leukemia. Tax governs the transcription from the viral 5'LTR, enhancing thereby its own expression, via the recruitment of dimers of phosphorylated CREB to cAMP-response elements located within the U3 region (vCRE). In addition to phosphorylation, CREB is also the target of O-GlcNAcylation, another reversible post-translational modification involved in a wide range of diseases, including cancers. O-GlcNAcylation consists in the addition of O-linked-N-acetylglucosamine (O-GlcNAc) on Serine or Threonine residues, a process controlled by two enzymes: O-GlcNAc transferase (OGT), which transfers O-GlcNAc on proteins, and O-GlcNAcase (OGA), which removes it. In this study, we investigated the status of O-GlcNAcylation enzymes in HTLV-1-transformed T cells. We found that OGA mRNA and protein expression levels are increased in HTLV-1-transformed T cells as compared to control T cell lines while OGT expression is unchanged. However, higher OGA production coincides with a reduction in OGA specific activity, showing that HTLV-1-transformed T cells produce high level of a less active form of OGA. Introducing Tax into HEK-293T cells or Tax-negative HTLV-1-transformed TL-om1 T cells is sufficient to inhibit OGA activity and increase total O-GlcNAcylation, without any change in OGT activity. Furthermore, Tax interacts with the OGT/OGA complex and inhibits the activity of OGT-bound OGA. Pharmacological inhibition of OGA increases CREB O-GlcNAcylation as well as HTLV-1-LTR transactivation by Tax and CREB recruitment to the LTR. Moreover, overexpression of wild-type CREB but not a CREB protein mutated on a previously described O-GlcNAcylation site enhances Tax-mediated LTR transactivation. Finally, both OGT and OGA are recruited to the LTR. These findings reveal the interplay between Tax and the O-GlcNAcylation pathway and identify new key molecular actors involved in the assembly of the Tax-dependent transactivation complex.
[Mh] Termos MeSH primário: Produtos do Gene tax/metabolismo
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/metabolismo
N-Acetilglucosaminiltransferases/metabolismo
Linfócitos T/virologia
beta-N-Acetil-Hexosaminidases/metabolismo
[Mh] Termos MeSH secundário: Acetilglucosamina/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/genética
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Regulação Viral da Expressão Gênica
Produtos do Gene tax/genética
Infecções por HTLV-I/enzimologia
Infecções por HTLV-I/genética
Infecções por HTLV-I/metabolismo
Interações Hospedeiro-Patógeno
Vírus 1 Linfotrópico T Humano/genética
Seres Humanos
N-Acetilglucosaminiltransferases/genética
Processamento de Proteína Pós-Traducional
Linfócitos T/enzimologia
Linfócitos T/metabolismo
Transcrição Genética
beta-N-Acetil-Hexosaminidases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic AMP Response Element-Binding Protein); 0 (Gene Products, tax); 0 (tax protein, Human T-lymphotrophic virus 1); EC 2.4.1.- (N-Acetylglucosaminyltransferases); EC 2.4.1.- (O-GlcNAc transferase); EC 3.2.1.50 (hexosaminidase C); EC 3.2.1.52 (beta-N-Acetylhexosaminidases); V956696549 (Acetylglucosamine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171213
[Lr] Data última revisão:
171213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006518


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[PMID]:28866351
[Au] Autor:Sakihama S; Saito M; Kuba-Miyara M; Tomoyose T; Taira N; Miyagi T; Hayashi M; Kinjo S; Nakachi S; Tedokon I; Nishi Y; Tamaki K; Morichika K; Uchihara JN; Morishima S; Karube KN; Tanaka Y; Masuzaki H; Fukushima T
[Ad] Endereço:Laboratory of Hematoimmunology, Graduate School of Health Sciences, University of the Ryukyus, Nishihara, Japan.
[Ti] Título:Human T-cell leukemia virus type I Tax genotype analysis in Okinawa, the southernmost and remotest islands of Japan: Different distributions compared with mainland Japan and the potential value for the prognosis of aggressive adult T-cell leukemia/lymphoma.
[So] Source:Leuk Res;61:18-24, 2017 Oct.
[Is] ISSN:1873-5835
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Okinawa, comprising remote islands off the mainland of Japan, is an endemic area of human T-cell leukemia virus type I (HTLV-1), the causative virus of adult T-cell leukemia-lymphoma (ATL) and HTLV-1-associated myelopathy (HAM). We investigated the tax genotype of HTLV-1 among 29 HTLV-1 carriers, 74 ATL patients, and 33 HAM patients in Okinawa. The genotype distribution-60 (44%) taxA cases and 76 (56%) taxB cases-differed from that of a previous report from Kagoshima Prefecture in mainland Japan (taxA, 10%; taxB, 90%). A comparison of the clinical outcomes of 45 patients (taxA, 14; taxB, 31) with aggressive ATL revealed that the overall response and 1-year overall survival rates for taxA (50% and 35%, respectively) were lower than those for taxB (71% and 49%, respectively). In a multivariate analysis of two prognostic indices for aggressive ATL, Japan Clinical Oncology Group-Prognostic Index and Prognostic Index for acute and lymphoma ATL, with respect to age, performance status, corrected calcium, soluble interleukin-2 receptor, and tax genotype, the estimated hazard ratio of taxA compared with taxB was 2.68 (95% confidence interval, 0.87-8.25; P=0.086). Our results suggest that the tax genotype has clinical value as a prognostic factor for aggressive ATL.
[Mh] Termos MeSH primário: Produtos do Gene tax/genética
Infecções por HTLV-I/patologia
Leucemia-Linfoma de Células T do Adulto/patologia
Leucemia-Linfoma de Células T do Adulto/virologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Feminino
Genótipo
Infecções por HTLV-I/tratamento farmacológico
Infecções por HTLV-I/mortalidade
Vírus 1 Linfotrópico T Humano/genética
Seres Humanos
Japão
Estimativa de Kaplan-Meier
Leucemia-Linfoma de Células T do Adulto/mortalidade
Masculino
Meia-Idade
Reação em Cadeia da Polimerase
Polimorfismo de Fragmento de Restrição
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, tax); 0 (tax protein, Human T-lymphotrophic virus 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170904
[St] Status:MEDLINE


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[PMID]:28821586
[Au] Autor:Wang J; Kang L; Song D; Liu L; Yang S; Ma L; Guo Z; Ding H; Wang H; Yang B
[Ad] Endereço:Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang 453003, China.
[Ti] Título:Ku70 Senses HTLV-1 DNA and Modulates HTLV-1 Replication.
[So] Source:J Immunol;199(7):2475-2482, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human T lymphotropic virus type 1 (HTLV-1) belongs to the deltaretrovirus family and has been linked to multiple diseases. However, the innate host defense against HTLV-1 is unclear. In this study, we report that the expression of Ku70, a known DNA sensor against DNA viruses, could be induced by HTLV-1 infection in HeLa, PMA-differentiated THP1 cells, primary human monocytes, and human monocyte-derived macrophages. In these cells, the overexpression of Ku70 inhibited the HTLV-1 protein expression, whereas the knockdown of Ku70 promoted the HTLV-1 protein expression. Furthermore, the overexpression of Ku70 enhanced the cellular response to HTLV-1 infection, whereas Ku70 knockdown yielded the opposite effect. Additionally, Ku70 was found to interact with HTLV-1 reverse transcription intermediate ssDNA90. ssDNA90 stimulation induced Ku70 expression and Ku70 promoted ssDNA90-triggered innate immune responses. Finally, HTLV-1 infection enhanced the association between Ku70 and stimulator of IFN genes, suggesting that stimulator of IFN genes was involved in Ku70-mediated host defenses against HTLV-1 infection. Taken together, our findings suggest a new sensor that detects HTLV-1 reverse transcription intermediate and controls HTLV-1 replication. These findings may provide new angles to understand host defenses against HTLV-1 infection and HTLV-1-associated diseases.
[Mh] Termos MeSH primário: DNA Viral
Vírus 1 Linfotrópico T Humano/fisiologia
Autoantígeno Ku/genética
Autoantígeno Ku/metabolismo
Replicação Viral
[Mh] Termos MeSH secundário: Células Cultivadas
Produtos do Gene tax/genética
Células HeLa
Vírus 1 Linfotrópico T Humano/genética
Vírus 1 Linfotrópico T Humano/imunologia
Seres Humanos
Imunidade Inata
Interferons/genética
Interferons/imunologia
Autoantígeno Ku/deficiência
Autoantígeno Ku/imunologia
Macrófagos/virologia
Monócitos/virologia
Produtos do Gene gag do Vírus da Imunodeficiência Humana/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Viral); 0 (Gene Products, tax); 0 (gag Gene Products, Human Immunodeficiency Virus); 0 (p19 protein, Human T-lymphotropic virus 1); 9008-11-1 (Interferons); EC 4.2.99.- (Ku Autoantigen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700111


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[PMID]:28724769
[Au] Autor:Termini JM; Magnani DM; Maxwell HS; Lauer W; Castro I; Pecotte J; Barber GN; Watkins DI; Desrosiers RC
[Ad] Endereço:Department of Pathology, University of Miami Miller School of Medicine, Miami, Florida, USA.
[Ti] Título:Simian T Lymphotropic Virus 1 Infection of Papio anubis: Sequence Heterogeneity and T Cell Recognition.
[So] Source:J Virol;91(20), 2017 Oct 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Baboons naturally infected with simian T lymphotropic virus (STLV) are a potentially useful model system for the study of vaccination against human T lymphotropic virus (HTLV). Here we expanded the number of available full-length baboon STLV-1 sequences from one to three and related the T cell responses that recognize the immunodominant Tax protein to the sequences present in two individual baboons. Continuously growing T cell lines were established from two baboons, animals 12141 and 12752. Next-generation sequencing (NGS) of complete STLV genome sequences from these T cell lines revealed them to be closely related but distinct from each other and from the baboon STLV-1 sequence in the NCBI sequence database. Overlapping peptides corresponding to each unique Tax sequence and to the reference baboon Tax sequence were used to analyze recognition by T cells from each baboon using intracellular cytokine staining (ICS). Individual baboons expressed more gamma interferon and tumor necrosis factor alpha in response to Tax peptides corresponding to their own STLV-1 sequence than in response to Tax peptides corresponding to the reference baboon STLV-1 sequence. Thus, our analyses revealed distinct but closely related STLV-1 genome sequences in two baboons, extremely low heterogeneity of STLV sequences within each baboon, no evidence for superinfection within each baboon, and a ready ability of T cells in each baboon to recognize circulating Tax sequences. While amino acid substitutions that result in escape from CD8 T cell recognition were not observed, premature stop codons were observed in 7% and 56% of sequences from peripheral blood mononuclear cells from animals 12141 and 12752, respectively. It has been estimated that approximately 100,000 people suffer serious morbidity and 10,000 people die each year from the consequences associated with human T lymphotropic virus (HTLV) infection. There are no antiviral drugs and no preventive vaccine. A preventive vaccine would significantly impact the global burden associated with HTLV infections. Here we provide fundamental information on the simian T lymphotropic virus (STLV) naturally transmitted in a colony of captive baboons. The limited viral sequence heterogeneity in individual baboons, the identity of the viral gene product that is the major target of cellular immune responses, the persistence of viral amino acid sequences that are the major targets of cellular immune responses, and the emergence of truncated variants in the major target of cellular immune responses all parallel what are seen with HTLV infection of humans. These results justify the use of STLV-infected baboons as a model system for vaccine development efforts.
[Mh] Termos MeSH primário: Produtos do Gene tax/química
Produtos do Gene tax/genética
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T de Símios/isolamento & purificação
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
DNA Viral/genética
Produtos do Gene tax/imunologia
Genoma Viral
Infecções por HTLV-I/imunologia
Infecções por HTLV-I/transmissão
Sequenciamento de Nucleotídeos em Larga Escala
Imunidade Celular
Interferon gama/biossíntese
Interferon gama/imunologia
Papio anubis
Filogenia
Reação em Cadeia da Polimerase
Vírus 1 Linfotrópico T de Símios/imunologia
Linfócitos T/virologia
Fator de Necrose Tumoral alfa/biossíntese
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Viral); 0 (Gene Products, tax); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma)
[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:170721
[St] Status:MEDLINE


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[PMID]:28724766
[Au] Autor:Ishihara Y; Tanaka Y; Kobayashi S; Kawamura K; Nakasone H; Gomyo A; Hayakawa J; Tamaki M; Akahoshi Y; Harada N; Kusuda M; Kameda K; Ugai T; Wada H; Sakamoto K; Sato M; Terasako-Saito K; Kikuchi M; Kimura SI; Tanihara A; Kako S; Uchimaru K; Kanda Y
[Ad] Endereço:Division of Hematology, Saitama Medical Center, Jichi Medical University, Saitama, Japan.
[Ti] Título:A Unique T-Cell Receptor Amino Acid Sequence Selected by Human T-Cell Lymphotropic Virus Type 1 Tax -Specific Cytotoxic T Cells in HLA-A24:02-Positive Asymptomatic Carriers and Adult T-Cell Leukemia/Lymphoma Patients.
[So] Source:J Virol;91(19), 2017 Oct 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that the T-cell receptor (TCR) repertoire of human T-cell lymphotropic virus type 1 (HTLV-1) Tax -specific CD8 cytotoxic T cells (Tax -CTLs) was highly restricted and a particular amino acid sequence motif, the PDR motif, was conserved among HLA-A*24:02-positive (HLA-A*24:02 ) adult T-cell leukemia/lymphoma (ATL) patients who had undergone allogeneic hematopoietic cell transplantation (allo-HSCT). Furthermore, we found that donor-derived PDR CTLs selectively expanded in ATL long-term HSCT survivors with strong CTL activity against HTLV-1. On the other hand, the TCR repertoires in Tax -CTLs of asymptomatic HTLV-1 carriers (ACs) remain unclear. In this study, we directly identified the DNA sequence of complementarity-determining region 3 (CDR3) of the TCR-ß chain of Tax -CTLs at the single-cell level and compared not only the TCR repertoires but also the frequencies and phenotypes of Tax -CTLs between ACs and ATL patients. We did not observe any essential difference in the frequencies of Tax -CTLs between ACs and ATL patients. In the single-cell TCR repertoire analysis of Tax -CTLs, 1,458 Tax -CTLs and 140 clones were identified in this cohort. Tax -CTLs showed highly restricted TCR repertoires with a strongly biased usage of BV7, and PDR, the unique motif in TCR-ß CDR3, was exclusively observed in all ACs and ATL patients. However, there was no correlation between PDR CTL frequencies and HTLV-1 proviral load (PVL). In conclusion, we have identified, for the first time, a unique amino acid sequence, PDR, as a public TCR-CDR3 motif against Tax in HLA-A*24:02 HTLV-1-infected individuals. Further investigations are warranted to elucidate the role of the PDR CTL response in the progression from carrier state to ATL. ATL is an aggressive T-cell malignancy caused by HTLV-1 infection. The HTLV-1 regulatory protein Tax aggressively promotes the proliferation of HTLV-1-infected lymphocytes and is also a major target antigen for CD8 CTLs. In our previous evaluation of Tax -CTLs, we found that a unique amino acid sequence motif, PDR, in CDR3 of the TCR-ß chain of Tax -CTLs was conserved among ATL patients after allo-HSCT. Furthermore, the PDR Tax -CTL clones selectively expanded and showed strong cytotoxic activities against HTLV-1. On the other hand, it remains unclear how Tax -CTL repertoire exists in ACs. In this study, we comprehensively compared Tax-specific TCR repertoires at the single-cell level between ACs and ATL patients. Tax -CTLs showed highly restricted TCR repertoires with a strongly biased usage of BV7, and PDR, the unique motif in TCR-ß CDR3, was conserved in all ACs and ATL patients, regardless of clinical subtype in HTLV-1 infection.
[Mh] Termos MeSH primário: Produtos do Gene tax/imunologia
Antígeno HLA-A24/imunologia
Vírus 1 Linfotrópico T Humano/imunologia
Leucemia-Linfoma de Células T do Adulto/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
Linfócitos T Citotóxicos/imunologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos/genética
Antígenos CD7/metabolismo
Molécula 1 de Adesão Celular
Moléculas de Adesão Celular/metabolismo
Células Cultivadas
Produtos do Gene tax/genética
Antígeno HLA-A24/genética
Infecções por HTLV-I/patologia
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/genética
Seres Humanos
Imunoglobulinas/metabolismo
Memória Imunológica/imunologia
Leucemia-Linfoma de Células T do Adulto/genética
Receptores de Antígenos de Linfócitos T/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD7); 0 (CADM1 protein, human); 0 (Cell Adhesion Molecule-1); 0 (Cell Adhesion Molecules); 0 (Gene Products, tax); 0 (HLA-A24 Antigen); 0 (Immunoglobulins); 0 (Receptors, Antigen, T-Cell); 0 (tax protein, Human T-lymphotrophic virus 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE


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[PMID]:28669733
[Au] Autor:Permatasari HK; Nakahata S; Ichikawa T; Morishita K
[Ad] Endereço:Division of Tumor and Cellular Biochemistry, Department of Medical Sciences, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan.
[Ti] Título:BCL11B is frequently downregulated in HTLV-1-infected T-cells through Tax-mediated proteasomal degradation.
[So] Source:Biochem Biophys Res Commun;490(3):1086-1092, 2017 Aug 26.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human T-cell leukemia virus type 1 (HTLV-1) is a causative agent of adult T-cell leukemia-lymphoma (ATLL). The HTLV-1-encoded protein Tax plays important roles in the proliferation of HTLV-1-infected T-cells by affecting cellular proteins. In this study, we showed that Tax transcriptionally and post-transcriptionally downregulates the expression of the tumor suppressor gene B-cell leukemia/lymphoma 11B (BCL11B), which encodes a lymphoid-related transcription factor. BCL11B expression was downregulated in HTLV-1-infected T-cell lines at the mRNA and protein levels, and forced expression of BCL11B suppressed the proliferation of these cells. The proteasomal inhibitor MG132 increased BCL11B expression in HTLV-1-infected cell lines, and colocalization of Tax with BCL11B was detected in the cytoplasm of HTLV-1-infected T-cells following MG132 treatment. shRNA knock-down of Tax expression also increased the expression of BCL11B in HTLV-1-infected cells. Moreover, we found that Tax physically binds to BCL11B protein and induces the polyubiquitination of BCL11B and proteasome-dependent degradation of BCL11B. Thus, inactivation of BCL11B by Tax protein may play an important role in the Tax-mediated leukemogenesis.
[Mh] Termos MeSH primário: Produtos do Gene tax/metabolismo
Infecções por HTLV-I/metabolismo
Vírus 1 Linfotrópico T Humano/fisiologia
Leucemia-Linfoma Linfoblástico de Células T Precursoras/metabolismo
Complexo de Endopeptidases do Proteassoma/metabolismo
Proteínas Repressoras/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Regulação para Baixo
Infecções por HTLV-I/genética
Infecções por HTLV-I/virologia
Seres Humanos
Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética
Leucemia-Linfoma Linfoblástico de Células T Precursoras/virologia
Proteólise
Proteínas Repressoras/genética
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCL11B protein, human); 0 (Gene Products, tax); 0 (Repressor Proteins); 0 (Tumor Suppressor Proteins); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE


  8 / 1462 MEDLINE  
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[PMID]:28478312
[Au] Autor:Lin HC; Simon PJ; Ysla RM; Zeichner SL; Brewer G; Rabson AB
[Ad] Endereço:Child Health Institute of New Jersey, Rutgers Robert Wood Johnson Medical School, 89 French Street, New Brunswick, NJ 08903, USA; Rutgers Cancer Institute of New Jersey, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
[Ti] Título:RNA stability regulates human T cell leukemia virus type 1 gene expression in chronically-infected CD4 T cells.
[So] Source:Virology;508:7-17, 2017 Aug.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulation of expression of HTLV-1 gene products from integrated proviruses plays an important role in HTLV-1-associated disease pathogenesis. Previous studies have shown that T cell receptor (TCR)- and phorbol ester (PMA) stimulation of chronically infected CD4 T cells increases the expression of integrated HTLV-1 proviruses in latently infected cells, however the mechanism remains unknown. Analysis of HTLV-1 RNA and protein species following PMA treatment of the latently HTLV-1-infected, FS and SP T cell lines demonstrated rapid induction of tax/rex mRNA. This rapid increase in tax/rex mRNA was associated with markedly enhanced tax/rex mRNA stability while the stability of unspliced or singly spliced HTLV-1 RNAs did not increase. Tax/rex mRNA in the HTLV-1 constitutively expressing cell lines exhibited high basal stability even without PMA treatment. Our data support a model whereby T cell activation leads to increased HTLV-1 gene expression at least in part through increased tax/rex mRNA stability.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/virologia
Regulação Viral da Expressão Gênica
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/genética
RNA Viral/química
[Mh] Termos MeSH secundário: Produtos do Gene tax/genética
Produtos do Gene tax/metabolismo
Vírus 1 Linfotrópico T Humano/química
Vírus 1 Linfotrópico T Humano/fisiologia
Seres Humanos
Estabilidade de RNA
RNA Viral/genética
Latência Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gene Products, tax); 0 (RNA, Viral)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170508
[St] Status:MEDLINE


  9 / 1462 MEDLINE  
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[PMID]:28302940
[Au] Autor:Ohsugi T
[Ad] Endereço:Department of Laboratory Animal Science, School of Veterinary Medicine, Rakuno-Gakuen University, 582 Bunkyodai-Midorimachi, Ebetsu, Hokkaido 069-8501, Japan.
[Ti] Título:Effects of expressing human T-cell leukemia virus type 1 (HTLV-I) oncoprotein Tax on DOK1, DOK2 and DOK3 gene expression in mice.
[So] Source:J Vet Med Sci;79(5):935-938, 2017 May 23.
[Is] ISSN:1347-7439
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Transgenic mice expressing the tax gene from human T-cell leukemia virus type 1 (HTLV-I) genome developed T-cell leukemia or histiocytic sarcoma after at least 12 months. The transgenic mice showed low expression of the downstream of tyrosine kinase (DOK) family members, DOK1, DOK2 and DOK3, which were recently reported to be tumor suppressor genes. Mice showed low DOK2 expression at 5-6 months of age, before disease onset. The expression of DOK1 and DOK3 was not significantly reduced at any age tested. These results suggest that downregulation of DOK2 by the expression of the viral tax gene is the first step in the development of T-cell leukemia or histiocytic sarcoma.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Proteínas de Ligação a DNA/metabolismo
Produtos do Gene tax/metabolismo
Vírus 1 Linfotrópico T Humano/genética
Fosfoproteínas/metabolismo
Proteínas de Ligação a RNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo
Regulação da Expressão Gênica/genética
Regulação da Expressão Gênica/fisiologia
Infecções por HTLV-I/metabolismo
Seres Humanos
Linfoma de Células T/metabolismo
Camundongos
Camundongos Transgênicos
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (DNA-Binding Proteins); 0 (Dok1 protein, mouse); 0 (Dok2 protein, mouse); 0 (Dok3 protein, mouse); 0 (Gene Products, tax); 0 (Phosphoproteins); 0 (RNA-Binding Proteins); 0 (tax protein, Human T-lymphotrophic virus 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE
[do] DOI:10.1292/jvms.17-0034


  10 / 1462 MEDLINE  
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[PMID]:28152383
[Au] Autor:Geddes VEV; José DP; Leal FE; Nixon DF; Tanuri A; Aguiar RS
[Ad] Endereço:Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, 21941-902, Brazil.
[Ti] Título:HTLV-1 Tax activates HIV-1 transcription in latency models.
[So] Source:Virology;504:45-51, 2017 Apr.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HIV-1 latency is a major obstacle to HIV-1 eradication. Coinfection with HTLV-1 has been associated with faster progression to AIDS. HTLV-1 encodes the transactivator Tax which can activate both HTLV-1 and HIV-1 transcription. Here, we demonstrate that Tax activates HIV transcription in latent CD4 T cells. Tax promotes the activation of P-TEFb, releasing CDK9 and Cyclin T1 from inactive forms, promoting transcription elongation and reactivation of latent HIV-1. Tax mutants lacking interaction with the HIV-1-LTR promoter were not able to activate P-TEFb, with no subsequent activation of latent HIV. In HIV-infected primary resting CD4 T cells, Tax-1 reactivated HIV-1 transcription up to five fold, confirming these findings in an ex vivo latency model. Finally, our results confirms that HTLV-1/Tax hijacks cellular partners, promoting HIV-1 transcription, and this interaction should be further investigated in HIV-1 latency studies in patients with HIV/HTLV-1 co-infection.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/virologia
Produtos do Gene tax/genética
HIV-1/genética
Vírus 1 Linfotrópico T Humano/genética
Transcrição Genética/genética
Ativação Transcricional/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Coinfecção
Ciclina T/metabolismo
Quinase 9 Dependente de Ciclina/metabolismo
Proteínas de Fluorescência Verde/genética
Seres Humanos
Células Jurkat
Fator B de Elongação Transcricional Positiva/metabolismo
Regiões Promotoras Genéticas/genética
Latência Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCNT1 protein, human); 0 (Cyclin T); 0 (Gene Products, tax); 0 (tax protein, Human T-lymphotrophic virus 1); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.11.- (Positive Transcriptional Elongation Factor B); EC 2.7.11.22 (CDK9 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 9)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170203
[St] Status:MEDLINE



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