Base de dados : MEDLINE
Pesquisa : D12.644.360.262.700 [Categoria DeCS]
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[PMID]:28409330
[Au] Autor:Ke S; Li RC; Lu J; Meng FK; Feng YK; Fang MH
[Ad] Endereço:Department of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
[Ti] Título:MicroRNA-192 regulates cell proliferation and cell cycle transition in acute myeloid leukemia via interaction with CCNT2.
[So] Source:Int J Hematol;106(2):258-265, 2017 Aug.
[Is] ISSN:1865-3774
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) are a class of small non-coding RNAs approximately 18-22 nucleotides in length, which play an important role in malignant transformation. The roles of miR-192 as an oncogene or tumor suppressor in solid tumors have been previously reported. However, little is known about the role of miR-192 in human acute myeloid leukemia. The results of the present study indicate that miR-192 is significantly downregulated in specimens from acute myeloid leukemia patients. Functional assays demonstrated that overexpression of miR-192 in NB4 and HL-60 cells significantly inhibited cell proliferation compared with that in control cells, and induced G0/G1 cell cycle arrest, cell differentiation, and apoptosis in vitro. Dual-luciferase reporter gene assays showed that miR-192 significantly suppressed the activity of a reporter gene containing the wild type 3'-UTR of CCNT2, but it did not suppress the activity of a reporter gene containing mutated 3'-UTR of CCNT2. QRT-PCR and Western blot assays showed that miR-192 significantly downregulated the expression of CCNT2 in human leukemia cells. Exogenous expression of CCNT2 attenuated the cell cycle arrest induced by miR-192 in NB4 and HL-60 cells. Collectively, miR-192 inhibits cell proliferation and induces G0/G1 cell cycle arrest in AML by regulating the expression of CCNT2.
[Mh] Termos MeSH primário: Ciclo Celular/genética
Proliferação Celular/genética
Transformação Celular Neoplásica/genética
Ciclina T/genética
Ciclina T/fisiologia
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/patologia
MicroRNAs/genética
MicroRNAs/fisiologia
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Apoptose/genética
Pontos de Checagem do Ciclo Celular/genética
Regulação para Baixo
Expressão Gênica
Células HL-60
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (CCNT2 protein, human); 0 (Cyclin T); 0 (MIRN192 microRNA, human); 0 (MicroRNAs)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1007/s12185-017-2232-2


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[PMID]:28326644
[Au] Autor:Shida H; Okada H; Suzuki H; Zhang X; Chen J; Tsunetsugu-Yokota Y; Tanaka Y; Yakushiji F; Hayashi Y
[Ad] Endereço:Institute for Genetic Medicine, Hokkaido University, Kita-ku, Sapporo, 060-0815, Japan.
[Ti] Título:HIV-1 susceptibility of transgenic rat-derived primary macrophage/T cells and a T cell line that express human receptors, CyclinT1 and CRM1 genes.
[So] Source:Genes Cells;22(5):424-435, 2017 May.
[Is] ISSN:1365-2443
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We developed transgenic (Tg) rats that express human CD4, CCR5, CXCR4, CyclinT1, and CRM1 genes. Tg rat macrophages were efficiently infected with HIV-1 and supported production of infectious progeny virus. By contrast, both rat primary CD4 T cells and established T cell lines expressing human CD4, CCR5, CyclinT1, and CRM1 genes were infected inefficiently, but this was ameliorated by inhibition of cyclophilin A. The infectivity of rat T cell-derived virus was lower than that of human T cell-derived virus.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Ciclina T/metabolismo
Infecções por HIV/imunologia
Carioferinas/metabolismo
Macrófagos/imunologia
Receptores Citoplasmáticos e Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/virologia
Linhagem Celular
Células Cultivadas
Ciclina T/genética
Suscetibilidade a Doenças
HIV-1/patogenicidade
Seres Humanos
Carioferinas/genética
Macrófagos/virologia
Ratos
Receptores CXCR4/genética
Receptores CXCR4/metabolismo
Receptores Citoplasmáticos e Nucleares/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin T); 0 (Karyopherins); 0 (Receptors, CXCR4); 0 (Receptors, Cytoplasmic and Nuclear); 0 (exportin 1 protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1111/gtc.12486


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[PMID]:28262505
[Au] Autor:Cheung KL; Zhang F; Jaganathan A; Sharma R; Zhang Q; Konuma T; Shen T; Lee JY; Ren C; Chen CH; Lu G; Olson MR; Zhang W; Kaplan MH; Littman DR; Walsh MJ; Xiong H; Zeng L; Zhou MM
[Ad] Endereço:Department of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
[Ti] Título:Distinct Roles of Brd2 and Brd4 in Potentiating the Transcriptional Program for Th17 Cell Differentiation.
[So] Source:Mol Cell;65(6):1068-1080.e5, 2017 Mar 16.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The BET proteins are major transcriptional regulators and have emerged as new drug targets, but their functional distinction has remained elusive. In this study, we report that the BET family members Brd2 and Brd4 exert distinct genomic functions at genes whose transcription they co-regulate during mouse T helper 17 (Th17) cell differentiation. Brd2 is associated with the chromatin insulator CTCF and the cohesin complex to support cis-regulatory enhancer assembly for gene transcriptional activation. In this context, Brd2 binds the transcription factor Stat3 in an acetylation-sensitive manner and facilitates Stat3 recruitment to active enhancers occupied with transcription factors Irf4 and Batf. In parallel, Brd4 temporally controls RNA polymerase II (Pol II) processivity during transcription elongation through cyclin T1 and Cdk9 recruitment and Pol II Ser2 phosphorylation. Collectively, our study uncovers both separate and interdependent Brd2 and Brd4 functions in potentiating the genetic program required for Th17 cell development and adaptive immunity.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Diferenciação Celular
Cromatina/enzimologia
Proteínas Cromossômicas não Histona/metabolismo
Proteínas Nucleares/metabolismo
Células Th17/enzimologia
Fatores de Transcrição/metabolismo
Transcrição Genética
[Mh] Termos MeSH secundário: Acetilação
Animais
Fator de Ligação a CCCTC
Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Células Cultivadas
Cromatina/genética
Proteínas Cromossômicas não Histona/química
Proteínas Cromossômicas não Histona/genética
Ciclina T/genética
Ciclina T/metabolismo
Quinase 9 Dependente de Ciclina/genética
Quinase 9 Dependente de Ciclina/metabolismo
Regulação da Expressão Gênica
Fatores Reguladores de Interferon/genética
Fatores Reguladores de Interferon/metabolismo
Camundongos Endogâmicos C57BL
Modelos Moleculares
Proteínas Nucleares/genética
Fenótipo
Fosforilação
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Interferência de RNA
RNA Polimerase II/metabolismo
Proteínas Repressoras/genética
Proteínas Repressoras/metabolismo
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Relação Estrutura-Atividade
Células Th17/imunologia
Fatores de Transcrição/genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brd4 protein, mouse); 0 (CCCTC-Binding Factor); 0 (Ccnt1 protein, mouse); 0 (Cell Cycle Proteins); 0 (Chromatin); 0 (Chromosomal Proteins, Non-Histone); 0 (Ctcf protein, mouse); 0 (Cyclin T); 0 (Interferon Regulatory Factors); 0 (Nuclear Proteins); 0 (Repressor Proteins); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (Transcription Factors); 0 (cohesins); 0 (interferon regulatory factor-4); EC 2.7.1.- (Brd2 protein, mouse); EC 2.7.11.22 (Cdk9 protein, mouse); EC 2.7.11.22 (Cyclin-Dependent Kinase 9); EC 2.7.7.- (RNA Polymerase II)
[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:170307
[St] Status:MEDLINE


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[PMID]:28178316
[Au] Autor:Asamitsu K; Hirokawa T; Okamoto T
[Ad] Endereço:Department of Molecular and Cellular Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, Japan.
[Ti] Título:MD simulation of the Tat/Cyclin T1/CDK9 complex revealing the hidden catalytic cavity within the CDK9 molecule upon Tat binding.
[So] Source:PLoS One;12(2):e0171727, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we applied molecular dynamics (MD) simulation to analyze the dynamic behavior of the Tat/CycT1/CDK9 tri-molecular complex and revealed the structural changes of P-TEFb upon Tat binding. We found that Tat could deliberately change the local flexibility of CycT1. Although the structural coordinates of the H1 and H2 helices did not substantially change, H1', H2', and H3' exhibited significant changes en masse. Consequently, the CycT1 residues involved in Tat binding, namely Tat-recognition residues (TRRs), lost their flexibility with the addition of Tat to P-TEFb. In addition, we clarified the structural variation of CDK9 in complex with CycT1 in the presence or absence of Tat. Interestingly, Tat addition significantly reduced the structural variability of the T-loop, thus consolidating the structural integrity of P-TEFb. Finally, we deciphered the formation of the hidden catalytic cavity of CDK9 upon Tat binding. MD simulation revealed that the PITALRE signature sequence of CDK9 flips the inactive kinase cavity of CDK9 into the active form by connecting with Thr186, which is crucial for its activity, thus presumably recruiting the substrate peptide such as the C-terminal domain of RNA pol II. These findings provide vital information for the development of effective novel anti-HIV drugs with CDK9 catalytic activity as the target.
[Mh] Termos MeSH primário: Ciclina T/química
Quinase 9 Dependente de Ciclina/química
Simulação de Dinâmica Molecular
Complexos Multiproteicos/química
Produtos do Gene tat do Vírus da Imunodeficiência Humana/química
[Mh] Termos MeSH secundário: Sítios de Ligação
Catálise
Ciclina T/metabolismo
Quinase 9 Dependente de Ciclina/metabolismo
Complexos Multiproteicos/metabolismo
Ligação Proteica
Conformação Proteica
Estabilidade Proteica
Relação Estrutura-Atividade
Produtos do Gene tat do Vírus da Imunodeficiência Humana/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin T); 0 (Multiprotein Complexes); 0 (tat Gene Products, Human Immunodeficiency Virus); EC 2.7.11.22 (Cyclin-Dependent Kinase 9)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0171727


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Tanuri, Amilcar
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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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[PMID]:27627980
[Au] Autor:Broholm C; Olsson AH; Perfilyev A; Hansen NS; Schrölkamp M; Strasko KS; Scheele C; Ribel-Madsen R; Mortensen B; Jørgensen SW; Ling C; Vaag A
[Ad] Endereço:Department of Endocrinology, Diabetes and Metabolism, Rigshospitalet - Section 7652, Tagensvej 20, DK-2200, Copenhagen, Denmark. christa.broholm@gmail.com.
[Ti] Título:Epigenetic programming of adipose-derived stem cells in low birthweight individuals.
[So] Source:Diabetologia;59(12):2664-2673, 2016 Dec.
[Is] ISSN:1432-0428
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:AIMS/HYPOTHESIS: Low birthweight (LBW) is associated with dysfunctions of adipose tissue and metabolic disease in adult life. We hypothesised that altered epigenetic and transcriptional regulation of adipose-derived stem cells (ADSCs) could play a role in programming adipose tissue dysfunction in LBW individuals. METHODS: ADSCs were isolated from the subcutaneous adipose tissue of 13 normal birthweight (NBW) and 13 LBW adult men. The adipocytes were cultured in vitro, and genome-wide differences in RNA expression and DNA methylation profiles were analysed in ADSCs and differentiated adipocytes. RESULTS: We demonstrated that ADSCs from LBW individuals exhibit multiple expression changes as well as genome-wide alterations in methylation pattern. Reduced expression of the transcription factor cyclin T2 encoded by CCNT2 may play a key role in orchestrating several of the gene expression changes in ADSCs from LBW individuals. Indeed, silencing of CCNT2 in human adipocytes decreased leptin secretion as well as the mRNA expression of several genes involved in adipogenesis, including MGLL, LIPE, PPARG, LEP and ADIPOQ. Only subtle genome-wide mRNA expression and DNA methylation changes were seen in mature cultured adipocytes from LBW individuals. CONCLUSIONS/INTERPRETATION: Epigenetic and transcriptional changes in LBW individuals are most pronounced in immature ADSCs that in turn may programme physiological characteristics of the mature adipocytes that influence the risk of metabolic diseases. Reduced expression of CCNT2 may play a key role in the developmental programming of adipose tissue.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Tecido Adiposo/citologia
Tecido Adiposo/metabolismo
Metilação de DNA/genética
Epigênese Genética/genética
Células-Tronco/citologia
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Adipogenia/genética
Adiponectina/genética
Adulto
Peso ao Nascer/genética
Peso ao Nascer/fisiologia
Células Cultivadas
Ciclina T/genética
Seres Humanos
Masculino
RNA Interferente Pequeno/genética
Reação em Cadeia da Polimerase em Tempo Real
Fator de Transcrição STAT2/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Adiponectin); 0 (CCNT2 protein, human); 0 (Cyclin T); 0 (RNA, Small Interfering); 0 (STAT2 Transcription Factor); 0 (STAT2 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160916
[St] Status:MEDLINE


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[PMID]:27343897
[Au] Autor:Hatch VL; Marin-Barba M; Moxon S; Ford CT; Ward NJ; Tomlinson ML; Desanlis I; Hendry AE; Hontelez S; van Kruijsbergen I; Veenstra GJ; Münsterberg AE; Wheeler GN
[Ad] Endereço:School of Biological Sciences, University of East Anglia, Norwich Research Park, Norwich NR4 7TJ, UK.
[Ti] Título:The positive transcriptional elongation factor (P-TEFb) is required for neural crest specification.
[So] Source:Dev Biol;416(2):361-72, 2016 08 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulation of gene expression at the level of transcriptional elongation has been shown to be important in stem cells and tumour cells, but its role in the whole animal is only now being fully explored. Neural crest cells (NCCs) are a multipotent population of cells that migrate during early development from the dorsal neural tube throughout the embryo where they differentiate into a variety of cell types including pigment cells, cranio-facial skeleton and sensory neurons. Specification of NCCs is both spatially and temporally regulated during embryonic development. Here we show that components of the transcriptional elongation regulatory machinery, CDK9 and CYCLINT1 of the P-TEFb complex, are required to regulate neural crest specification. In particular, we show that expression of the proto-oncogene c-Myc and c-Myc responsive genes are affected. Our data suggest that P-TEFb is crucial to drive expression of c-Myc, which acts as a 'gate-keeper' for the correct temporal and spatial development of the neural crest.
[Mh] Termos MeSH primário: Ciclina T/genética
Quinase 9 Dependente de Ciclina/genética
Regulação da Expressão Gênica no Desenvolvimento
Genes myc
Crista Neural/embriologia
Fator B de Elongação Transcricional Positiva/genética
Elongação da Transcrição Genética
Proteínas de Xenopus/genética
Xenopus laevis/embriologia
[Mh] Termos MeSH secundário: Animais
Ciclina T/deficiência
Quinase 9 Dependente de Ciclina/deficiência
Isoxazóis/farmacologia
Morfolinos/farmacologia
Fator B de Elongação Transcricional Positiva/deficiência
Proteínas Proto-Oncogênicas c-myc/biossíntese
RNA Polimerase II/metabolismo
Fatores de Transcrição SOXE/biossíntese
Fatores de Transcrição SOXE/genética
Elongação da Transcrição Genética/efeitos dos fármacos
Transcrição Genética
Proteínas de Xenopus/deficiência
Xenopus laevis/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cyclin T); 0 (Isoxazoles); 0 (Morpholinos); 0 (Proto-Oncogene Proteins c-myc); 0 (SOXE Transcription Factors); 0 (Xenopus Proteins); EC 2.7.11.- (Positive Transcriptional Elongation Factor B); EC 2.7.11.22 (Cyclin-Dependent Kinase 9); EC 2.7.7.- (RNA Polymerase II); G162GK9U4W (leflunomide)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160626
[St] Status:MEDLINE


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[PMID]:27286828
[Au] Autor:Borkar AN; Bardaro MF; Camilloni C; Aprile FA; Varani G; Vendruscolo M
[Ad] Endereço:Department of Chemistry, University of Cambridge, Cambridge CB2 1EW, United Kingdom;
[Ti] Título:Structure of a low-population binding intermediate in protein-RNA recognition.
[So] Source:Proc Natl Acad Sci U S A;113(26):7171-6, 2016 06 28.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interaction of the HIV-1 protein transactivator of transcription (Tat) and its cognate transactivation response element (TAR) RNA transactivates viral transcription and represents a paradigm for the widespread occurrence of conformational rearrangements in protein-RNA recognition. Although the structures of free and bound forms of TAR are well characterized, the conformations of the intermediates in the binding process are still unknown. By determining the free energy landscape of the complex using NMR residual dipolar couplings in replica-averaged metadynamics simulations, we observe two low-population intermediates. We then rationally design two mutants, one in the protein and another in the RNA, that weaken specific nonnative interactions that stabilize one of the intermediates. By using surface plasmon resonance, we show that these mutations lower the release rate of Tat, as predicted. These results identify the structure of an intermediate for RNA-protein binding and illustrate a general strategy to achieve this goal with high resolution.
[Mh] Termos MeSH primário: Repetição Terminal Longa de HIV/fisiologia
RNA Viral/metabolismo
Produtos do Gene tat do Vírus da Imunodeficiência Humana/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Ciclina T/metabolismo
Quinase 9 Dependente de Ciclina/metabolismo
Espectroscopia de Ressonância Magnética
Simulação de Dinâmica Molecular
Ressonância de Plasmônio de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (CCNT1 protein, human); 0 (Cyclin T); 0 (RNA, Viral); 0 (tat Gene Products, Human Immunodeficiency Virus); EC 2.7.11.22 (CDK9 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 9)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160612
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1521349113


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[PMID]:27193293
[Au] Autor:Asamitsu K; Omagari K; Okuda T; Hibi Y; Okamoto T
[Ad] Endereço:Department of Molecular and Cellular Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, 467-8601, Japan.
[Ti] Título:Quantification of the HIV transcriptional activator complex in live cells by image-based protein-protein interaction analysis.
[So] Source:Genes Cells;21(7):706-16, 2016 Jul.
[Is] ISSN:1365-2443
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The virus-encoded Tat protein is essential for HIV transcription in infected cells. The interaction of Tat with the cellular transcription elongation factor P-TEFb (positive transcriptional elongation factor b) containing cyclin T1 (CycT1) and cyclin-dependent kinase 9 (CDK9) is critical for its activity. In this study, we use the Fluoppi (fluorescent-based technology detecting protein-protein interaction) system, which enables the quantification of interactions between biomolecules, such as proteins, in live cells. Quantitative measurement of the molecular interactions among Tat, CycT1 and CDK9 has showed that any third molecule enhances the binding between the other two molecules. These findings suggest that each component of the Tat:P-TEFb complex stabilizes the overall complex, thereby supporting the efficient transcriptional elongation during viral RNA synthesis. These interactions may serve as appropriate targets for novel anti-HIV therapy.
[Mh] Termos MeSH primário: Ciclina T/genética
Quinase 9 Dependente de Ciclina/genética
HIV/genética
Fator B de Elongação Transcricional Positiva/genética
Produtos do Gene tat do Vírus da Imunodeficiência Humana/genética
[Mh] Termos MeSH secundário: Ciclina T/metabolismo
Quinase 9 Dependente de Ciclina/metabolismo
HIV/patogenicidade
Infecções por HIV/genética
Infecções por HIV/virologia
Seres Humanos
Complexos Multiproteicos/genética
Fator B de Elongação Transcricional Positiva/metabolismo
Mapas de Interação de Proteínas/genética
Transcrição Genética
Replicação Viral/genética
Produtos do Gene tat do Vírus da Imunodeficiência Humana/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCNT1 protein, human); 0 (Cyclin T); 0 (Multiprotein Complexes); 0 (tat Gene Products, Human Immunodeficiency Virus); 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:1702
[Cu] Atualização por classe:170213
[Lr] Data última revisão:
170213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160520
[St] Status:MEDLINE
[do] DOI:10.1111/gtc.12375


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[PMID]:27068475
[Au] Autor:Zhao Y; Wang L; Ren S; Wang L; Blackburn PR; McNulty MS; Gao X; Qiao M; Vessella RL; Kohli M; Zhang J; Karnes RJ; Tindall DJ; Kim Y; MacLeod R; Ekker SC; Kang T; Sun Y; Huang H
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA; Department of Urology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA; Mayo Clinic Cancer Center, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
[Ti] Título:Activation of P-TEFb by Androgen Receptor-Regulated Enhancer RNAs in Castration-Resistant Prostate Cancer.
[So] Source:Cell Rep;15(3):599-610, 2016 Apr 19.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The androgen receptor (AR) is required for castration-resistant prostate cancer (CRPC) progression, but the function and disease relevance of AR-bound enhancers remain unclear. Here, we identify a group of AR-regulated enhancer RNAs (e.g., PSA eRNA) that are upregulated in CRPC cells, patient-derived xenografts (PDXs), and patient tissues. PSA eRNA binds to CYCLIN T1, activates P-TEFb, and promotes cis and trans target gene transcription by increasing serine-2 phosphorylation of RNA polymerase II (Pol II-Ser2p). We define an HIV-1 TAR RNA-like (TAR-L) motif in PSA eRNA that is required for CYCLIN T1 binding. Using TALEN-mediated gene editing we further demonstrate that this motif is essential for increased Pol II-Ser2p occupancy levels and CRPC cell growth. We have uncovered a P-TEFb activation mechanism and reveal altered eRNA expression that is related to abnormal AR function and may potentially be a therapeutic target in CRPC.
[Mh] Termos MeSH primário: Fator B de Elongação Transcricional Positiva/metabolismo
Neoplasias de Próstata Resistentes à Castração/genética
RNA/metabolismo
Receptores Androgênicos/metabolismo
[Mh] Termos MeSH secundário: Sequência de Bases
Linhagem Celular Tumoral
Proliferação Celular
Ciclina T/metabolismo
Elementos Facilitadores Genéticos/genética
Regulação Neoplásica da Expressão Gênica
Loci Gênicos
Seres Humanos
Masculino
Modelos Biológicos
Motivos de Nucleotídeos/genética
Fosforilação
Antígeno Prostático Específico/genética
Neoplasias de Próstata Resistentes à Castração/patologia
Ligação Proteica
RNA Polimerase II/metabolismo
Serina/metabolismo
Regulação para Cima/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 (AR protein, human); 0 (Cyclin T); 0 (Receptors, Androgen); 452VLY9402 (Serine); 63231-63-0 (RNA); EC 2.7.11.- (Positive Transcriptional Elongation Factor B); EC 2.7.7.- (RNA Polymerase II); EC 3.4.21.77 (Prostate-Specific Antigen)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160413
[St] Status:MEDLINE



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