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  1 / 15836 MEDLINE  
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[PMID]:28470612
[Au] Autor:Berger I; Jiang Q; Schulze RJ; Collinson I; Schaffitzel C
[Ad] Endereço:The School of Biochemistry, University Walk, University of Bristol, Clifton, BS8 1TD, UK. imre.berger@bristol.ac.uk.
[Ti] Título:Multiprotein Complex Production in E. coli: The SecYEG-SecDFYajC-YidC Holotranslocon.
[So] Source:Methods Mol Biol;1586:279-290, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A modular approach for balanced overexpression of recombinant multiprotein complexes in E. coli is described, with the prokaryotic protein secretase/insertase complex, the SecYEG-SecDFYajC-YidC holotranslocon (HTL), used as an example. This procedure has been implemented here in the ACEMBL system. The protocol details the design principles of the monocistronic or polycistronic DNA constructs, the expression and purification of functional HTL and its association with translating ribosome nascent chain (RNC) complexes into a RNC-HTL supercomplex.
[Mh] Termos MeSH primário: Escherichia coli/genética
Complexos Multiproteicos/genética
Canais de Translocação SEC/genética
[Mh] Termos MeSH secundário: Clonagem Molecular/métodos
DNA Recombinante/genética
Proteínas de Escherichia coli/genética
Proteínas de Membrana Transportadoras/genética
Plasmídeos/genética
Proteínas Recombinantes/genética
Ribossomos/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Recombinant); 0 (Escherichia coli Proteins); 0 (Membrane Transport Proteins); 0 (Multiprotein Complexes); 0 (Recombinant Proteins); 0 (SEC Translocation Channels); 0 (SecD protein, E coli); 0 (YIDC protein, E coli)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6887-9_18


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[PMID]:29206240
[Au] Autor:Treat BR; Bidula SM; Ramachandran S; St Leger AJ; Hendricks RL; Kinchington PR
[Ad] Endereço:Molecular Virology and Microbiology Graduate Program, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
[Ti] Título:Influence of an immunodominant herpes simplex virus type 1 CD8+ T cell epitope on the target hierarchy and function of subdominant CD8+ T cells.
[So] Source:PLoS Pathog;13(12):e1006732, 2017 Dec.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Herpes simplex virus type 1 (HSV-1) latency in sensory ganglia such as trigeminal ganglia (TG) is associated with a persistent immune infiltrate that includes effector memory CD8+ T cells that can influence HSV-1 reactivation. In C57BL/6 mice, HSV-1 induces a highly skewed CD8+ T cell repertoire, in which half of CD8+ T cells (gB-CD8s) recognize a single epitope on glycoprotein B (gB498-505), while the remainder (non-gB-CD8s) recognize, in varying proportions, 19 subdominant epitopes on 12 viral proteins. The gB-CD8s remain functional in TG throughout latency, while non-gB-CD8s exhibit varying degrees of functional compromise. To understand how dominance hierarchies relate to CD8+ T cell function during latency, we characterized the TG-associated CD8+ T cells following corneal infection with a recombinant HSV-1 lacking the immunodominant gB498-505 epitope (S1L). S1L induced a numerically equivalent CD8+ T cell infiltrate in the TG that was HSV-specific, but lacked specificity for gB498-505. Instead, there was a general increase of non-gB-CD8s with specific subdominant epitopes arising to codominance. In a latent S1L infection, non-gB-CD8s in the TG showed a hierarchy targeting different epitopes at latency compared to at acute times, and these cells retained an increased functionality at latency. In a latent S1L infection, these non-gB-CD8s also display an equivalent ability to block HSV reactivation in ex vivo ganglionic cultures compared to TG infected with wild type HSV-1. These data indicate that loss of the immunodominant gB498-505 epitope alters the dominance hierarchy and reduces functional compromise of CD8+ T cells specific for subdominant HSV-1 epitopes during viral latency.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/virologia
Herpes Simples/imunologia
Herpesvirus Humano 1/imunologia
Epitopos Imunodominantes/metabolismo
Gânglio Trigeminal/virologia
Proteínas do Envelope Viral/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/patologia
Linhagem Celular
Células Cultivadas
Cercopithecus aethiops
DNA Recombinante/metabolismo
Infecções Oculares Virais/imunologia
Infecções Oculares Virais/metabolismo
Infecções Oculares Virais/patologia
Infecções Oculares Virais/virologia
Feminino
Deleção de Genes
Herpes Simples/metabolismo
Herpes Simples/patologia
Herpes Simples/virologia
Herpesvirus Humano 1/fisiologia
Camundongos Endogâmicos C57BL
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/metabolismo
Mutação Puntual
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Gânglio Trigeminal/imunologia
Gânglio Trigeminal/patologia
Células Vero
Proteínas do Envelope Viral/química
Proteínas do Envelope Viral/genética
Ativação Viral
Latência Viral
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Recombinant); 0 (Immunodominant Epitopes); 0 (Peptide Fragments); 0 (Recombinant Fusion Proteins); 0 (Viral Envelope Proteins); 0 (glycoprotein B, human herpesvirus 1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006732


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[PMID]:28749559
[Au] Autor:Li G; Zhu Y; Shao D; Chang H; Zhang X; Zhou D; Gao Y; Lan K; Deng Q
[Ad] Endereço:CAS Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Shanghai, China.
[Ti] Título:Recombinant covalently closed circular DNA of hepatitis B virus induces long-term viral persistence with chronic hepatitis in a mouse model.
[So] Source:Hepatology;67(1):56-70, 2018 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Covalently closed circular DNA of hepatitis B virus (HBV) is critical for viral persistence in vivo. We recently reported a technique involving recombinant covalently closed circular DNA (rcccDNA) of HBV by site-specific DNA recombination. Using hydrodynamic injection, rcccDNA induces a temporarily prolonged HBV antigenemia in immunocompetent mice, similar to acute resolving HBV infection. In this study, we simulated the pathophysiological impact of chronic hepatitis to reproduce rcccDNA persistence in mouse models. We showed that rcccDNA achieved long-lasting persistence in the presence of a compromised immune response or when transcriptional activity was repressed. To closely mimic chronic hepatitis, we used a replication-defective recombinant adenoviral vector to deliver rcccDNA to the liver, which led to prominent HBV persistence throughout the experiment duration (>62 weeks) in transgenic mice expressing Cre recombinase under the albumin promoter. A sustained necroinflammatory response and fibrosis were identified in mouse livers, with dysplastic lesions commonly seen during the late stage of viral persistence, analogous to the progressive pathology of clinical chronic hepatitis. CONCLUSION: rcccDNA was intrinsically stable in vivo, enabling long-term persistence in the context of chronic hepatitis, and viral persistence, in turn, may promote progression of chronic liver disease; our study also presented a surrogate model of HBV cccDNA persistence in mice that could advance our understanding of the pathogenesis of chronic hepatitis B. (Hepatology 2018;67:56-70).
[Mh] Termos MeSH primário: Replicação do DNA/genética
Vírus da Hepatite B/genética
Vírus da Hepatite B/fisiologia
Hepatite B Crônica/patologia
Replicação Viral/genética
[Mh] Termos MeSH secundário: Animais
Biópsia por Agulha
DNA Circular/genética
DNA Recombinante/genética
DNA Viral
Modelos Animais de Doenças
Hepatite B Crônica/genética
Hepatite B Crônica/virologia
Imuno-Histoquímica
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Distribuição Aleatória
Reação em Cadeia da Polimerase em Tempo Real
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Circular); 0 (DNA, Recombinant); 0 (DNA, Viral)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29406


  4 / 15836 MEDLINE  
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[PMID]:28696257
[Au] Autor:Zhi X; Dages S; Dages K; Liu Y; Hua ZC; Makemson J; Leng F
[Ad] Endereço:From the Biomolecular Sciences Institute and.
[Ti] Título:Transient and dynamic DNA supercoiling potently stimulates the promoter in .
[So] Source:J Biol Chem;292(35):14566-14575, 2017 Sep 01.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The inactive prokaryotic promoter (P ) contains a single A-to-G point mutation in the -10 region of the leucine operon promoter, which causes leucine auxotrophy. This promoter can be activated by (-) DNA supercoiling in strains. However, whether this activation arises from global, permanent, or transient, dynamic supercoiling is still not fully understood. In this article, using a newly established system carrying a pair of divergently coupled promoters, an IPTG-inducible promoter and P that control the expression of and (the firefly luciferase gene), respectively, we demonstrate that transient, dynamic (-) DNA supercoiling provided by divergent transcription in both wild-type and strains can potently activate P We found that this activation depended on the promoter strength and the length of RNA transcripts, which are functional characteristics of transcription-coupled DNA supercoiling (TCDS) precisely predicted by the twin-supercoiled domain model of transcription in which a (+) supercoiled domain is produced ahead of the RNA polymerase and a (-) supercoiled domain behind it. We also demonstrate that TCDS can be generated on topologically open DNA molecules, linear DNA molecules, in , suggesting that topological boundaries or barriers are not required for the production of TCDS This work demonstrates that transient, dynamic TCDS by RNA polymerases is a major chromosome remodeling force in and greatly influences the nearby, coupled promoters/transcription.
[Mh] Termos MeSH primário: DNA Bacteriano/metabolismo
DNA Super-Helicoidal/metabolismo
Escherichia coli/metabolismo
Regulação Bacteriana da Expressão Gênica
Mutação Puntual
Regiões Promotoras Genéticas
Ativação Transcricional
[Mh] Termos MeSH secundário: Montagem e Desmontagem da Cromatina
DNA Bacteriano/química
DNA Circular
DNA Recombinante/química
DNA Recombinante/metabolismo
DNA Super-Helicoidal/química
RNA Polimerases Dirigidas por DNA/genética
RNA Polimerases Dirigidas por DNA/metabolismo
Escherichia coli/genética
Escherichia coli/crescimento & desenvolvimento
Deleção de Genes
Cinética
Leucina/metabolismo
Luciferases de Vaga-Lume/genética
Luciferases de Vaga-Lume/metabolismo
Óperon
Plasmídeos/genética
Plasmídeos/metabolismo
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Especificidade da Espécie
Transcrição Genética
Proteínas Virais/genética
Proteínas Virais/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Bacterial); 0 (DNA, Circular); 0 (DNA, Recombinant); 0 (DNA, Superhelical); 0 (Recombinant Proteins); 0 (Viral Proteins); EC 1.13.12.7 (Luciferases, Firefly); EC 2.7.7.- (bacteriophage T7 RNA polymerase); EC 2.7.7.6 (DNA-Directed RNA Polymerases); GMW67QNF9C (Leucine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.794628


  5 / 15836 MEDLINE  
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[PMID]:28684419
[Au] Autor:Akinfenwa PY; Bond WS; Ildefonso CJ; Hurwitz MY; Hurwitz RL
[Ad] Endereço:From the Interdepartmental Program in Translational Biology and Molecular Medicine.
[Ti] Título:Versican G1 domain enhances adenoviral-mediated transgene expression and can be modulated by inhibitors of the Janus kinase (JAK)/STAT and Src family kinase pathways.
[So] Source:J Biol Chem;292(35):14381-14390, 2017 Sep 01.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To examine the biochemical influences that may contribute to the success of gene therapy for ocular disorders, the role of versican, a vitreous component, in adenoviral-mediated transgene expression was examined. Versican is a large chondroitin sulfate-containing, hyaluronic acid-binding proteoglycan present in the extracellular matrix and in ocular vitreous body. Y79 retinoblastoma cells and CD44-negative SK-N-DZ neuroblastoma cells transduced with adenoviral vectors in the presence of versican respond with an activation of transgene expression. Proteolysis of versican generates a hyaluronan-binding G1 domain. The addition of recombinant versican G1 to SK-N-DZ cells results in a similar activation of transgene expression, and treatment with dasatinib, an inhibitor of Src family kinases, also mimics the effects of versican. Enhancement is accompanied by an increase in signal transducer and activator of transcription 5 (STAT5) phosphorylation and is abrogated by treatment with C188-9, a STAT3/5 inhibitor, or with ruxolitinib, a Janus kinase 1/2 (JAK1/2) inhibitor. These data implicate versican G1 in enhancing adenoviral vector transgene expression in a hyaluronic acid-CD44 independent manner that is down-regulated by inhibitors of the JAK/STAT pathway and enhanced by inhibitors of the Src kinase pathway.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Proteínas de Neoplasias/metabolismo
Neoplasias/genética
Neoplasias/terapia
Inibidores de Proteínas Quinases/farmacologia
Versicanas/metabolismo
[Mh] Termos MeSH secundário: Adenoviridae/crescimento & desenvolvimento
Adenoviridae/fisiologia
Animais
Células COS
Linhagem Celular Tumoral
Cercopithecus aethiops
DNA Recombinante/metabolismo
DNA Viral/metabolismo
Genes Reporter/efeitos dos fármacos
Vetores Genéticos
Seres Humanos
Janus Quinases/antagonistas & inibidores
Janus Quinases/metabolismo
Proteínas de Neoplasias/antagonistas & inibidores
Proteínas de Neoplasias/química
Proteínas de Neoplasias/genética
Neoplasias/metabolismo
Neoplasias/virologia
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Fatores de Transcrição STAT/antagonistas & inibidores
Fatores de Transcrição STAT/metabolismo
Transdução de Sinais/efeitos dos fármacos
Versicanas/química
Versicanas/genética
Replicação Viral/efeitos dos fármacos
Quinases da Família src/antagonistas & inibidores
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (DNA, Recombinant); 0 (DNA, Viral); 0 (Neoplasm Proteins); 0 (Peptide Fragments); 0 (Protein Kinase Inhibitors); 0 (Recombinant Fusion Proteins); 0 (STAT Transcription Factors); 0 (VCAN protein, human); 126968-45-4 (Versicans); EC 2.7.10.2 (Janus Kinases); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.773549


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[PMID]:28637869
[Au] Autor:Chen Z; Eggerman TL; Bocharov AV; Baranova IN; Vishnyakova TG; Kurlander R; Patterson AP
[Ad] Endereço:From the Department of Laboratory Medicine, Clinical Center.
[Ti] Título:Heat shock proteins stimulate APOBEC-3-mediated cytidine deamination in the hepatitis B virus.
[So] Source:J Biol Chem;292(32):13459-13479, 2017 Aug 11.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Apolipoprotein B mRNA-editing enzyme catalytic subunit 3 (APOBEC-3) enzymes are cytidine deaminases that are broadly and constitutively expressed. They are often up-regulated during carcinogenesis and candidate genes for causing the major single-base substitution in cancer-associated DNA mutations. Moreover, APOBEC-3s are involved in host innate immunity against many viruses. However, how APOBEC-3 mutational activity is regulated in normal and pathological conditions remains largely unknown. Heat shock protein levels are often elevated in both carcinogenesis and viral infection and are associated with DNA mutations. Here, using mutational analyses of hepatitis B virus (HBV), we found that Hsp90 stimulates deamination activity of APOBEC-3G (A3G), A3B, and A3C during co-expression in human liver HepG2 cells. Hsp90 directly stimulated A3G deamination activity when the purified proteins were used in reactions. Hsp40, -60, and -70 also had variable stimulatory effects in the cellular assay, but not Sequencing analyses further demonstrated that Hsp90 increased both A3G cytosine mutation efficiency on HBV DNA and total HBV mutation frequency. In addition, Hsp90 shifted A3G's cytosine region selection in HBV DNA and increased A3G's 5' nucleoside preference for deoxycytidine (5'-CC). Furthermore, the Hsp90 inhibitor 17- -allylamino-17-demethoxygeldanamycin dose dependently inhibited A3G and A3B mutational activity on HBV viral DNA. Hsp90 knockdown by siRNA or by Hsp90 active-site mutation also decreased A3G activity. These results indicate that heat shock proteins, in particular Hsp90, stimulate APOBEC-3-mediated DNA deamination activity, suggesting a potential physiological role in carcinogenesis and viral innate immunity.
[Mh] Termos MeSH primário: Desaminase APOBEC-3G/metabolismo
Citidina Desaminase/metabolismo
DNA Viral/metabolismo
Proteínas de Choque Térmico HSP90/metabolismo
Vírus da Hepatite B/metabolismo
Hepatócitos/metabolismo
Antígenos de Histocompatibilidade Menor/metabolismo
[Mh] Termos MeSH secundário: Desaminase APOBEC-3G/química
Desaminase APOBEC-3G/genética
Carcinogênese
Citidina/metabolismo
Citidina Desaminase/química
Citidina Desaminase/genética
Análise Mutacional de DNA
DNA Recombinante/química
DNA Recombinante/metabolismo
DNA Viral/química
Desaminação
Proteínas de Choque Térmico HSP90/antagonistas & inibidores
Proteínas de Choque Térmico HSP90/genética
Células Hep G2
Vírus da Hepatite B/genética
Vírus da Hepatite B/imunologia
Hepatócitos/imunologia
Hepatócitos/virologia
Seres Humanos
Imunidade Inata
Antígenos de Histocompatibilidade Menor/química
Antígenos de Histocompatibilidade Menor/genética
Mutagênese
Taxa de Mutação
Fragmentos de Peptídeos/agonistas
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Mutação Puntual
Interferência de RNA
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Recombinant); 0 (DNA, Viral); 0 (HSP90 Heat-Shock Proteins); 0 (Minor Histocompatibility Antigens); 0 (Peptide Fragments); 0 (Recombinant Fusion Proteins); 0 (Recombinant Proteins); 5CSZ8459RP (Cytidine); EC 3.5.4.5 (APOBEC-3G Deaminase); EC 3.5.4.5 (APOBEC3B protein, human); EC 3.5.4.5 (APOBEC3C protein, human); EC 3.5.4.5 (APOBEC3G protein, human); EC 3.5.4.5 (Cytidine Deaminase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.760637


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[PMID]:28539359
[Au] Autor:Wang J; Zhao S; He W; Wei Y; Zhang Y; Pegg H; Shore P; Roberts SGE; Deng W
[Ad] Endereço:From the Institute of Biology and Medicine, Wuhan University of Science and Technology, Wuhan City, Hubei Province 430065, China.
[Ti] Título:A transcription factor IIA-binding site differentially regulates RNA polymerase II-mediated transcription in a promoter context-dependent manner.
[So] Source:J Biol Chem;292(28):11873-11885, 2017 Jul 14.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RNA polymerase II (pol II) is required for the transcription of all protein-coding genes and as such represents a major enzyme whose activity is tightly regulated. Transcriptional initiation therefore requires numerous general transcriptional factors and cofactors that associate with pol II at the core promoter to form a pre-initiation complex. Transcription factor IIA (TFIIA) is a general cofactor that binds TFIID and stabilizes the TFIID-DNA complex during transcription initiation. Previous studies showed that TFIIA can make contact with the DNA sequence upstream or downstream of the TATA box, and that the region bound by TFIIA could overlap with the elements recognized by another factor, TFIIB, at adenovirus major late core promoter. Whether core promoters contain a DNA motif recognized by TFIIA remains unknown. Here we have identified a core promoter element upstream of the TATA box that is recognized by TFIIA. A search of the human promoter database revealed that many natural promoters contain a TFIIA recognition element (IIARE). We show that the IIARE enhances TFIIA-promoter binding and enhances the activity of TATA-containing promoters, but represses or activates promoters that lack a TATA box. Chromatin immunoprecipitation assays revealed that the IIARE activates transcription by increasing the recruitment of pol II, TFIIA, TAF4, and P300 at TATA-dependent promoters. These findings extend our understanding of the role of TFIIA in transcription, and provide new insights into the regulatory mechanism of core promoter elements in gene transcription by pol II.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Regiões Promotoras Genéticas
RNA Polimerase II/metabolismo
Elementos de Resposta
TATA Box
Fatores Associados à Proteína de Ligação a TATA/metabolismo
Fator de Transcrição TFIIA/metabolismo
Fator de Transcrição TFIID/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Imunoprecipitação da Cromatina
DNA Recombinante
Proteína p300 Associada a E1A/química
Proteína p300 Associada a E1A/metabolismo
Genes Reporter
Células HEK293
Seres Humanos
Mutagênese Sítio-Dirigida
Mutação
Motivos de Nucleotídeos
Subunidades Proteicas/química
Subunidades Proteicas/genética
Subunidades Proteicas/metabolismo
RNA Polimerase II/química
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Fatores Associados à Proteína de Ligação a TATA/química
Proteína de Ligação a TATA-Box/química
Proteína de Ligação a TATA-Box/genética
Proteína de Ligação a TATA-Box/metabolismo
Fator de Transcrição TFIIA/química
Fator de Transcrição TFIIA/genética
Fator de Transcrição TFIID/química
Fatores Estimuladores Upstream/química
Fatores Estimuladores Upstream/genética
Fatores Estimuladores Upstream/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Recombinant); 0 (Protein Subunits); 0 (Recombinant Proteins); 0 (TAF4 protein, human); 0 (TATA-Binding Protein Associated Factors); 0 (TATA-Box Binding Protein); 0 (TBP protein, human); 0 (Transcription Factor TFIIA); 0 (Transcription Factor TFIID); 0 (USF1 protein, human); 0 (Upstream Stimulatory Factors); EC 2.3.1.48 (E1A-Associated p300 Protein); EC 2.3.1.48 (EP300 protein, human); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.770412


  8 / 15836 MEDLINE  
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[PMID]:28533432
[Au] Autor:Manning BJ; Yusufzai T
[Ad] Endereço:From the Department of Radiation Oncology, Dana-Farber Cancer Institute and Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02215.
[Ti] Título:The ATP-dependent chromatin remodeling enzymes CHD6, CHD7, and CHD8 exhibit distinct nucleosome binding and remodeling activities.
[So] Source:J Biol Chem;292(28):11927-11936, 2017 Jul 14.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Proper chromatin regulation is central to genome function and maintenance. The group III chromodomain-helicase-DNA-binding (CHD) family of ATP-dependent chromatin remodeling enzymes, comprising CHD6, CHD7, CHD8, and CHD9, has well-documented roles in transcription regulation, impacting both organism development and disease etiology. These four enzymes are similar in their constituent domains, but they fill surprisingly non-redundant roles in the cell, with deficiencies in individual enzymes leading to dissimilar disease states such as CHARGE syndrome or autism spectrum disorders. The mechanisms explaining their divergent, non-overlapping functions are unclear. In this study, we performed an in-depth biochemical analysis of purified CHD6, CHD7, and CHD8 and discovered distinct differences in chromatin remodeling specificities and activities among them. We report that CHD6 and CHD7 both bind with high affinity to short linker DNA, whereas CHD8 requires longer DNA for binding. As a result, CHD8 slides nucleosomes into positions with more flanking linker DNA than CHD7. Moreover, we found that, although CHD7 and CHD8 slide nucleosomes, CHD6 disrupts nucleosomes in a distinct non-sliding manner. The different activities of these enzymes likely lead to differences in chromatin structure and, thereby, transcriptional control, at the enhancer and promoter loci where these enzymes bind. Overall, our work provides a mechanistic basis for both the non-redundant roles and the diverse mutant disease states of these enzymes .
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Montagem e Desmontagem da Cromatina
DNA Helicases/metabolismo
Proteínas de Ligação a DNA/metabolismo
DNA/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Nucleossomos/enzimologia
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Transporte Biológico
DNA/química
DNA Helicases/química
DNA Helicases/genética
DNA Helicases/isolamento & purificação
DNA Recombinante/química
DNA Recombinante/metabolismo
DNA Viral/química
DNA Viral/metabolismo
Proteínas de Ligação a DNA/química
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/isolamento & purificação
Células HeLa
Seres Humanos
Hidrólise
Cinética
Peso Molecular
Proteínas do Tecido Nervoso/química
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/isolamento & purificação
Nucleossomos/metabolismo
Filogenia
Proteínas Recombinantes/química
Proteínas Recombinantes/isolamento & purificação
Proteínas Recombinantes/metabolismo
Células Sf9
Spodoptera
Fatores de Transcrição/química
Fatores de Transcrição/genética
Fatores de Transcrição/isolamento & purificação
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CHD6 protein, human); 0 (CHD8 protein, human); 0 (DNA, Recombinant); 0 (DNA, Viral); 0 (DNA-Binding Proteins); 0 (Nerve Tissue Proteins); 0 (Nucleosomes); 0 (Recombinant Proteins); 0 (Transcription Factors); 8L70Q75FXE (Adenosine Triphosphate); 9007-49-2 (DNA); EC 3.6.4.- (DNA Helicases); EC 3.6.4.12 (CHD7 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.779470


  9 / 15836 MEDLINE  
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[PMID]:28412323
[Au] Autor:Tsuboi K; Nagatomo T; Gohno T; Higuchi T; Sasaki S; Fujiki N; Kurosumi M; Takei H; Yamaguchi Y; Niwa T; Hayashi SI
[Ad] Endereço:Department of Molecular and Functional Dynamics, Graduate School of Medicine, Tohoku University, Aoba-ku, Sendai, 980-8575, Japan.
[Ti] Título:Single CpG site methylation controls estrogen receptor gene transcription and correlates with hormone therapy resistance.
[So] Source:J Steroid Biochem Mol Biol;171:209-217, 2017 Jul.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hormone therapy is the most effective treatment for patients with estrogen receptor α-positive breast cancers. However, although resistance occurs during treatment in some cases and often reflects changed estrogen receptor α status, the relationship between changes in estrogen receptor α expression and resistance to therapy are poorly understood. In this study, we identified a mechanism for altered estrogen receptor α expression during disease progression and acquired hormone therapy resistance in aromatase inhibitor-resistant breast cancer cell lines. Subsequently, we investigated promoter switching and DNA methylation status of the estrogen receptor α promoter, and found marked changes of methylation at a single CpG site (CpG4) in resistant cells. In addition, luciferase reporter assays showed reduced transcriptional activity from this methylated CpG site. This CpG region was also completely conserved among species, suggesting that it acts as a methylation-sensitive Ets-2 transcription factor binding site, as confirmed using chromatin immunoprecipitation assays. In estrogen receptor α-positive tumors, CpG4 methylation levels were inversely correlated with estrogen receptor α expression status, suggesting that single CpG site plays an important role in the regulation of estrogen receptor α transcription.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Metilação de DNA
Fosfatos de Dinucleosídeos/metabolismo
Receptor alfa de Estrogênio/metabolismo
Regiões Promotoras Genéticas
Proteína Proto-Oncogênica c-ets-2/metabolismo
Transcrição Genética
[Mh] Termos MeSH secundário: Antineoplásicos Hormonais/farmacologia
Inibidores da Aromatase/farmacologia
Sequência de Bases
Neoplasias da Mama/tratamento farmacológico
Sequência Conservada
Metilação de DNA/efeitos dos fármacos
DNA Recombinante/metabolismo
Resistência a Medicamentos Antineoplásicos
Receptor alfa de Estrogênio/química
Receptor alfa de Estrogênio/genética
Feminino
Genes Reporter/efeitos dos fármacos
Seres Humanos
Células MCF-7
Meia-Idade
Mutação
Proteínas de Neoplasias/química
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Regiões Promotoras Genéticas/efeitos dos fármacos
Proteína Proto-Oncogênica c-ets-2/genética
Proteínas Recombinantes/metabolismo
Elementos de Resposta/efeitos dos fármacos
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Aromatase Inhibitors); 0 (DNA, Recombinant); 0 (Dinucleoside Phosphates); 0 (ETS2 protein, human); 0 (Estrogen Receptor alpha); 0 (Neoplasm Proteins); 0 (Proto-Oncogene Protein c-ets-2); 0 (Recombinant Proteins); 0 (estrogen receptor alpha, human); 2382-65-2 (cytidylyl-3'-5'-guanosine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170417
[St] Status:MEDLINE


  10 / 15836 MEDLINE  
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[PMID]:28322993
[Au] Autor:Rezaie ES; Visser NJ; Friedrich PF; Shin AY; Bishop AT
[Ad] Endereço:Mayo Clinic, Department of Orthopedic Surgery, 200 1st St. SW, Rochester, MN 55905, United States. Electronic address: rezaie.elisa@mayo.edu.
[Ti] Título:Intra-luminal gene therapy in the porcine artery using a recombinant adeno-associated virus 9.
[So] Source:Gene;618:24-27, 2017 Jun 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The ability to improve or restore blood flow and promote healing in ischemic tissue has many potential clinical applications. Augmentation by direct delivery of growth factors may further enhance results, but requires a method for sustained delivery. In this study, we have tested the ability of adeno-associated virus 9 (AAV9) delivered within the lumen of a porcine artery to transfect the vessel and produce a desired product. The marker chosen was green fluorescent protein (GFP) (Ke et al., 2011). In 4 farm pigs the cranial tibial artery was surgically exposed. The vessel was temporarily clamped proximally, and divided distally. A cannula was placed intraluminally, and the arterial segment was injected with 1×10E13 particles of AAV9.CB7.CI.GFP·WPRE.rBG. At 14days the transfected cranial tibial artery as well as the liver, spleen and kidneys were harvested. ELISA and reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) were used to analyze the artery for GFP production. Significant GFP expression was seen in all transfected cranial tibial vessels, as determined by both GFP protein production (ELISA) and mRNA (RT-qPCR). No GFP was identified in liver, spleen or kidney, nor in the no-GFP control animal artery. Adeno-associated virus 9 is an appropriate vector for gene therapy experiments in the porcine artery model. This vector, and the intraluminal deliver method described result in robust gene expression at 2weeks without evident systemic spill of the virus. The ability to limit delivery of the gene to an isolated segment of vessel is desirable for future research applications.
[Mh] Termos MeSH primário: Dependovirus/genética
Terapia Genética/métodos
Artérias da Tíbia
[Mh] Termos MeSH secundário: Animais
DNA Recombinante/administração & dosagem
DNA Recombinante/genética
Técnicas de Transferência de Genes
Vetores Genéticos/administração & dosagem
Vetores Genéticos/genética
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Injeções Intra-Arteriais
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Recombinant); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE



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