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[PMID]:29339154
[Au] Autor:Cao M; Zhao Z; Tang Y; Wei Q; Wang L; Xiang Q; Zhang Y; Zhang H; Lai G
[Ad] Endereço:Chongqing Medical University Laboratory Animal Center, Chongqing, China.
[Ti] Título:A new hepatitis B virus e antigen-negative strain gene used as a reference sequence in an animal model.
[So] Source:Biochem Biophys Res Commun;496(2):502-507, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infection with hepatitis B virus (HBV) e-antigen (HBeAg)-negative strains is increasingly prevalent. Currently, detailed information of the obtained natural HBV strain is not available except for the B genotype and HBeAg-negative. The aim of the present study was to characterize the natural genetic variation of the HBeAg-negative strain and investigate its function. The genic sequence was determined using Sanger sequencing, and compared to related sequences using alignment and phylogenetic analysis. In vivo, virus-specific serum markers were investigated in CBA/CaJ mice. The sequence had a full genome length of 3215 nucleotides. Sites 122, 125, 127, and 160 in S regions were identified as lysine, threonine, proline, and lysine respectively. The main four point variants including A1762T, G1764A, G1896A, and G1899A were detected in the full-length genome. The genotype of the sequence was B, with sub-genotype B2 and serological subtype adw2. The characterize of the natural genetic variation strain showed no reported drug-resistant variant in P region and no reported immune escape site in S region. The strain will increase viral replication and infection for mutations A1762T and G1764A in the basal core promoter region, and mutations G1896A and G1899A in the pre-core region. The G1896A variant resulted in a premature stop codon and abolished HBeAg expression. HBsAg persisted for 26 weeks and HBeAg was still negative in CBA/CaJ mice. The present sequence is representative of the HBeAg-negative genome and may serve as a valuable reference for studying HBeAg-negative strains. The present findings were successfully verified in CBA/CaJ mice, demonstrating good applicability of the sequence.
[Mh] Termos MeSH primário: DNA Viral/genética
Genoma Viral
Antígenos E da Hepatite B/genética
Vírus da Hepatite B/genética
Hepatite B/virologia
[Mh] Termos MeSH secundário: Animais
DNA Circular/genética
DNA Circular/imunologia
DNA Viral/imunologia
Modelos Animais de Doenças
Variação Genética
Genótipo
Hepatite B/imunologia
Antígenos E da Hepatite B/imunologia
Vírus da Hepatite B/crescimento & desenvolvimento
Vírus da Hepatite B/metabolismo
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos CBA
Mutação
Regiões Promotoras Genéticas
Padrões de Referência
Análise de Sequência de DNA
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Circular); 0 (DNA, Viral); 0 (Hepatitis B e Antigens)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:27771387
[Au] Autor:Alfaiate D; Lucifora J; Abeywickrama-Samarakoon N; Michelet M; Testoni B; Cortay JC; Sureau C; Zoulim F; Dény P; Durantel D
[Ad] Endereço:INSERM U1052, CNRS UMR-5286, Cancer Research Center of Lyon (CRCL), 69008 Lyon, France; University of Lyon, Université Claude-Bernard (UCBL), 69008 Lyon, France.
[Ti] Título:HDV RNA replication is associated with HBV repression and interferon-stimulated genes induction in super-infected hepatocytes.
[So] Source:Antiviral Res;136:19-31, 2016 12.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Hepatitis D virus (HDV) super-infection of Hepatitis B virus (HBV)-infected patients is the most aggressive form of viral hepatitis. HDV infection is not susceptible to direct anti-HBV drugs, and only suboptimal antiviral responses are obtained with interferon (IFN)-alpha-based therapy. To get insights on HDV replication and interplay with HBV in physiologically relevant hepatocytes, differentiated HepaRG (dHepaRG) cells, previously infected or not with HBV, were infected with HDV, and viral markers were extensively analyzed. Innate and IFN responses to HDV were monitored by measuring pro-inflammatory and interferon-stimulated gene (ISG) expression. Both mono- and super-infected dHepaRG cells supported a strong HDV intracellular replication, which was accompanied by a strong secretion of infectious HDV virions only in the super-infection setting and despite the low number of co-infected cells. Upon HDV super-infection, HBV replication markers including HBeAg, total HBV-DNA and pregenomic RNA were significantly decreased, confirming the interference of HDV on HBV. Yet, no decrease of circular covalently closed HBV DNA (cccDNA) and HBsAg levels was evidenced. At the peak of HDV-RNA accumulation and onset of interference on HBV replication, a strong type-I IFN response was observed, with interferon stimulated genes, RSAD2 (Viperin) and IFI78 (MxA) being highly induced. We established a cellular model to characterize in more detail the direct interference of HBV and HDV, and the indirect interplay between the two viruses via innate immune responses. This model will be instrumental to assess molecular and immunological mechanisms of this viral interference.
[Mh] Termos MeSH primário: Vírus da Hepatite B/fisiologia
Vírus Delta da Hepatite/fisiologia
Hepatócitos/virologia
Imunidade Inata
Interferons/imunologia
Interferência Viral
Replicação Viral
[Mh] Termos MeSH secundário: Células Cultivadas
Coinfecção
Replicação do DNA
DNA Circular
Hepatite B/virologia
Antígenos E da Hepatite B/genética
Hepatite D/virologia
Vírus Delta da Hepatite/genética
Seres Humanos
Interferon Tipo I/imunologia
Proteínas de Resistência a Myxovirus/genética
Proteínas/genética
RNA Viral/biossíntese
RNA Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Circular); 0 (Hepatitis B e Antigens); 0 (Interferon Type I); 0 (MX1 protein, human); 0 (Myxovirus Resistance Proteins); 0 (Proteins); 0 (RNA, Viral); 0 (RSAD2 protein, human); 9008-11-1 (Interferons)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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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


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[PMID]:28945802
[Au] Autor:Guo F; Zhao Q; Sheraz M; Cheng J; Qi Y; Su Q; Cuconati A; Wei L; Du Y; Li W; Chang J; Guo JT
[Ad] Endereço:Baruch S. Blumberg Institute, Doylestown, Pennsylvania, United States of America.
[Ti] Título:HBV core protein allosteric modulators differentially alter cccDNA biosynthesis from de novo infection and intracellular amplification pathways.
[So] Source:PLoS Pathog;13(9):e1006658, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatitis B virus (HBV) core protein assembles viral pre-genomic (pg) RNA and DNA polymerase into nucleocapsids for reverse transcriptional DNA replication to take place. Several chemotypes of small molecules, including heteroaryldihydropyrimidines (HAPs) and sulfamoylbenzamides (SBAs), have been discovered to allosterically modulate core protein structure and consequentially alter the kinetics and pathway of core protein assembly, resulting in formation of irregularly-shaped core protein aggregates or "empty" capsids devoid of pre-genomic RNA and viral DNA polymerase. Interestingly, in addition to inhibiting nucleocapsid assembly and subsequent viral genome replication, we have now demonstrated that HAPs and SBAs differentially modulate the biosynthesis of covalently closed circular (ccc) DNA from de novo infection and intracellular amplification pathways by inducing disassembly of nucleocapsids derived from virions as well as double-stranded DNA-containing progeny nucleocapsids in the cytoplasm. Specifically, the mistimed cuing of nucleocapsid uncoating prevents cccDNA formation during de novo infection of hepatocytes, while transiently accelerating cccDNA synthesis from cytoplasmic progeny nucleocapsids. Our studies indicate that elongation of positive-stranded DNA induces structural changes of nucleocapsids, which confers ability of mature nucleocapsids to bind CpAMs and triggers its disassembly. Understanding the molecular mechanism underlying the dual effects of the core protein allosteric modulators on nucleocapsid assembly and disassembly will facilitate the discovery of novel core protein-targeting antiviral agents that can more efficiently suppress cccDNA synthesis and cure chronic hepatitis B.
[Mh] Termos MeSH primário: DNA Circular/biossíntese
Vírus da Hepatite B/fisiologia
Hepatite B Crônica/virologia
Replicação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antivirais/farmacologia
Linhagem Celular
DNA Circular/genética
DNA Viral
DNA Polimerase Dirigida por DNA/metabolismo
Hepatócitos/virologia
Seres Humanos
Nucleocapsídeo/efeitos dos fármacos
Nucleocapsídeo/genética
Reação em Cadeia da Polimerase em Tempo Real
Replicação Viral/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (DNA, Circular); 0 (DNA, Viral); EC 2.7.7.7 (DNA-Directed DNA Polymerase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171022
[Lr] Data última revisão:
171022
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006658


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[PMID]:28877255
[Au] Autor:Mehanna P; Gagné V; Lajoie M; Spinella JF; St-Onge P; Sinnett D; Brukner I; Krajinovic M
[Ad] Endereço:CHU Sainte-Justine Research Center, University of Montreal, Montreal, Qc, Canada.
[Ti] Título:Characterization of the microDNA through the response to chemotherapeutics in lymphoblastoid cell lines.
[So] Source:PLoS One;12(9):e0184365, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recently, a new class of extrachromosomal circular DNA, called microDNA, was identified. They are on average 100 to 400 bp long and are derived from unique non-repetitive genomic regions with high gene density. MicroDNAs are thought to arise from DNA breaks associated with RNA metabolism or replication slippage. Given the paucity of information on this entirely novel phenomenon, we aimed to get an additional insight into microDNA features by performing the microDNA analysis in 20 independent human lymphoblastoid cell lines (LCLs) prior and after treatment with chemotherapeutic drugs. The results showed non-random genesis of microDNA clusters from the active regions of the genome. The size periodicity of 190 bp was observed, which matches DNA fragmentation typical for apoptotic cells. The chemotherapeutic drug-induced apoptosis of LCLs increased both number and size of clusters further suggesting that part of microDNAs could result from the programmed cell death. Interestingly, proportion of identified microDNA sequences has common loci of origin when compared between cell line experiments. While compatible with the original observation that microDNAs originate from a normal physiological process, obtained results imply complementary source of its production. Furthermore, non-random genesis of microDNAs depicted by redundancy between samples makes these entities possible candidates for new biomarker generation.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
DNA Circular/genética
Linfócitos/citologia
Linfócitos/efeitos dos fármacos
Análise em Microsséries
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
[Mh] Termos MeSH secundário: Apoptose
Biomarcadores/metabolismo
Linhagem Celular
Linhagem Celular Tumoral
Replicação do DNA
Genoma Humano
Genômica
Seres Humanos
Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers); 0 (DNA, Circular)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184365


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[PMID]:28854738
[Au] Autor:Toliusis P; Zaremba M; Silanskas A; Szczelkun MD; Siksnys V
[Ad] Endereço:Department of Protein-DNA Interactions, Institute of Biotechnology, Vilnius University, Sauletekio al. 7, LT-10257, Vilnius, Lithuania.
[Ti] Título:CgII cleaves DNA using a mechanism distinct from other ATP-dependent restriction endonucleases.
[So] Source:Nucleic Acids Res;45(14):8435-8447, 2017 Aug 21.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The restriction endonuclease CglI from Corynebacterium glutamicum recognizes an asymmetric 5'-GCCGC-3' site and cleaves the DNA 7 and 6/7 nucleotides downstream on the top and bottom DNA strands, respectively, in an NTP-hydrolysis dependent reaction. CglI is composed of two different proteins: an endonuclease (R.CglI) and a DEAD-family helicase-like ATPase (H.CglI). These subunits form a heterotetrameric complex with R2H2 stoichiometry. However, the R2H2·CglI complex has only one nuclease active site sufficient to cut one DNA strand suggesting that two complexes are required to introduce a double strand break. Here, we report studies to evaluate the DNA cleavage mechanism of CglI. Using one- and two-site circular DNA substrates we show that CglI does not require two sites on the same DNA for optimal catalytic activity. However, one-site linear DNA is a poor substrate, supporting a mechanism where CglI complexes must communicate along the one-dimensional DNA contour before cleavage is activated. Based on experimental data, we propose that adenosine triphosphate (ATP) hydrolysis by CglI produces translocation on DNA preferentially in a downstream direction from the target, although upstream translocation is also possible. Our results are consistent with a mechanism of CglI action that is distinct from that of other ATP-dependent restriction-modification enzymes.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
RNA Helicases DEAD-box/metabolismo
Clivagem do DNA
Enzimas de Restrição do DNA/metabolismo
DNA/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Sequência de Bases
Biocatálise
Corynebacterium glutamicum/enzimologia
DNA/genética
DNA Circular/genética
DNA Circular/metabolismo
Modelos Genéticos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (DNA, Circular); 8L70Q75FXE (Adenosine Triphosphate); 9007-49-2 (DNA); EC 3.1.21.- (DNA Restriction Enzymes); EC 3.6.4.13 (DEAD-box RNA Helicases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx580


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[PMID]:28715975
[Au] Autor:Shulman LM; Davidson I
[Ad] Endereço:Department of Epidemiology and Preventive Medicine, School of Public Health, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, 69978, Israel; email: lester.shulman@bezeqint.net.
[Ti] Título:Viruses with Circular Single-Stranded DNA Genomes Are Everywhere!
[So] Source:Annu Rev Virol;4(1):159-180, 2017 Sep 29.
[Is] ISSN:2327-0578
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Circular single-stranded DNA viruses infect archaea, bacteria, and eukaryotic organisms. The relatively recent emergence of single-stranded DNA viruses, such as chicken anemia virus (CAV) and porcine circovirus 2 (PCV2), as serious pathogens of eukaryotes is due more to growing awareness than to the appearance of new pathogens or alteration of existing pathogens. In the case of the ubiquitous human circular single-stranded DNA virus family Anelloviridae, there is still no convincing direct causal relation to any specific disease. However, infections may play a role in autoimmunity by changing the homeostatic balance of proinflammatory cytokines and the human immune system, indirectly affecting the severity of diseases caused by other pathogens. Infections with CAV (family Anelloviridae, genus Gyrovirus) and PCV2 (family Circoviridae, genus Circovirus) are presented here because they are immunosuppressive and affect health in domesticated animals. CAV shares genomic organization, genomic orientation, and common features of major proteins with human anelloviruses, and PCV2 DNA may be present in human food and vaccines.
[Mh] Termos MeSH primário: Infecções por Circoviridae/veterinária
Infecções por Vírus de DNA/virologia
Vírus de DNA/genética
DNA Circular
DNA de Cadeia Simples/genética
Genoma Viral
[Mh] Termos MeSH secundário: Anelloviridae/genética
Anelloviridae/isolamento & purificação
Animais
Animais Domésticos/virologia
Archaea/virologia
Autoimunidade
Bactérias/virologia
Vírus da Anemia da Galinha/genética
Vírus da Anemia da Galinha/isolamento & purificação
Infecções por Circoviridae/imunologia
Infecções por Circoviridae/virologia
Circovirus/genética
Circovirus/isolamento & purificação
Infecções por Vírus de DNA/imunologia
Vírus de DNA/isolamento & purificação
Vírus de DNA/fisiologia
DNA Viral
Seres Humanos
Suínos/virologia
Doenças dos Suínos/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (DNA, Circular); 0 (DNA, Single-Stranded); 0 (DNA, Viral)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1146/annurev-virology-101416-041953


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[PMID]:28707271
[Au] Autor:Cui L; Wu B; Zhu X; Guo X; Ge Y; Zhao K; Qi X; Shi Z; Zhu F; Sun L; Zhou M
[Ad] Endereço:Institute of Pathogenic Microbiology, Jiangsu Provincial Center for Disease Control and Prevention, Key Laboratories of Enteric Pathogenic Microbiology (Ministry of Health), Nanjing, China.
[Ti] Título:Identification and genetic characterization of a novel circular single-stranded DNA virus in a human upper respiratory tract sample.
[So] Source:Arch Virol;162(11):3305-3312, 2017 Nov.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Metagenomic analysis through high-throughput sequencing is a tool for detecting both known and novel viruses. Using this technique, a novel circular single-stranded DNA (ssDNA) virus genome was discovered in respiratory secretions from a febrile traveler. The virus, named human respiratory-associated PSCV-5-like virus (HRAPLV), has a genome comprising 3,018 bases, with two major putative ORFs inversely encoding capsid (Cap) and replicase (Rep) protein and separated by two intergenic regions. One stem-loop structure was predicted in the larger intergenic region (LIR). The predicted amino acid sequences of the Cap and Rep proteins of HRAPLV showed highest identity to those of porcine stool-associated circular virus 5 isolate CP3 (PoSCV 5) (53.0% and 48.9%, respectively). The host tropism of the virus is unknown, and further study is warranted to determine whether this novel virus is associated with human disease.
[Mh] Termos MeSH primário: Circovirus/genética
Circovirus/isolamento & purificação
DNA Circular/genética
DNA de Cadeia Simples/genética
DNA Viral/genética
Faringe/virologia
[Mh] Termos MeSH secundário: Genoma Viral
Seres Humanos
Masculino
Meia-Idade
Filogenia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Circular); 0 (DNA, Single-Stranded); 0 (DNA, Viral)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3481-3


  9 / 5420 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


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[PMID]:28694331
[Au] Autor:Francisco JC; Dai Q; Luo Z; Wang Y; Chong RH; Tan YJ; Xie W; Lee GH; Lin C
[Ad] Endereço:Transcriptional Control in Development and Disease Laboratory, Institute of Molecular and Cell Biology, Singapore, Singapore.
[Ti] Título:Transcriptional Elongation Control of Hepatitis B Virus Covalently Closed Circular DNA Transcription by Super Elongation Complex and BRD4.
[So] Source:Mol Cell Biol;37(19), 2017 Oct 01.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic hepatitis B virus (HBV) infection can lead to liver cirrhosis and hepatocellular carcinoma. HBV reactivation during or after chemotherapy is a potentially fatal complication for cancer patients with chronic HBV infection. Transcription of HBV is a critical intermediate step of the HBV life cycle. However, factors controlling HBV transcription remain largely unknown. Here, we found that different P-TEFb complexes are involved in the transcription of the HBV viral genome. Both BRD4 and the super elongation complex (SEC) bind to the HBV genome. The treatment of bromodomain inhibitor JQ1 stimulates HBV transcription and increases the occupancy of BRD4 on the HBV genome, suggesting the bromodomain-independent recruitment of BRD4 to the HBV genome. JQ1 also leads to the increased binding of SEC to the HBV genome, and SEC is required for JQ1-induced HBV transcription. These findings reveal a novel mechanism by which the HBV genome hijacks the host P-TEFb-containing complexes to promote its own transcription. Our findings also point out an important clinical implication, that is, the potential risk of HBV reactivation during therapy with a BRD4 inhibitor, such as JQ1 or its analogues, which are a potential treatment for acute myeloid leukemia.
[Mh] Termos MeSH primário: DNA Circular/genética
DNA Viral/genética
Vírus da Hepatite B/fisiologia
Proteínas Nucleares/metabolismo
Fator B de Elongação Transcricional Positiva/metabolismo
Elongação da Transcrição Genética
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Azepinas/farmacologia
DNA Circular/metabolismo
DNA Viral/metabolismo
Células HeLa
Células Hep G2
Vírus da Hepatite B/genética
Seres Humanos
Ligação Proteica
Elongação da Transcrição Genética/efeitos dos fármacos
Fatores de Elongação da Transcrição
Triazóis/farmacologia
Ativação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((+)-JQ1 compound); 0 (Azepines); 0 (BRD4 protein, human); 0 (DNA, Circular); 0 (DNA, Viral); 0 (Nuclear Proteins); 0 (Transcription Factors); 0 (Transcriptional Elongation Factors); 0 (Triazoles); EC 2.7.11.- (Positive Transcriptional Elongation Factor B)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE



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