Base de dados : MEDLINE
Pesquisa : D13.150 [Categoria DeCS]
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[PMID]:28357596
[Au] Autor:Ma Z; Kong X; Liu S; Yin S; Zhao Y; Liu C; Lv Z; Wang X
[Ad] Endereço:Department of Genetics, Hebei Medical University, Hebei Key Lab of Laboratory Animal, Shijiazhuang, Hebei Province, 050017, China.
[Ti] Título:Combined sense-antisense Alu elements activate the EGFP reporter gene when stable transfection.
[So] Source:Mol Genet Genomics;292(4):833-846, 2017 Aug.
[Is] ISSN:1617-4623
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Alu elements in the human genome are present in more than one million copies, accounting for 10% of the genome. However, the biological functions of most Alu repeats are unknown. In this present study, we detected the effects of Alu elements on EGFP gene expression using a plasmid system to find the roles of Alu elements in human genome. We inserted 5'-4TMI-Alus-CMV promoter-4TMI-Alus (or antisense Alus)-3' sequences into the pEGFP-C1 vector to construct expression vectors. We altered the copy number of Alus, the orientation of the Alus, and the presence of an enhancer (4TMI) in the inserted 5'-4TMI-Alus-CMV promoter-4TMI-Alus (or antisense Alus)-3' sequences. These expression vectors were stably transfected into HeLa cells, and EGFP reporter gene expression was determined. Our results showed that combined sense-antisense Alu elements activated the EGFP reporter gene in the presence of enhancers and stable transfection. The combined sense-antisense Alu vectors carrying four copies of Alus downstream of inserted CMV induced much stronger EGFP gene expression than two copies. Alus downstream of inserted CMV were replaced to AluJBs (having 76% homology with Alu) to construct expression vectors. We found that combined sense-antisense Alu (or antisense AluJB) vectors induced strong EGFP gene expression after stable transfection and heat shock. To further explore combined sense-antisense Alus activating EGFP gene expression, we constructed Tet-on system vectors, mini-C1-Alu-sense-sense and mini-C1-Alu-sense-antisense (EGFP gene was driven by mini-CMV). We found that combined sense-antisense Alus activated EGFP gene in the presence of reverse tetracycline repressor (rTetR) and doxycycline (Dox). Clone experiments showed that Mini-C1-Alu-sense-antisense vector had more positive cells than that of Mini-C1-Alu-sense-sense vector. The results in this paper proved that Alu repetitive sequences inhibited gene expression and combined sense-antisense Alus activated EGFP reporter gene when Alu transcribes, which suggests that Alus play roles in maintaining gene expression (silencing genes or activating genes) in human genome.
[Mh] Termos MeSH primário: Elementos Alu/genética
Elementos Antissenso (Genética)/genética
Regulação da Expressão Gênica/genética
Proteínas de Fluorescência Verde/biossíntese
Proteínas de Fluorescência Verde/genética
Sequências Reguladoras de Ácido Nucleico/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Dosagem de Genes/genética
Genoma Humano
Células HeLa
Seres Humanos
Regiões Promotoras Genéticas
Ativação Transcricional/genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antisense Elements (Genetics)); 0 (enhanced green fluorescent protein); 147336-22-9 (Green Fluorescent Proteins)
[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:170331
[St] Status:MEDLINE
[do] DOI:10.1007/s00438-017-1312-6


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[PMID]:27487356
[Au] Autor:Lavender CA; Cannady KR; Hoffman JA; Trotter KW; Gilchrist DA; Bennett BD; Burkholder AB; Burd CJ; Fargo DC; Archer TK
[Ad] Endereço:Epigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America.
[Ti] Título:Downstream Antisense Transcription Predicts Genomic Features That Define the Specific Chromatin Environment at Mammalian Promoters.
[So] Source:PLoS Genet;12(8):e1006224, 2016 Aug.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Antisense transcription is a prevalent feature at mammalian promoters. Previous studies have primarily focused on antisense transcription initiating upstream of genes. Here, we characterize promoter-proximal antisense transcription downstream of gene transcription starts sites in human breast cancer cells, investigating the genomic context of downstream antisense transcription. We find extensive correlations between antisense transcription and features associated with the chromatin environment at gene promoters. Antisense transcription downstream of promoters is widespread, with antisense transcription initiation observed within 2 kb of 28% of gene transcription start sites. Antisense transcription initiates between nucleosomes regularly positioned downstream of these promoters. The nucleosomes between gene and downstream antisense transcription start sites carry histone modifications associated with active promoters, such as H3K4me3 and H3K27ac. This region is bound by chromatin remodeling and histone modifying complexes including SWI/SNF subunits and HDACs, suggesting that antisense transcription or resulting RNA transcripts contribute to the creation and maintenance of a promoter-associated chromatin environment. Downstream antisense transcription overlays additional regulatory features, such as transcription factor binding, DNA accessibility, and the downstream edge of promoter-associated CpG islands. These features suggest an important role for antisense transcription in the regulation of gene expression and the maintenance of a promoter-associated chromatin environment.
[Mh] Termos MeSH primário: Elementos Antissenso (Genética)/genética
Proteínas Nucleares/genética
Regiões Promotoras Genéticas
Transcrição Genética
[Mh] Termos MeSH secundário: Elementos Antissenso (Genética)/biossíntese
Cromatina/genética
Ilhas de CpG/genética
Regulação Fúngica da Expressão Gênica
Genômica
Código das Histonas/genética
Histonas/genética
Seres Humanos
Proteínas Nucleares/biossíntese
Nucleossomos/genética
Ligação Proteica/genética
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antisense Elements (Genetics)); 0 (Chromatin); 0 (Histones); 0 (Nuclear Proteins); 0 (Nucleosomes)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160804
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006224


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[PMID]:27318213
[Au] Autor:Jin JL; Guo YL; Li JJ
[Ad] Endereço:Division of Dyslipidemia, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No 167 Bei Li Shi Road, Xi Cheng District, Beijing 100037, China. Electronic address: lijianjun938@126.com.
[Ti] Título:Apoprotein C-III: A review of its clinical implications.
[So] Source:Clin Chim Acta;460:50-4, 2016 Sep 01.
[Is] ISSN:1873-3492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Apoprotein C-III (apoC-III), originating from the apoA-I/C-III/A-IV gene cluster affected by multiple regulating factors, has been demonstrated to have a validated link with hypertriglyceridemia in humans. Following genome studies establishing the impact of apoC-III on both plasma triglyceride (TG) level and cardiovascular disease (CVD), apoC-III offers us a novel explanation attempting to resolve the long-existing confusion with regard to the atherogenic effect of TG. Notably, apoC-III exerts its atherogenic effect by means of not only intervening in the function and metabolism of various lipid molecules, but also accelerating pro-inflammatory effects between monocytes and endothelial cells. Data have suggested that diabetes, a common endocrine disease, also correlates closely with apoC-III in its apoptosis process of islet ßcells. In fact, apoC-III genes, with various mutations among individuals, are also found to have relevance to other diseases, including fatty liver disease. Fortunately, besides present day therapeutic strategies, such as lifestyle changes and lipid-lowering drug treatments, a promising new antisense drug specifically targeting on apoC-III gene expression opens up new avenues. This article mainly summarizes the clinical implication of apoC-III and its future directions of treatment.
[Mh] Termos MeSH primário: Apolipoproteína C-III/fisiologia
[Mh] Termos MeSH secundário: Elementos Antissenso (Genética)/uso terapêutico
Apolipoproteína C-III/sangue
Apolipoproteína C-III/efeitos dos fármacos
Doenças Cardiovasculares/sangue
Doenças Cardiovasculares/terapia
Suscetibilidade a Doenças/sangue
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antisense Elements (Genetics)); 0 (Apolipoprotein C-III)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170202
[Lr] Data última revisão:
170202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160619
[St] Status:MEDLINE


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[PMID]:26896950
[Au] Autor:Tretina K; Pelle R; Silva JC
[Ad] Endereço:Institute for Genome Sciences and Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA. ktretina@som.umaryland.edu.
[Ti] Título:Cis regulatory motifs and antisense transcriptional control in the apicomplexan Theileria parva.
[So] Source:BMC Genomics;17:128, 2016 Feb 20.
[Is] ISSN:1471-2164
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Theileria parva is an intracellular parasite that causes a lymphoproliferative disease in cattle. It does so by inducing cancer-like phenotypes in the host cells it infects, although the molecular and regulatory mechanisms involved remain poorly understood. RNAseq data, and the resulting updated genome annotation now available for this parasite, offer an unprecedented opportunity to characterize the genomic features associated with gene regulation in this species. Our previous analyses revealed a T. parva genome even more gene-dense than previously thought, with many adjacent loci overlapping each other, not only at the level of untranslated sequences (UTRs) but even in coding sequences. RESULTS: Despite this compactness, Theileria intergenic regions show a pattern of size distribution indicative of monocistronic gene transcription. Three previously described motifs are conserved among Theileria species and highly prevalent in promoter regions near or at the transcription start sites. We found novel motifs at many transcription termination sites, as well as upstream of parasite genes thought to be critical for host transformation. Adjacent genes that could be regulated by antisense transcription from an overlapping transcriptional unit are syntenic between T. parva and P. falciparum at a frequency higher than expected by chance, suggesting the presence of common, and evolutionary old, regulatory mechanisms in the phylum Apicomplexa. CONCLUSIONS: We propose a model of transcription with conserved sense and antisense transcription from a few taxonomically ubiquitous and several species-specific promoter motifs. Interestingly, the gene networks regulated by conserved promoters are themselves, in most cases, not conserved between species or genera.
[Mh] Termos MeSH primário: Elementos Antissenso (Genética)
Genoma de Protozoário
Sequências Reguladoras de Ácido Nucleico
Theileria parva/genética
Transcrição Genética
[Mh] Termos MeSH secundário: DNA de Protozoário/genética
Éxons
Regulação da Expressão Gênica
Regiões Promotoras Genéticas
Análise de Sequência de RNA
Sítio de Iniciação de Transcrição
Regiões não Traduzidas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Antisense Elements (Genetics)); 0 (DNA, Protozoan); 0 (Untranslated Regions)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160222
[St] Status:MEDLINE
[do] DOI:10.1186/s12864-016-2444-5


  5 / 1334 MEDLINE  
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[PMID]:26755557
[Au] Autor:Uprety B; Kaja A; Ferdoush J; Sen R; Bhaumik SR
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Southern Illinois University School of Medicine, Carbondale, Illinois, USA.
[Ti] Título:Regulation of Antisense Transcription by NuA4 Histone Acetyltransferase and Other Chromatin Regulatory Factors.
[So] Source:Mol Cell Biol;36(6):992-1006, 2016 Jan 11.
[Is] ISSN:1098-5549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NuA4 histone lysine (K) acetyltransferase (KAT) promotes transcriptional initiation of TATA-binding protein (TBP)-associated factor (TAF)-dependent ribosomal protein genes. TAFs have also been recently found to enhance antisense transcription from the 3' end of the GAL10 coding sequence. However, it remains unknown whether, like sense transcription of the ribosomal protein genes, TAF-dependent antisense transcription of GAL10 also requires NuA4 KAT. Here, we show that NuA4 KAT associates with the GAL10 antisense transcription initiation site at the 3' end of the coding sequence. Such association of NuA4 KAT depends on the Reb1p-binding site that recruits Reb1p activator to the GAL10 antisense transcription initiation site. Targeted recruitment of NuA4 KAT to the GAL10 antisense transcription initiation site promotes GAL10 antisense transcription. Like NuA4 KAT, histone H3 K4/36 methyltransferases and histone H2B ubiquitin conjugase facilitate GAL10 antisense transcription, while the Swi/Snf and SAGA chromatin remodeling/modification factors are dispensable for antisense, but not sense, transcription of GAL10. Taken together, our results demonstrate for the first time the roles of NuA4 KAT and other chromatin regulatory factors in controlling antisense transcription, thus illuminating chromatin regulation of antisense transcription.
[Mh] Termos MeSH primário: Elementos Antissenso (Genética)/genética
Regulação Fúngica da Expressão Gênica
Histona Acetiltransferases/metabolismo
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
Transativadores/genética
[Mh] Termos MeSH secundário: Elementos Antissenso (Genética)/metabolismo
Histona-Lisina N-Metiltransferase/metabolismo
Histonas/metabolismo
Transativadores/metabolismo
Sítio de Iniciação de Transcrição
Ativação Transcricional
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antisense Elements (Genetics)); 0 (GAL10 protein, S cerevisiae); 0 (Histones); 0 (SAGA complex, S cerevisiae); 0 (Saccharomyces cerevisiae Proteins); 0 (Trans-Activators); EC 2.1.1.- (histone methyltransferase); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.3.1.48 (Histone Acetyltransferases); EC 2.3.1.48 (NuA4 protein, S cerevisiae)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160113
[St] Status:MEDLINE
[do] DOI:10.1128/MCB.00808-15


  6 / 1334 MEDLINE  
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[PMID]:26660659
[Au] Autor:Beilharz TH
[Ad] Endereço:Development and Stem Cells Program, Department of Biochemistry and Molecular Biology, Monash Biomedicine Discovery Institute, Monash University, Melbourne, VIC, 3800, Australia. traude.beilharz@monash.edu.
[Ti] Título:Understanding the regulation of coding and noncoding transcription in cell populations.
[So] Source:Curr Genet;62(2):317-9, 2016 May.
[Is] ISSN:1432-0983
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Whole transcriptome analyses have unveiled the uncomfortable truth that we know less about how transcription is regulated then we thought. In addition to its role in classic promoter-driven transcription of coding RNA, it is now clear that RNA Pol II also drives abundant expression of noncoding RNA. For the majority of this the functional significance remains unclear. Moreover, its regulation and impact are hard to predict because it often proceeds in unexpected ways from cryptic promoters, including by driving convergent antisense transcription from within 3' UTRs. This review suggests that its time to rethink how we envisage gene expression by inclusion of the regulatory architecture of the full genetic locus, and expanding our thinking to encompass the fact that we generally study cells within heterogeneous populations.
[Mh] Termos MeSH primário: Fases de Leitura Aberta
Transcrição Genética
Regiões não Traduzidas
[Mh] Termos MeSH secundário: Elementos Antissenso (Genética)
Regulação da Expressão Gênica
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antisense Elements (Genetics)); 0 (Untranslated Regions)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[St] Status:MEDLINE
[do] DOI:10.1007/s00294-015-0547-1


  7 / 1334 MEDLINE  
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[PMID]:26369550
[Au] Autor:Grierson D
[Ad] Endereço:Plant & Crop Sciences Division, School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough, Leicestershire, UK.
[Ti] Título:Identifying and silencing tomato ripening genes with antisense genes.
[So] Source:Plant Biotechnol J;14(3):835-8, 2016 Mar.
[Is] ISSN:1467-7652
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Elementos Antissenso (Genética)
Frutas/genética
Inativação Gênica
Genes de Plantas
Lycopersicon esculentum/genética
[Mh] Termos MeSH secundário: Técnicas de Inativação de Genes
Plantas Geneticamente Modificadas
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antisense Elements (Genetics)); 0 (RNA, Messenger)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150916
[St] Status:MEDLINE
[do] DOI:10.1111/pbi.12463


  8 / 1334 MEDLINE  
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[PMID]:26731993
[Au] Autor:Dang Y; Wang Y; Ouyang X; Wang L; Huang Q
[Ti] Título:High Expression of IncRNA-PCNA-AS1 in Human Gastric Cancer and its Clinical Significances.
[So] Source:Clin Lab;61(11):1679-85, 2015.
[Is] ISSN:1433-6510
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Long noncoding RNAs (IncRNAs) have been demonstrated to be associated with human cancer. However, the clinical value of most lncRNAs to serve as the biomarkers for gastric cancer remains largely unknown. In this study, we examined the relationship between the expression levels of IncRNA, PCNA antisense RNA 1 (PCNA-AS1), and clinicopathological characteristics of gastric cancer. METHODS: A total of 90 tissue samples from patients with gastric cancer were collected, and the IncRNA PCNA-AS1 levels in cancer and paired non-cancer tissues was detected by real-time quantitative RT-PCR (qRT-PCR). The relationship between PCNA-AS1 levels and the clinicopathological characteristics were then evaluated. RESULTS: PCNA-AS1 expression levels were increased in 68 of 90 gastric cancer tissues (75.56%) and were associated with invasion (p = 0.038), but not associated with other clinicopathological characteristics. The expression levels of PCNA-AS1 were also related with immunohistochemical biomarkers of BRCA1 (p = 0.043) and RRM1 (p = 0.023). CONCLUSIONS: These data indicated that IncRNA-PCNA-AS1 may participate in the gastric cancer carcinogenesis and development and may serve as a new biomarker for patients with gastric cancer.
[Mh] Termos MeSH primário: Elementos Antissenso (Genética)/genética
Antígeno Nuclear de Célula em Proliferação/genética
RNA Longo não Codificante/genética
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Biomarcadores Tumorais
Feminino
Seres Humanos
Masculino
Meia-Idade
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antisense Elements (Genetics)); 0 (Biomarkers, Tumor); 0 (Proliferating Cell Nuclear Antigen); 0 (RNA, Long Noncoding)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:160106
[Lr] Data última revisão:
160106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160107
[St] Status:MEDLINE


  9 / 1334 MEDLINE  
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[PMID]:26559642
[Au] Autor:Ananta JS; Paulmurugan R; Massoud TF
[Ad] Endereço:Laboratory of Experimental and Molecular Neuroimaging, Molecular Imaging Program at Stanford (MIPS), and Bio-X Program, Stanford University School of Medicine , Stanford, California 94305-5427, United States.
[Ti] Título:Nanoparticle-Delivered Antisense MicroRNA-21 Enhances the Effects of Temozolomide on Glioblastoma Cells.
[So] Source:Mol Pharm;12(12):4509-17, 2015 Dec 07.
[Is] ISSN:1543-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma (GBM) generally exhibits high IC50 values for its standard drug treatment, temozolomide (TMZ). MicroRNA-21 (miR-21) is an oncomiR overexpressed in GBM, thus controlling important aspects of glioma biology. We hypothesized that PLGA nanoparticles carrying antisense miR-21 to glioblastoma cells might beneficially knock down endogenous miR-21 prior to TMZ treatment. PLGA nanoparticles encapsulating antisense miR-21 were effective in intracellular delivery and sustained silencing (p < 0.01) of miR-21 function in U87 MG, LN229, and T98G cells. Prior antisense miR-21 delivery significantly reduced the number of viable cells (p < 0.001), and increased (1.6-fold) cell cycle arrest at G2/M phase upon TMZ treatment in U87 MG cells. There was overexpression of the miR-21 target genes PTEN (by 67%) and caspase-3 (by 15%) upon cotreatment. This promising PLGA nanoparticle-based platform for antisense miR-21 delivery to GBM is an effective cotherapeutic strategy in cell culture, warranting the need for further studies prior to future clinical translation.
[Mh] Termos MeSH primário: Elementos Antissenso (Genética)/genética
Dacarbazina/análogos & derivados
Glioblastoma/tratamento farmacológico
MicroRNAs/genética
Nanopartículas/administração & dosagem
[Mh] Termos MeSH secundário: Antineoplásicos Alquilantes/farmacologia
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/genética
Caspase 3/genética
Linhagem Celular Tumoral
Dacarbazina/farmacologia
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Glioblastoma/genética
Glioma/tratamento farmacológico
Glioma/genética
Seres Humanos
PTEN Fosfo-Hidrolase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Antisense Elements (Genetics)); 0 (MIRN21 microRNA, human); 0 (MicroRNAs); 7GR28W0FJI (Dacarbazine); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human); EC 3.4.22.- (Caspase 3); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151113
[St] Status:MEDLINE
[do] DOI:10.1021/acs.molpharmaceut.5b00694


  10 / 1334 MEDLINE  
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[PMID]:26216517
[Au] Autor:Philippen LE; Dirkx E; Wit JB; Burggraaf K; de Windt LJ; da Costa Martins PA
[Ad] Endereço:Department of Cardiology, CARIM School for Cardiovascular Diseases, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, The Netherlands.
[Ti] Título:Antisense MicroRNA Therapeutics in Cardiovascular Disease: Quo Vadis?
[So] Source:Mol Ther;23(12):1810-8, 2015 Dec.
[Is] ISSN:1525-0024
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heart failure (HF) is the end result of a diverse set of causes such as genetic cardiomyopathies, coronary artery disease, and hypertension and represents the primary cause of hospitalization in Europe. This serious clinical disorder is mostly associated with pathological remodeling of the myocardium, pump failure, and sudden death. While the survival of HF patients can be prolonged with conventional pharmacological therapies, the prognosis remains poor. New therapeutic modalities are thus needed that will target the underlying causes and not only the symptoms of the disease. Under chronic cardiac stress, small noncoding RNAs, in particular microRNAs, act as critical regulators of cardiac tissue remodeling and represent a new class of therapeutic targets in patients suffering from HF. Here, we focus on the potential use of microRNA inhibitors as a new treatment paradigm for HF.
[Mh] Termos MeSH primário: Elementos Antissenso (Genética)/uso terapêutico
Insuficiência Cardíaca/diagnóstico
Insuficiência Cardíaca/genética
MicroRNAs/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Elementos Antissenso (Genética)/genética
Modelos Animais de Doenças
Regulação da Expressão Gênica
Insuficiência Cardíaca/terapia
Seres Humanos
MicroRNAs/genética
Miocárdio/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Antisense Elements (Genetics)); 0 (MicroRNAs)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150729
[St] Status:MEDLINE
[do] DOI:10.1038/mt.2015.133



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