Base de dados : MEDLINE
Pesquisa : D13.150.200 [Categoria DeCS]
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  1 / 2033 MEDLINE  
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[PMID]:28476952
[Au] Autor:Rogell B; Fischer B; Rettel M; Krijgsveld J; Castello A; Hentze MW
[Ad] Endereço:European Molecular Biology Laboratory (EMBL), 69117 Heidelberg, Germany.
[Ti] Título:Specific RNP capture with antisense LNA/DNA mixmers.
[So] Source:RNA;23(8):1290-1302, 2017 Aug.
[Is] ISSN:1469-9001
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RNA-binding proteins (RBPs) play essential roles in RNA biology, responding to cellular and environmental stimuli to regulate gene expression. Important advances have helped to determine the (near) complete repertoires of cellular RBPs. However, identification of RBPs associated with specific transcripts remains a challenge. Here, we describe "specific ribonucleoprotein (RNP) capture," a versatile method for the determination of the proteins bound to specific transcripts in vitro and in cellular systems. Specific RNP capture uses UV irradiation to covalently stabilize protein-RNA interactions taking place at "zero distance." Proteins bound to the target RNA are captured by hybridization with antisense locked nucleic acid (LNA)/DNA oligonucleotides covalently coupled to a magnetic resin. After stringent washing, interacting proteins are identified by quantitative mass spectrometry. Applied to in vitro extracts, specific RNP capture identifies the RBPs bound to a reporter mRNA containing the Sex-lethal (Sxl) binding motifs, revealing that the Sxl homolog sister of Sex lethal (Ssx) displays similar binding preferences. This method also revealed the repertoire of RBPs binding to 18S or 28S rRNAs in HeLa cells, including previously unknown rRNA-binding proteins.
[Mh] Termos MeSH primário: DNA Antissenso/metabolismo
Oligonucleotídeos/metabolismo
RNA/metabolismo
Ribonucleoproteínas/isolamento & purificação
[Mh] Termos MeSH secundário: DNA Antissenso/genética
Células HeLa
Seres Humanos
Oligonucleotídeos/genética
RNA/genética
Ribonucleoproteínas/genética
Ribonucleoproteínas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Antisense); 0 (Oligonucleotides); 0 (Ribonucleoproteins); 0 (locked nucleic acid); 63231-63-0 (RNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE
[do] DOI:10.1261/rna.060798.117


  2 / 2033 MEDLINE  
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[PMID]:28289142
[Au] Autor:Yeganeh M; Praz V; Cousin P; Hernandez N
[Ad] Endereço:Center for Integrative Genomics, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland.
[Ti] Título:Transcriptional interference by RNA polymerase III affects expression of the gene.
[So] Source:Genes Dev;31(4):413-421, 2017 Feb 15.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Overlapping gene arrangements can potentially contribute to gene expression regulation. A mammalian interspersed repeat (MIR) nested in antisense orientation within the first intron of the gene, encoding an RNA polymerase III (Pol III) subunit, is conserved in mammals and highly occupied by Pol III. Using a fluorescence assay, CRISPR/Cas9-mediated deletion of the MIR in mouse embryonic stem cells, and chromatin immunoprecipitation assays, we show that the MIR affects expression through transcriptional interference. Our study reveals a mechanism by which a Pol II gene can be regulated at the transcription elongation level by transcription of an embedded antisense Pol III gene.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/genética
RNA Polimerase III/metabolismo
[Mh] Termos MeSH secundário: Animais
Sequência Conservada/genética
DNA Antissenso/genética
Células-Tronco Embrionárias
Sequências Repetitivas Dispersas/genética
Íntrons/genética
Camundongos
RNA Polimerase II/genética
RNA Polimerase III/genética
RNA Mensageiro/genética
Deleção de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Antisense); 0 (RNA, Messenger); EC 2.7.7.- (RNA Polymerase II); EC 2.7.7.6 (Polr3e protein, mouse); EC 2.7.7.6 (RNA Polymerase III)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE
[do] DOI:10.1101/gad.293324.116


  3 / 2033 MEDLINE  
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[PMID]:28262506
[Au] Autor:Swarts DC; Szczepaniak M; Sheng G; Chandradoss SD; Zhu Y; Timmers EM; Zhang Y; Zhao H; Lou J; Wang Y; Joo C; van der Oost J
[Ad] Endereço:Laboratory of Microbiology, Department of Agrotechnology and Food Sciences, Wageningen University, 6708 WE Wageningen, the Netherlands.
[Ti] Título:Autonomous Generation and Loading of DNA Guides by Bacterial Argonaute.
[So] Source:Mol Cell;65(6):985-998.e6, 2017 Mar 16.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Several prokaryotic Argonaute proteins (pAgos) utilize small DNA guides to mediate host defense by targeting invading DNA complementary to the DNA guide. It is unknown how these DNA guides are being generated and loaded onto pAgo. Here, we demonstrate that guide-free Argonaute from Thermus thermophilus (TtAgo) can degrade double-stranded DNA (dsDNA), thereby generating small dsDNA fragments that subsequently are loaded onto TtAgo. Combining single-molecule fluorescence, molecular dynamic simulations, and structural studies, we show that TtAgo loads dsDNA molecules with a preference toward a deoxyguanosine on the passenger strand at the position opposite to the 5' end of the guide strand. This explains why in vivo TtAgo is preferentially loaded with guides with a 5' end deoxycytidine. Our data demonstrate that TtAgo can independently generate and selectively load functional DNA guides.
[Mh] Termos MeSH primário: Proteínas Argonauta/metabolismo
Proteínas de Bactérias/metabolismo
DNA Antissenso/metabolismo
DNA Bacteriano/metabolismo
Thermus thermophilus/enzimologia
[Mh] Termos MeSH secundário: Proteínas Argonauta/química
Proteínas Argonauta/genética
Proteínas de Bactérias/genética
Sítios de Ligação
DNA Antissenso/química
DNA Antissenso/genética
DNA Bacteriano/química
DNA Bacteriano/genética
Desoxicitidina/metabolismo
Desoxiguanosina/metabolismo
Transferência Ressonante de Energia de Fluorescência
Simulação de Dinâmica Molecular
Conformação de Ácido Nucleico
Ligação Proteica
Conformação Proteica
Imagem Individual de Molécula
Relação Estrutura-Atividade
Thermus thermophilus/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Argonaute Proteins); 0 (Bacterial Proteins); 0 (DNA, Antisense); 0 (DNA, Bacterial); 0W860991D6 (Deoxycytidine); G9481N71RO (Deoxyguanosine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE


  4 / 2033 MEDLINE  
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[PMID]:28167103
[Au] Autor:Inouye M; Ishida Y; Inouye K
[Ad] Endereço:Department of Biochemistry, Rutgers-Robert Wood Johnson Medical School, Center for Advance Biotechnology and Medicine, Piscataway, NJ 08854, USA. Electronic address: inouye@cabm.rutgers.edu.
[Ti] Título:Designing of a single gene encoding four functional proteins.
[So] Source:J Theor Biol;419:266-268, 2017 Apr 21.
[Is] ISSN:1095-8541
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the genomes of some organisms such as bacteriophages and bacteria, a DNA sequence is able to encode two different proteins, indicating that genetic information is compacted in DNA twice denser than in usual DNA. In theory, a DNA sequence has a maximal capacity to produce six different mRNAs, however, it is an intriguing question how many of these mRNAs are able to synthesize functional proteins. Here, we design a DNA sequence encoding four collagen-like proteins, two, (Gly-Arg-Pro)n and (Gly-Ala-Pro)n, from a sense mRNA and the other two, also (Gly-Arg-Pro)n and (Gly-Ala-Pro)n from its antisense mRNA, all of which are expected to form triple-helical structures unique to collagens. Other designs such as the combination of (Gly-Arg-Pro)n, (Gly-Val-Pro)n, (Gly-Thr-Pro)n and (Gly-Arg-Pro)n are also possible. The proposed DNA sequence is considered to contain the most compact genetic information ever created.
[Mh] Termos MeSH primário: DNA/genética
Homologia de Genes/genética
Genes Sintéticos/genética
Proteínas/genética
RNA Mensageiro/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Sequência de Bases
Colágeno/genética
DNA Antissenso/genética
Modelos Genéticos
Biossíntese de Proteínas
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Antisense); 0 (Proteins); 0 (RNA, Messenger); 9007-34-5 (Collagen); 9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE


  5 / 2033 MEDLINE  
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[PMID]:28145081
[Au] Autor:Zhao HY; Wu HJ; He JL; Zhuang JH; Liu ZY; Huang LQ; Zhao ZX
[Ad] Endereço:Department of Neurology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
[Ti] Título:Chronic Sleep Restriction Induces Cognitive Deficits and Cortical Beta-Amyloid Deposition in Mice via BACE1-Antisense Activation.
[So] Source:CNS Neurosci Ther;23(3):233-240, 2017 Mar.
[Is] ISSN:1755-5949
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: To clarify the correlation between chronic sleep restriction (CSR) and sporadic Alzheimer disease (AD), we determined in wild-type mice the impact of CSR, on cognitive performance, beta-amyloid (Aß) peptides, and its feed-forward regulators regarding AD pathogenesis. METHODS: Sixteen nine-month-old C57BL/6 male mice were equally divided into the CSR and control groups. CSR was achieved by application of a slowly rotating drum for 2 months. The Morris water maze test was used to assess cognitive impairment. The concentrations of Aß peptides, amyloid precursor protein (APP) and ß-secretase 1 (BACE1), and the mRNA levels of BACE1 and BACE1-antisense (BACE1-AS) were measured. RESULTS: Following CSR, impairments of spatial learning and memory consolidation were observed in the mice, accompanied by Aß plaque deposition and an increased Aß concentration in the prefrontal and temporal lobe cortex. CSR also upregulated the ß-secretase-induced cleavage of APP by increasing the protein and mRNA levels of BACE1, particularly the BACE1-AS. CONCLUSIONS: This study shows that a CSR accelerates AD pathogenesis in wild-type mice. An upregulation of the BACE1 pathway appears to participate in both cortical Aß plaque deposition and memory impairment caused by CSR. BACE1-AS is likely activated to initiate a cascade of events that lead to AD pathogenesis. Our study provides, therefore, a molecular mechanism that links CSR to sporadic AD.
[Mh] Termos MeSH primário: Secretases da Proteína Precursora do Amiloide/metabolismo
Ácido Aspártico Endopeptidases/metabolismo
Córtex Cerebral/metabolismo
Transtornos Cognitivos/etiologia
Privação do Sono/complicações
Privação do Sono/patologia
[Mh] Termos MeSH secundário: Secretases da Proteína Precursora do Amiloide/genética
Peptídeos beta-Amiloides/metabolismo
Precursor de Proteína beta-Amiloide/metabolismo
Animais
Ácido Aspártico Endopeptidases/genética
DNA Antissenso/farmacologia
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Masculino
Camundongos
Camundongos Endogâmicos C57BL
RNA Mensageiro/metabolismo
Tempo de Reação/efeitos dos fármacos
Aprendizagem Espacial/fisiologia
Memória Espacial/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Amyloid beta-Protein Precursor); 0 (DNA, Antisense); 0 (RNA, Messenger); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.23.- (Aspartic Acid Endopeptidases); EC 3.4.23.46 (Bace1 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170202
[St] Status:MEDLINE
[do] DOI:10.1111/cns.12667


  6 / 2033 MEDLINE  
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[PMID]:27888605
[Au] Autor:Ostrowski LA; Saville BJ
[Ad] Endereço:Environmental and Life Sciences Graduate Program, Trent University, Peterborough, ON, Canada, K9L 0G2.
[Ti] Título:Natural antisense transcripts are linked to the modulation of mitochondrial function and teliospore dormancy in Ustilago maydis.
[So] Source:Mol Microbiol;103(5):745-763, 2017 Mar.
[Is] ISSN:1365-2958
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The basidiomycete smut fungus Ustilago maydis causes common smut of corn. This disease is spread through the production of teliospores, which are thick-walled dormant structures characterized by low rates of respiration and metabolism. Teliospores are formed when the fungus grows within the plant, and the morphological steps involved in their formation have been described, but the molecular events leading to dormancy are not known. In U. maydis, natural antisense transcripts (NATs) can function to alter gene expression and many NATs have increased levels in the teliospore. One such NAT is as-ssm1 which is complementary to the gene for the mitochondrial seryl-tRNA synthetase (ssm1), an enzyme important to mitochondrial function. The disruption of ssm1 leads to cell lysis, indicating it is also essential for cellular viability. To assess the function of as-ssm1, it was ectopically expressed in haploid cells, where it is not normally present. This expression led to reductions in growth rate, virulence, mitochondrial membrane potential and oxygen consumption. It also resulted in the formation of as-ssm1/ssm1 double-stranded RNA and increased ssm1 transcript levels, but no change in Ssm1 protein levels was detected. Together, these findings suggest a role for as-ssm1 in facilitating teliospore dormancy through dsRNA formation and reduction of mitochondrial function.
[Mh] Termos MeSH primário: DNA Antissenso/genética
Regulação Fúngica da Expressão Gênica
Mitocôndrias/fisiologia
RNA não Traduzido/genética
Ustilago/genética
[Mh] Termos MeSH secundário: DNA Antissenso/metabolismo
Genes Fúngicos
Mitocôndrias/enzimologia
Mitocôndrias/genética
Oxigênio/metabolismo
Serina-tRNA Ligase/genética
Serina-tRNA Ligase/metabolismo
Esporos Fúngicos/genética
Ustilago/crescimento & desenvolvimento
Ustilago/fisiologia
Virulência
Zea mays/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Antisense); 0 (RNA, Untranslated); EC 6.1.1.11 (Serine-tRNA Ligase); S88TT14065 (Oxygen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161127
[St] Status:MEDLINE
[do] DOI:10.1111/mmi.13587


  7 / 2033 MEDLINE  
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[PMID]:27718524
[Au] Autor:Da F; Yao L; Su Z; Hou Z; Li Z; Xue X; Meng J; Luo X
[Ad] Endereço:Department of Pharmacology, School of Pharmacy, Fourth Military Medical University, Xi'an, China.
[Ti] Título:Antisense locked nucleic acids targeting agrA inhibit quorum sensing and pathogenesis of community-associated methicillin-resistant Staphylococcus aureus.
[So] Source:J Appl Microbiol;122(1):257-267, 2017 Jan.
[Is] ISSN:1365-2672
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is commonly associated with nonnosocomial skin and soft tissue infections due to its virulence, which is mainly controlled by the accessory gene regulator (agr) quorum sensing (QS) system. In this study (KFF) K peptide-conjugated locked nucleic acids (PLNAs) targeting agrA mRNA were developed to inhibit agr activity and arrest the pathogenicity of CA-MRSA. METHODS AND RESULTS: Two PLNAs were designed, and synthesized, after predicting the secondary structure of agrA mRNA. The influence on bacterial growth was tested using a growth curve assay. RT-qPCR, haemolysis assay, lactate dehydrogenase release assay and chemotaxis assay were used to evaluate the effects of the PLNAs on inhibiting agr QS. A mouse skin infection model was employed to test the protective effect of the PLNAs in vivo. None of the PLNAs were found to be bacteriostatic or bactericidal in vitro. However, one PLNA, PLNA34, showed strong ability to suppress expression of agrA and the effector molecule RNAIII in USA300 LAC strain. Furthermore, PLNA34 inhibited the expression of virulence genes that are upregulated by agr, including hla, psmα, psmß and pvl. The haemolytic activity of the supernatants from PLNA34-treated bacteria was also dramatically reduced, as well as the capacity to lyse and recruit neutrophils. Moreover, PLNA34 showed high levels of protection in the CA-MRSA mouse skin infection model. CONCLUSIONS: The anti-agrA PLNA34 can effectively inhibit the agr QS and suppress CA-MRSA pathogenicity. SIGNIFICANCE AND IMPACT OF THE STUDY: agrA is a promising target for the development of antisense oligonucleotides to block agr QS.
[Mh] Termos MeSH primário: Proteínas de Bactérias/genética
Infecções Comunitárias Adquiridas/microbiologia
DNA Antissenso/genética
Staphylococcus aureus Resistente à Meticilina/genética
Staphylococcus aureus Resistente à Meticilina/patogenicidade
Oligonucleotídeos/genética
Percepção de Quorum
Infecções Estafilocócicas/microbiologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Bactérias/metabolismo
Infecções Comunitárias Adquiridas/terapia
DNA Antissenso/metabolismo
Seres Humanos
Staphylococcus aureus Resistente à Meticilina/crescimento & desenvolvimento
Staphylococcus aureus Resistente à Meticilina/fisiologia
Camundongos
Oligonucleotídeos/metabolismo
Infecções Estafilocócicas/terapia
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (DNA, Antisense); 0 (Oligonucleotides); 0 (locked nucleic acid)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161009
[St] Status:MEDLINE
[do] DOI:10.1111/jam.13321


  8 / 2033 MEDLINE  
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[PMID]:27801428
[Au] Autor:Bryzghalov O; Szczesniak MW; Makalowska I
[Ad] Endereço:Department of Integrative Genomics, Institute of Antropology, Adam Mickiewicz University in Poznan, Poznan, Poland.
[Ti] Título:Retroposition as a source of antisense long non-coding RNAs with possible regulatory functions.
[So] Source:Acta Biochim Pol;63(4):825-833, 2016.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Long non-coding RNAs (lncRNAs) are a class of intensely studied, yet enigmatic molecules that make up a substantial portion of the human transcriptome. In this work, we link the origins and functions of some lncRNAs to retroposition, a process resulting in the creation of intronless copies (retrocopies) of the so-called parental genes. We found 35 human retrocopies transcribed in antisense and giving rise to 58 lncRNA transcripts. These lncRNAs share sequence similarity with the corresponding parental genes but in the sense/antisense orientation, meaning they have the potential to interact with each other and to form RNA:RNA duplexes. We took a closer look at these duplexes and found that 10 of the lncRNAs might regulate parental gene expression and processing at the pre-mRNA and mRNA levels. Further analysis of the co-expression and expression correlation provided support for the existence of functional coupling between lncRNAs and their mate parental gene transcripts.
[Mh] Termos MeSH primário: RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Sequência Conservada
DNA Antissenso/genética
Seres Humanos
Camundongos
Anotação de Sequência Molecular
Pan troglodytes
Interferência de RNA
Retroelementos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Antisense); 0 (RNA, Long Noncoding); 0 (Retroelements)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170119
[Lr] Data última revisão:
170119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161102
[St] Status:MEDLINE


  9 / 2033 MEDLINE  
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[PMID]:27548692
[Au] Autor:Khanna R; Feagan BG
[Ad] Endereço:Department of Medicine, University of Western Ontario, London, Ont., Canada.
[Ti] Título:Emerging Therapies for Inflammatory Bowel Diseases.
[So] Source:Dig Dis;34 Suppl 1:67-73, 2016.
[Is] ISSN:1421-9875
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The past decade has seen important advances in the management of chronic inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis. The development of TNF antagonists, the recognition of interrupting lymphocyte trafficking as an effective treatment strategy, confirmation of the value of combination therapy, and the need, particularly in CD, for the treatment of high-risk patients early in the disease course are all fundamental concepts upon which the next generation of IBD treatment algorithms will be built. Emerging concepts that will continue to evolve and shape the field include an increased emphasis on personalized medicine (right drug, right dose, right time) and the development of new therapeutic classes. In this article, we review the clinical data and provide some insights into recent data regarding IBD therapies. KEY MESSAGES: In this article, we review the mechanism of action and data for novel therapies in IBD with particular focus on the evidence for agents targeting leukocyte trafficking, cytokine signaling, including interleukin-12/23 and the Janus kinase-signal transducers/activators of transcription pathway, and the emergence of antisense therapy for the treatment of IBD. CONCLUSIONS: Multiple new therapies are emerging for IBD; however, the potential positioning of these agents in treatment algorithms is difficult to predict in the absence of comparative effectiveness studies.
[Mh] Termos MeSH primário: Terapia Biológica/métodos
Colite Ulcerativa/tratamento farmacológico
Doença de Crohn/tratamento farmacológico
Drogas em Investigação/uso terapêutico
[Mh] Termos MeSH secundário: Citocinas/efeitos dos fármacos
DNA Antissenso/efeitos dos fármacos
Seres Humanos
Doenças Inflamatórias Intestinais/tratamento farmacológico
Interleucina-12/metabolismo
Interleucina-23/metabolismo
Leucócitos/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (DNA, Antisense); 0 (Drugs, Investigational); 0 (Interleukin-23); 187348-17-0 (Interleukin-12)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170113
[Lr] Data última revisão:
170113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160823
[St] Status:MEDLINE
[do] DOI:10.1159/000447378


  10 / 2033 MEDLINE  
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[PMID]:27035516
[Au] Autor:Izumi H; Nagao S; Mochizuki S; Fujiwara N; Sakurai K; Morimoto Y
[Ad] Endereço:University of Occupational and Environmental Health, Yahatanishi-ku, Kitakyushu, Fukuoka 807-8555, Japan.
[Ti] Título:Optimal sequence of antisense DNA to silence YB-1 in lung cancer by use of a novel polysaccharide drug delivery system.
[So] Source:Int J Oncol;48(6):2472-8, 2016 Jun.
[Is] ISSN:1791-2423
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Silencing Y-box binding protein 1 (YB-1) can be an excellent target for cancer therapy and many lung cancer cells express the polysaccharide-recognition receptor Dectin-1. We designed a Dectin-1 targeting vehicle delivering YB-1-antisense DNA. First, we selected five optimal antisense DNA sequences to silence YB-1 from among 153 candidates. We chose the sequence closest to the start codon (AS014), and attached dA40 to the 3' end; dA40 promotes complex formation with a ß-(1➝3)-d-glucan called schizophyllan (SPG). The resultant complexes were applied to 12 human-oriented lung cancer cell lines, and cell viability was examined. The cell lines exhibited decreased viability and showed strong affinity to bind SPG, suggesting the AS014/SPG complex entered the cells via the Dectin-1 mediated pathway.
[Mh] Termos MeSH primário: DNA Antissenso/farmacologia
Lectinas Tipo C/química
Neoplasias Pulmonares/genética
Sizofirano/química
Proteína 1 de Ligação a Y-Box/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
DNA Antissenso/química
DNA Antissenso/genética
Sistemas de Liberação de Medicamentos
Inativação Gênica
Seres Humanos
Proteína 1 de Ligação a Y-Box/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Antisense); 0 (Lectins, C-Type); 0 (Y-Box-Binding Protein 1); 0 (YBX1 protein, human); 0 (dectin 1); 9050-67-3 (Sizofiran)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170310
[Lr] Data última revisão:
170310
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160402
[St] Status:MEDLINE
[do] DOI:10.3892/ijo.2016.3451



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