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[PMID]:29363539
[Au] Autor:Pirmohamed M
[Ad] Endereço:Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
[Ti] Título:Nucleic acid based therapies: developing frontier for precision medicine.
[So] Source:BMJ;360:k223, 2018 01 23.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Terapia Genética/utilização
Terapia de Alvo Molecular/utilização
Ácidos Nucleicos/uso terapêutico
Medicina de Precisão/métodos
[Mh] Termos MeSH secundário: Adenoviridae/genética
Aminofenóis/uso terapêutico
Agonistas dos Canais de Cloreto/uso terapêutico
Fibrose Cística/tratamento farmacológico
Fibrose Cística/genética
Regulador de Condutância Transmembrana em Fibrose Cística/efeitos dos fármacos
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Terapia Genética/economia
Genômica
Hemofilia A/classificação
Hemofilia A/tratamento farmacológico
Hemofilia A/genética
Seres Humanos
Doença dos Neurônios Motores/tratamento farmacológico
Doença dos Neurônios Motores/genética
Mutação
Oligonucleotídeos Antissenso/economia
Oligonucleotídeos Antissenso/uso terapêutico
Quinolonas/uso terapêutico
Reino Unido/epidemiologia
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (Aminophenols); 0 (CFTR protein, human); 0 (Chloride Channel Agonists); 0 (Nucleic Acids); 0 (Oligonucleotides, Antisense); 0 (Quinolones); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.k223


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[PMID]:29383373
[Au] Autor:Muth CC
[Ti] Título:ASO Therapy: Hope for Genetic Neurological Diseases.
[So] Source:JAMA;319(7):644-646, 2018 Feb 20.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Atrofia Muscular Espinal/tratamento farmacológico
Doenças Neurodegenerativas/tratamento farmacológico
Oligonucleotídeos Antissenso/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Seres Humanos
Camundongos
Atrofia Muscular Espinal/genética
Distrofia Muscular de Duchenne/tratamento farmacológico
Distrofia Muscular de Duchenne/genética
Mutação
Doenças Neurodegenerativas/genética
Ataxias Espinocerebelares/tratamento farmacológico
[Pt] Tipo de publicação:NEWS
[Nm] Nome de substância:
0 (Oligonucleotides, Antisense)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.18665


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Registro de Ensaios Clínicos
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[PMID]:29443664
[Au] Autor:Mercuri E; Darras BT; Chiriboga CA; Day JW; Campbell C; Connolly AM; Iannaccone ST; Kirschner J; Kuntz NL; Saito K; Shieh PB; Tulinius M; Mazzone ES; Montes J; Bishop KM; Yang Q; Foster R; Gheuens S; Bennett CF; Farwell W; Schneider E; De Vivo DC; Finkel RS; CHERISH Study Group
[Ad] Endereço:From the Department of Pediatric Neurology, Catholic University, Rome (E.M., E.S.M.); the Department of Neurology, Boston Children's Hospital, Boston (B.T.D.), and Biogen, Cambridge (R.F., S.G., W.F.) - both in Massachusetts; the Departments of Neurology (C.A.C., J.M., D.C.D.), Pediatrics (C.A.C., D
[Ti] Título:Nusinersen versus Sham Control in Later-Onset Spinal Muscular Atrophy.
[So] Source:N Engl J Med;378(7):625-635, 2018 02 15.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Nusinersen is an antisense oligonucleotide drug that modulates pre-messenger RNA splicing of the survival motor neuron 2 ( SMN2) gene. It has been developed for the treatment of spinal muscular atrophy (SMA). METHODS: We conducted a multicenter, double-blind, sham-controlled, phase 3 trial of nusinersen in 126 children with SMA who had symptom onset after 6 months of age. The children were randomly assigned, in a 2:1 ratio, to undergo intrathecal administration of nusinersen at a dose of 12 mg (nusinersen group) or a sham procedure (control group) on days 1, 29, 85, and 274. The primary end point was the least-squares mean change from baseline in the Hammersmith Functional Motor Scale-Expanded (HFMSE) score at 15 months of treatment; HFMSE scores range from 0 to 66, with higher scores indicating better motor function. Secondary end points included the percentage of children with a clinically meaningful increase from baseline in the HFMSE score (≥3 points), an outcome that indicates improvement in at least two motor skills. RESULTS: In the prespecified interim analysis, there was a least-squares mean increase from baseline to month 15 in the HFMSE score in the nusinersen group (by 4.0 points) and a least-squares mean decrease in the control group (by -1.9 points), with a significant between-group difference favoring nusinersen (least-squares mean difference in change, 5.9 points; 95% confidence interval, 3.7 to 8.1; P<0.001). This result prompted early termination of the trial. Results of the final analysis were consistent with results of the interim analysis. In the final analysis, 57% of the children in the nusinersen group as compared with 26% in the control group had an increase from baseline to month 15 in the HFMSE score of at least 3 points (P<0.001), and the overall incidence of adverse events was similar in the nusinersen group and the control group (93% and 100%, respectively). CONCLUSIONS: Among children with later-onset SMA, those who received nusinersen had significant and clinically meaningful improvement in motor function as compared with those in the control group. (Funded by Biogen and Ionis Pharmaceuticals; CHERISH ClinicalTrials.gov number, NCT02292537 .).
[Mh] Termos MeSH primário: Oligonucleotídeos Antissenso/uso terapêutico
Oligonucleotídeos/uso terapêutico
Atrofias Musculares Espinais da Infância/tratamento farmacológico
[Mh] Termos MeSH secundário: Idade de Início
Criança
Pré-Escolar
Método Duplo-Cego
Feminino
Seres Humanos
Lactente
Injeções Espinhais
Análise dos Mínimos Quadrados
Masculino
Destreza Motora
Oligonucleotídeos/efeitos adversos
Oligonucleotídeos Antissenso/efeitos adversos
Atrofias Musculares Espinais da Infância/fisiopatologia
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Oligonucleotides); 0 (Oligonucleotides, Antisense); 0 (nusinersen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180215
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1710504


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[PMID]:29261648
[Au] Autor:Zuin J; Casa V; Pozojevic J; Kolovos P; van den Hout MCGN; van Ijcken WFJ; Parenti I; Braunholz D; Baron Y; Watrin E; Kaiser FJ; Wendt KS
[Ad] Endereço:Department of Cell Biology, Erasmus MC, Rotterdam, The Netherlands.
[Ti] Título:Regulation of the cohesin-loading factor NIPBL: Role of the lncRNA NIPBL-AS1 and identification of a distal enhancer element.
[So] Source:PLoS Genet;13(12):e1007137, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cohesin is crucial for genome stability, cell division, transcription and chromatin organization. Its functions critically depend on NIPBL, the cohesin-loader protein that is found to be mutated in >60% of the cases of Cornelia de Lange syndrome (CdLS). Other mutations are described in the cohesin subunits SMC1A, RAD21, SMC3 and the HDAC8 protein. In 25-30% of CdLS cases no mutation in the known CdLS genes is detected. Until now, functional elements in the noncoding genome were not characterized in the molecular etiology of CdLS and therefore are excluded from mutation screening, although the impact of such mutations has now been recognized for a wide range of diseases. We have identified different elements of the noncoding genome involved in regulation of the NIPBL gene. NIPBL-AS1 is a long non-coding RNA transcribed upstream and antisense to NIPBL. By knockdown and transcription blocking experiments, we could show that not the NIPBL-AS1 gene product, but its actual transcription is important to regulate NIPBL expression levels. This reveals a possibility to boost the transcriptional activity of the NIPBL gene by interfering with the NIPBL-AS1 lncRNA. Further, we have identified a novel distal enhancer regulating both NIPBL and NIPBL-AS1. Deletion of the enhancer using CRISPR genome editing in HEK293T cells reduces expression of NIPBL, NIPBL-AS1 as well as genes found to be dysregulated in CdLS.
[Mh] Termos MeSH primário: Elementos Facilitadores Genéticos
Oligonucleotídeos Antissenso/genética
Oligonucleotídeos Antissenso/metabolismo
Proteínas/genética
Proteínas/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Proteínas Cromossômicas não Histona/genética
Proteínas Cromossômicas não Histona/metabolismo
Segregação de Cromossomos
Síndrome de Lange/genética
Regulação da Expressão Gênica
Genoma Humano
Células HEK293
Seres Humanos
Mutação
Fenótipo
Regiões Promotoras Genéticas
RNA Longo não Codificante/genética
RNA Longo não Codificante/metabolismo
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Chromosomal Proteins, Non-Histone); 0 (NIPBL protein, human); 0 (Oligonucleotides, Antisense); 0 (Proteins); 0 (RNA, Long Noncoding); 0 (cohesins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007137


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[PMID]:29337064
[Au] Autor:Knollenberg BJ; Liu J; Yu S; Lin H; Tian L
[Ad] Endereço:Department of Plant Sciences, University of California, Davis, CA, 95616, USA; The Huck Institutes of the Life Sciences, Pennsylvania State University, State College, PA, 16801, USA.
[Ti] Título:Cloning and functional characterization of a p-coumaroyl quinate/shikimate 3'-hydroxylase from potato (Solanum tuberosum).
[So] Source:Biochem Biophys Res Commun;496(2):462-467, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chlorogenic acid (CGA) plays an important role in protecting plants against pathogens and promoting human health. Although CGA accumulates to high levels in potato tubers, the key enzyme p-coumaroyl quinate/shikimate 3'-hydroxylase (C3'H) for CGA biosynthesis has not been isolated and functionally characterized in potato. In this work, we cloned StC3'H from potato and showed that it catalyzed the formation of caffeoylshikimate and CGA (caffeoylquinate) from p-coumaroyl shikimate and p-coumaroyl quinate, respectively, but was inactive towards p-coumaric acid in in vitro enzyme assays. When the expression of StC3'H proteins was blocked through antisense (AS) inhibition under the control of a tuber-specific patatin promoter, moderate changes in tuber yield as well as phenolic metabolites in the core tuber tissue were observed for several AS lines. On the other hand, the AS and control potato lines exhibited similar responses to a bacterial pathogen Pectobacterium carotovorum. These results suggest that StC3'H is implicated in phenolic metabolism in potato. They also suggest that CGA accumulation in the core tissue of potato tubers is an intricately controlled process and that additional C3'H activity may also be involved in CGA biosynthesis in potato.
[Mh] Termos MeSH primário: Ácido Clorogênico/metabolismo
Oxigenases de Função Mista/genética
Proteínas de Plantas/genética
Tubérculos/enzimologia
Solanum tuberosum/enzimologia
[Mh] Termos MeSH secundário: Hidrolases de Éster Carboxílico/genética
Hidrolases de Éster Carboxílico/metabolismo
Ácido Clorogênico/análogos & derivados
Clonagem Molecular
Expressão Gênica
Oxigenases de Função Mista/antagonistas & inibidores
Oxigenases de Função Mista/metabolismo
Oligonucleotídeos Antissenso/genética
Oligonucleotídeos Antissenso/metabolismo
Pectobacterium carotovorum/patogenicidade
Pectobacterium carotovorum/fisiologia
Pichia/genética
Pichia/metabolismo
Proteínas de Plantas/metabolismo
Tubérculos/genética
Tubérculos/microbiologia
Plantas Geneticamente Modificadas
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Ácido Chiquímico/análogos & derivados
Ácido Chiquímico/metabolismo
Solanum tuberosum/genética
Solanum tuberosum/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (4-coumaroylshikimic acid); 0 (Oligonucleotides, Antisense); 0 (Plant Proteins); 0 (Recombinant Proteins); 0 (patatin protein, Solanum tuberosum); 29MS2WI2NU (Shikimic Acid); 318ADP12RI (Chlorogenic Acid); 73263-62-4 (5-O-caffeoylshikimic acid); E57A0DKE0B (3,4-di-O-caffeoylquinic acid); EC 1.- (Mixed Function Oxygenases); EC 1.14.13.- (5-O-(4-coumaroyl)shikimate 3'-hydroxylase); EC 3.1.1.- (Carboxylic Ester Hydrolases)
[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:180117
[St] Status:MEDLINE


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[PMID]:29037661
[Au] Autor:Donaldson TN; Jennings KT; Cherep LA; McNeela AM; Depreux FF; Jodelka FM; Hastings ML; Wallace DG
[Ad] Endereço:Northern Illinois University, Department of Psychology, DeKalb, IL 60115, United States.
[Ti] Título:Antisense oligonucleotide therapy rescues disruptions in organization of exploratory movements associated with Usher syndrome type 1C in mice.
[So] Source:Behav Brain Res;338:76-87, 2018 Feb 15.
[Is] ISSN:1872-7549
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Usher syndrome, Type 1C (USH1C) is an autosomal recessive inherited disorder in which a mutation in the gene encoding harmonin is associated with multi-sensory deficits (i.e., auditory, vestibular, and visual). USH1C (Usher) mice, engineered with a human USH1C mutation, exhibit these multi-sensory deficits by circling behavior and lack of response to sound. Administration of an antisense oligonucleotide (ASO) therapeutic that corrects expression of the mutated USH1C gene, has been shown to increase harmonin levels, reduce circling behavior, and improve vestibular and auditory function. The current study evaluates the organization of exploratory movements to assess spatial organization in Usher mice and determine the efficacy of ASO therapy in attenuating any such deficits. Usher and heterozygous mice received the therapeutic ASO, ASO-29, or a control, non-specific ASO treatment at postnatal day five. Organization of exploratory movements was assessed under dark and light conditions at two and six-months of age. Disruptions in exploratory movement organization observed in control-treated Usher mice were consistent with impaired use of self-movement and environmental cues. In general, ASO-29 treatment rescued organization of exploratory movements at two and six-month testing points. These observations are consistent with ASO-29 rescuing processing of multiple sources of information and demonstrate the potential of ASO therapies to ameliorate topographical disorientation associated with other genetic disorders.
[Mh] Termos MeSH primário: Proteínas de Transporte/genética
Comportamento Exploratório/efeitos dos fármacos
Movimento/efeitos dos fármacos
Oligonucleotídeos Antissenso/farmacologia
Síndromes de Usher/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Proteínas de Transporte/metabolismo
Masculino
Camundongos
Síndromes de Usher/genética
Síndromes de Usher/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Oligonucleotides, Antisense); 0 (Ush1c protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE


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[PMID]:28745638
[Au] Autor:Xu X; You Y; Zhang L
[Ad] Endereço:Department of Entomology, China Agricultural University.
[Ti] Título:Localization of Odorant Receptor Genes in Locust Antennae by RNA In Situ Hybridization.
[So] Source:J Vis Exp;(125), 2017 Jul 13.
[Is] ISSN:1940-087X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Insects have evolved sophisticated olfactory reception systems to sense exogenous chemical signals. These chemical signals are transduced by Olfactory Receptor Neurons (ORNs) housed in hair-like structures, called chemosensilla, of the antennae. On the ORNs' membranes, Odorant Receptors (ORs) are believed to be involved in odor coding. Thus, being able to identify genes localized to the ORNs is necessary to recognize OR genes, and provides a fundamental basis for further functional in situ studies. The RNA expression levels of specific ORs in insect antennae are very low, and preserving insect tissue for histology is challenging. Thus, it is difficult to localize an OR to a specific type of sensilla using RNA in situ hybridization. In this paper, a detailed and highly effective RNA in situ hybridization protocol particularly for lowly expressed OR genes of insects, is introduced. In addition, a specific OR gene was identified by conducting double-color fluorescent in situ hybridization experiments using a co-expressing receptor gene, Orco, as a marker.
[Mh] Termos MeSH primário: Antenas de Artrópodes/patologia
Gafanhotos/metabolismo
RNA/metabolismo
Receptores Odorantes/genética
[Mh] Termos MeSH secundário: Animais
Antenas de Artrópodes/metabolismo
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Microscopia Confocal
Neurônios Receptores Olfatórios/metabolismo
Neurônios Receptores Olfatórios/patologia
Oligonucleotídeos Antissenso/química
Oligonucleotídeos Antissenso/metabolismo
Receptores Odorantes/metabolismo
Gravação em Vídeo
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (Oligonucleotides, Antisense); 0 (Receptors, Odorant); 63231-63-0 (RNA)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180126
[Lr] Data última revisão:
180126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.3791/55924


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[PMID]:29190672
[Au] Autor:Pfeiffer N; Voykov B; Renieri G; Bell K; Richter P; Weigel M; Thieme H; Wilhelm B; Lorenz K; Feindor M; Wosikowski K; Janicot M; Päckert D; Römmich R; Mala C; Fettes P; Leo E
[Ad] Endereço:Dpt. of Ophthalmology, University Medical Center Mainz, Mainz, Germany.
[Ti] Título:First-in-human phase I study of ISTH0036, an antisense oligonucleotide selectively targeting transforming growth factor beta 2 (TGF-ß2), in subjects with open-angle glaucoma undergoing glaucoma filtration surgery.
[So] Source:PLoS One;12(11):e0188899, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To evaluate the safety and tolerability of intravitreal ISTH0036, an antisense oligonucleotide selectively targeting transforming growth factor beta 2 (TGF-ß2), in patients with primary open angle glaucoma (POAG) undergoing trabeculectomy (TE; glaucoma filtration surgery). METHODS: In this prospective phase I trial glaucoma patients scheduled for TE with mitomycin C (MMC) received a single intravitreal injection of ISTH0036 at the end of surgery in escalating total doses of 6.75 µg, 22.5 µg, 67.5 µg or 225 µg, resulting in calculated intraocular ISTH0036 concentrations in the vitreous humor of approximately 0.3 µM, 1 µM, 3 µM or 10 µM after injection, respectively. Outcomes assessed included: type and frequency of adverse events (AEs), intraocular pressure (IOP), numbers of interventions post trabeculectomy, bleb survival, visual acuity, visual field, electroretinogram (ERG), slit lamp biomicroscopy and optic disc assessment. RESULTS: In total, 12 patients were treated in the 4 dose groups. Main ocular AEs observed were corneal erosion, corneal epithelium defect, or too high or too low IOP, among others. No AE was reported to be related to ISTH0036. All other safety-related analyses did not reveal any toxicities of concern, either. The mean medicated preoperative IOP at decision time-point for surgery was 27.3 mmHg +/- 12.6 mmHg (SD). Mean IOP (±SD) for dose levels 1, 2, 3, and 4 were at Day 43 9.8 mmHg ± 1.0 mmHg, 11.3 mmHg ± 6.7 mmHg, 5.5 mmHg ± 3.0 mmHg and 7.5 mmHg ± 2.3 mmHg SD; and at Day 85 9.7 mmHg ± 3.3 mmHg, 14.2 mmHg ± 6.5 mmHg, 5.8 mmHg ± 1.8 mmHg and 7.8 mmHg ± 0.6 mmHg, respectively. In contrast to IOP values for dose levels 1 and 2, IOP values for dose levels 3 and 4 persistently remained below 10 mmHg throughout the observation period. CONCLUSION: This first-in-human trial demonstrates that intravitreal injection of ISTH0036 at the end of TE is safe. Regarding IOP control, single-dose ISTH0036 administration of 67.5 µg or 225 µg at the time of TE resulted in IOP values persistently < 10 mmHg over the three month postoperative observation period.
[Mh] Termos MeSH primário: Implantes para Drenagem de Glaucoma
Glaucoma de Ângulo Aberto/tratamento farmacológico
Oligonucleotídeos Antissenso/uso terapêutico
Oligonucleotídeos/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Feminino
Glaucoma de Ângulo Aberto/cirurgia
Seres Humanos
Masculino
Meia-Idade
Oligonucleotídeos/efeitos adversos
Oligonucleotídeos/farmacologia
Oligonucleotídeos Antissenso/efeitos adversos
Oligonucleotídeos Antissenso/farmacologia
Estudos Prospectivos
Fatores de Crescimento Transformadores
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ISTH0036); 0 (Oligonucleotides); 0 (Oligonucleotides, Antisense); 76057-06-2 (Transforming Growth Factors)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188899


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[PMID]:29216448
[Au] Autor:Huynh TV; Liao F; Francis CM; Robinson GO; Serrano JR; Jiang H; Roh J; Finn MB; Sullivan PM; Esparza TJ; Stewart FR; Mahan TE; Ulrich JD; Cole T; Holtzman DM
[Ad] Endereço:Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA; Medical Scientist Training Program (MSTP), Washington University School of Medicine, St. Louis, MO 63110, USA.
[Ti] Título:Age-Dependent Effects of apoE Reduction Using Antisense Oligonucleotides in a Model of ß-amyloidosis.
[So] Source:Neuron;96(5):1013-1023.e4, 2017 Dec 06.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer disease. Previous studies suggest that reduction of apoE levels through genetic manipulation can reduce Aß pathology. However, it is not clear how reduction of apoE levels after birth would affect amyloid deposition. We utilize an antisense oligonucleotide (ASO) to reduce apoE expression in the brains of APP/PS1-21 mice homozygous for the APOE-ε4 or APOE-ε3 allele. ASO treatment starting after birth led to a significant decrease in Aß pathology when assessed at 4 months. Interestingly, ASO treatment starting at the onset of amyloid deposition led to an increase in Aß plaque size and a reduction in plaque-associated neuritic dystrophy with no change in overall plaque load. These results suggest that lowering apoE levels prior to plaque deposition can strongly affect the initiation of Aß pathology while lowering apoE after Aß seeding modulates plaque size and toxicity.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides
Amiloidose/tratamento farmacológico
Apolipoproteínas E/antagonistas & inibidores
Oligonucleotídeos Antissenso/uso terapêutico
[Mh] Termos MeSH secundário: Envelhecimento/fisiologia
Alelos
Doença de Alzheimer/patologia
Precursor de Proteína beta-Amiloide/biossíntese
Precursor de Proteína beta-Amiloide/genética
Amiloidose/patologia
Animais
Apolipoproteína E3/genética
Apolipoproteína E4/genética
Seres Humanos
Masculino
Camundongos
Camundongos Transgênicos
Placa Amiloide/patologia
Placa Amiloide/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Amyloid beta-Protein Precursor); 0 (Apolipoprotein E3); 0 (Apolipoprotein E4); 0 (Apolipoproteins E); 0 (Oligonucleotides, Antisense)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE


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[PMID]:29180822
[Au] Autor:Michelini F; Pitchiaya S; Vitelli V; Sharma S; Gioia U; Pessina F; Cabrini M; Wang Y; Capozzo I; Iannelli F; Matti V; Francia S; Shivashankar GV; Walter NG; d'Adda di Fagagna F
[Ad] Endereço:IFOM-The FIRC Institute of Molecular Oncology, Milan 20139, Italy.
[Ti] Título:Damage-induced lncRNAs control the DNA damage response through interaction with DDRNAs at individual double-strand breaks.
[So] Source:Nat Cell Biol;19(12):1400-1411, 2017 Dec.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The DNA damage response (DDR) preserves genomic integrity. Small non-coding RNAs termed DDRNAs are generated at DNA double-strand breaks (DSBs) and are critical for DDR activation. Here we show that active DDRNAs specifically localize to their damaged homologous genomic sites in a transcription-dependent manner. Following DNA damage, RNA polymerase II (RNAPII) binds to the MRE11-RAD50-NBS1 complex, is recruited to DSBs and synthesizes damage-induced long non-coding RNAs (dilncRNAs) from and towards DNA ends. DilncRNAs act both as DDRNA precursors and by recruiting DDRNAs through RNA-RNA pairing. Together, dilncRNAs and DDRNAs fuel DDR focus formation and associate with 53BP1. Accordingly, inhibition of RNAPII prevents DDRNA recruitment, DDR activation and DNA repair. Antisense oligonucleotides matching dilncRNAs and DDRNAs impair site-specific DDR focus formation and DNA repair. We propose that DDR signalling sites, in addition to sharing a common pool of proteins, individually host a unique set of site-specific RNAs necessary for DDR activation.
[Mh] Termos MeSH primário: Quebras de DNA de Cadeia Dupla
Dano ao DNA
Reparo do DNA
RNA Longo não Codificante/metabolismo
[Mh] Termos MeSH secundário: Transportadores de Cassetes de Ligação de ATP/metabolismo
Animais
Proteínas de Ciclo Celular/metabolismo
Linhagem Celular
Sistema Livre de Células
Dano ao DNA/genética
Dano ao DNA/fisiologia
Reparo do DNA/genética
Reparo do DNA/fisiologia
Proteína Homóloga a MRE11/metabolismo
Camundongos
Modelos Biológicos
Proteínas Nucleares/metabolismo
Oligonucleotídeos Antissenso/genética
RNA Polimerase II/metabolismo
RNA Longo não Codificante/genética
Transcrição Genética
Proteína 1 de Ligação à Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP-Binding Cassette Transporters); 0 (Cell Cycle Proteins); 0 (Mre11a protein, mouse); 0 (Nijmegen breakage syndrome 1 protein, mouse); 0 (Nuclear Proteins); 0 (Oligonucleotides, Antisense); 0 (RNA, Long Noncoding); 0 (Rad50 protein, mouse); 0 (Trp53bp1 protein, mouse); 0 (Tumor Suppressor p53-Binding Protein 1); EC 2.7.7.- (RNA Polymerase II); EC 3.1.- (MRE11 Homologue Protein)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3643



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