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[PMID]:29381918
[Au] Autor:Xu HY; Li CY; Su SS; Yang L; Ye M; Ye JR; Ke PP; Chen CS; Xie YP; Li YP
[Ad] Endereço:Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, PR China.
[Ti] Título:Diagnosis of tuberculous pleurisy with combination of adenosine deaminase and interferon-γ immunospot assay in a tuberculosis-endemic population: A prospective cohort study.
[So] Source:Medicine (Baltimore);96(47):e8412, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to identify the optimal cut-off value of T cell enzyme-linked immunospot assay for tuberculosis (T-SPOT.TB) and evaluate its diagnostic performance alone (in the peripheral blood) or in combination with the adenosine deaminase (ADA) activity test (in peripheral blood and the pleural fluid) in patients with tuberculous pleurisy.Adult patients presenting with pleural effusion were included in this prospective cohort study. Tuberculous pleurisy was diagnosed by T-SPOT.TB in peripheral blood and a combination of T-SPOT.TB and ADA activity test in pleural fluid and peripheral blood. Receiver operating characteristic (ROC) curve in combination with multivariate logistic regression was used to evaluate the diagnostic performance of the assays.Among a total of 189 patients with suspected tuberculous pleurisy who were prospectively enrolled in this study, 177 patients were validated for inclusion in the final analysis. ROC analysis revealed that the area under the ROC curve (AUC) for T-SPOT.TB in pleural fluid and peripheral blood was 0.918 and 0.881, respectively, and for the ADA activity test in pleural fluid was 0.944. In addition, 95.5 spot-forming cells (SFCs)/2.5 × 10 cells were determined as the optimal cut-off value for T-SPOT.TB in pleural fluid. Parallel combination of T-SPOT.TB and ADA activity test in pleural fluid showed increased sensitivity (96.9%) and specificity (87.5%), whereas serial combination showed increased specificity (97.5%). The combination of 3 assays had the highest sensitivity at 97.9%, with an AUC value of 0.964.T-SPOT.TB in pleural fluid performed better than that in peripheral blood and the ADA activity test in pleural fluid for tuberculous pleurisy diagnosis. The optimal cut-off value of T-SPOT.TB in pleural fluid was 95.5 SFCs/2.5 × 10 cells. Combination of 3 assays might be a promising approach for tuberculous pleurisy diagnosis.
[Mh] Termos MeSH primário: Adenosina Desaminase/imunologia
ELISPOT/métodos
Interferon gama/imunologia
Tuberculose Pleural/diagnóstico
Tuberculose Pleural/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
ELISPOT/normas
Feminino
Testes Hematológicos
Seres Humanos
Masculino
Meia-Idade
Derrame Pleural/imunologia
Estudos Prospectivos
Curva ROC
Valores de Referência
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
82115-62-6 (Interferon-gamma); EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008412


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[PMID]:28453786
[Au] Autor:Porath HT; Schaffer AA; Kaniewska P; Alon S; Eisenberg E; Rosenthal J; Levanon EY; Levy O
[Ad] Endereço:The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
[Ti] Título:A-to-I RNA Editing in the Earliest-Diverging Eumetazoan Phyla.
[So] Source:Mol Biol Evol;34(8):1890-1901, 2017 Aug 01.
[Is] ISSN:1537-1719
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The highly conserved ADAR enzymes, found in all multicellular metazoans, catalyze the editing of mRNA transcripts by the deamination of adenosines to inosines. This type of editing has two general outcomes: site specific editing, which frequently leads to recoding, and clustered editing, which is usually found in transcribed genomic repeats. Here, for the first time, we looked for both editing of isolated sites and clustered, non-specific sites in a basal metazoan, the coral Acropora millepora during spawning event, in order to reveal its editing pattern. We found that the coral editome resembles the mammalian one: it contains more than 500,000 sites, virtually all of which are clustered in non-coding regions that are enriched for predicted dsRNA structures. RNA editing levels were increased during spawning and increased further still in newly released gametes. This may suggest that editing plays a role in introducing variability in coral gametes.
[Mh] Termos MeSH primário: Adenosina Desaminase/genética
Antozoários/genética
Edição de RNA/genética
[Mh] Termos MeSH secundário: Adenosina Desaminase/metabolismo
Animais
Antozoários/metabolismo
Sequência de Bases
Evolução Molecular
Genoma
Genômica
Seres Humanos
Mamíferos/genética
Filogenia
RNA
RNA Mensageiro/genética
Proteínas de Ligação a RNA/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (RNA, immune); 0 (RNA-Binding Proteins); 63231-63-0 (RNA); EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/molbev/msx125


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[PMID]:29242208
[Au] Autor:Debatin KM
[Ad] Endereço:ULM UNIVERSITY MEDICAL CENTER.
[Ti] Título:HSCT cures ADA2 deficiency.
[So] Source:Blood;130(24):2582-2583, 2017 12 14.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Adenosina Desaminase/deficiência
Fenótipo
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-10-811125


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[PMID]:29045406
[Au] Autor:Diosa-Toro M; Echavarría-Consuegra L; Flipse J; Fernández GJ; Kluiver J; van den Berg A; Urcuqui-Inchima S; Smit JM
[Ad] Endereço:Department of Medical Microbiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
[Ti] Título:MicroRNA profiling of human primary macrophages exposed to dengue virus identifies miRNA-3614-5p as antiviral and regulator of ADAR1 expression.
[So] Source:PLoS Negl Trop Dis;11(10):e0005981, 2017 Oct.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Due to the high burden of dengue disease worldwide, a better understanding of the interactions between dengue virus (DENV) and its human host cells is of the utmost importance. Although microRNAs modulate the outcome of several viral infections, their contribution to DENV replication is poorly understood. METHODS AND PRINCIPAL FINDINGS: We investigated the microRNA expression profile of primary human macrophages challenged with DENV and deciphered the contribution of microRNAs to infection. To this end, human primary macrophages were challenged with GFP-expressing DENV and sorted to differentiate between truly infected cells (DENV-positive) and DENV-exposed but non-infected cells (DENV-negative cells). The miRNAome was determined by small RNA-Seq analysis and the effect of differentially expressed microRNAs on DENV yield was examined. Five microRNAs were differentially expressed in human macrophages challenged with DENV. Of these, miR-3614-5p was found upregulated in DENV-negative cells and its overexpression reduced DENV infectivity. The cellular targets of miR-3614-5p were identified by liquid chromatography/mass spectrometry and western blot. Adenosine deaminase acting on RNA 1 (ADAR1) was identified as one of the targets of miR-3614-5p and was shown to promote DENV infectivity at early time points post-infection. CONCLUSION/SIGNIFICANCE: Overall, miRNAs appear to play a limited role in DENV replication in primary human macrophages. The miRNAs that were found upregulated in DENV-infected cells did not control the production of infectious virus particles. On the other hand, miR-3614-5p, which was upregulated in DENV-negative macrophages, reduced DENV infectivity and regulated ADAR1 expression, a protein that facilitates viral replication.
[Mh] Termos MeSH primário: Adenosina Desaminase/metabolismo
Vírus da Dengue/fisiologia
Macrófagos/metabolismo
Macrófagos/virologia
MicroRNAs/metabolismo
Proteínas de Ligação a RNA/metabolismo
Transcriptoma
[Mh] Termos MeSH secundário: Adenosina Desaminase/genética
Deleção de Genes
Regulação da Expressão Gênica/imunologia
Seres Humanos
MicroRNAs/genética
Proteínas de Ligação a RNA/genética
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA-Binding Proteins); 0 (microRNA 3614, human); EC 3.5.4.37 (ADAR1 protein, human); EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0005981


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[PMID]:29022489
[Au] Autor:Song IH; Kim YA; Heo SH; Park IA; Lee M; Bang WS; Park HS; Gong G; Lee HJ
[Ad] Endereço:1 Department of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
[Ti] Título:ADAR1 expression is associated with tumour-infiltrating lymphocytes in triple-negative breast cancer.
[So] Source:Tumour Biol;39(10):1010428317734816, 2017 Oct.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumours with a high mutation burden exhibit considerable neoantigens and tumour-infiltrating lymphocytes. RNA editing by ADAR1 is a source of changes in epitope. However, ADAR1 expression in cancer cells and tumour-infiltrating lymphocyte levels in triple-negative breast cancer have not been well evaluated. We immunohistochemically examined ADAR1 expression in 681 triple-negative breast cancer patients and analysed their clinicopathological characteristics. We also analysed basal-like tumours using The Cancer Genome Atlas data. Among the 681 triple-negative breast cancer patients, 45.8% demonstrated high ADAR1 expression. Tumours with high ADAR1 expression exhibited high tumour-infiltrating lymphocyte levels, considerable CD8 + T lymphocyte infiltration, high histological grade and high expression of interferon-related proteins, including HLA-ABC, MxA and PKR. Among patients with lymph node metastasis, those with high tumour-infiltrating lymphocyte levels and low ADAR1 expression demonstrated the best disease-free survival. The Cancer Genome Atlas data analysis of basal-like tumours revealed significant positive correlation between ADAR1 and CD8B expression and positive association of high ADAR1 expression with immune responses and apoptosis pathways. We detected high ADAR1 expression in half of the triple-negative breast cancer patients. In addition to DNA mutations, RNA editing can be related to neoantigens; hence, we need to explore non-synonymous mutations exclusively found using RNA sequencing data to identify clinically relevant neoantigens.
[Mh] Termos MeSH primário: Adenosina Desaminase/biossíntese
Biomarcadores Tumorais/biossíntese
Proteínas de Ligação a RNA/biossíntese
Neoplasias de Mama Triplo Negativas/genética
[Mh] Termos MeSH secundário: Adenosina Desaminase/genética
Adulto
Idoso
Biomarcadores Tumorais/genética
Linfócitos T CD8-Positivos/patologia
Intervalo Livre de Doença
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Metástase Linfática
Linfócitos do Interstício Tumoral/patologia
Meia-Idade
Edição de RNA/genética
Proteínas de Ligação a RNA/genética
Análise Serial de Tecidos
Neoplasias de Mama Triplo Negativas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (RNA-Binding Proteins); EC 3.5.4.37 (ADAR1 protein, human); EC 3.5.4.4 (Adenosine Deaminase)
[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:171013
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317734816


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[PMID]:28985428
[Au] Autor:Qi L; Song Y; Chan THM; Yang H; Lin CH; Tay DJT; Hong H; Tang SJ; Tan KT; Huang XX; Lin JS; Ng VHE; Maury JJP; Tenen DG; Chen L
[Ad] Endereço:Cancer Science Institute of Singapore, National University of Singapore, Singapore.
[Ti] Título:An RNA editing/dsRNA binding-independent gene regulatory mechanism of ADARs and its clinical implication in cancer.
[So] Source:Nucleic Acids Res;45(18):10436-10451, 2017 Oct 13.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adenosine-to-inosine (A-to-I) RNA editing, catalyzed by Adenosine DeAminases acting on double-stranded RNA(dsRNA) (ADAR), occurs predominantly in the 3' untranslated regions (3'UTRs) of spliced mRNA. Here we uncover an unanticipated link between ADARs (ADAR1 and ADAR2) and the expression of target genes undergoing extensive 3'UTR editing. Using METTL7A (Methyltransferase Like 7A), a novel tumor suppressor gene with multiple editing sites at its 3'UTR, we demonstrate that its expression could be repressed by ADARs beyond their RNA editing and double-stranded RNA (dsRNA) binding functions. ADARs interact with Dicer to augment the processing of pre-miR-27a to mature miR-27a. Consequently, mature miR-27a targets the METTL7A 3'UTR to repress its expression level. In sum, our study unveils that the extensive 3'UTR editing of METTL7A is merely a footprint of ADAR binding, and there are a subset of target genes that are equivalently regulated by ADAR1 and ADAR2 through their non-canonical RNA editing and dsRNA binding-independent functions, albeit maybe less common. The functional significance of ADARs is much more diverse than previously appreciated and this gene regulatory function of ADARs is most likely to be of high biological importance beyond the best-studied editing function. This non-editing side of ADARs opens another door to target cancer.
[Mh] Termos MeSH primário: Adenosina Desaminase/metabolismo
Redes Reguladoras de Genes/fisiologia
Neoplasias/genética
Edição de RNA
RNA de Cadeia Dupla/metabolismo
Proteínas de Ligação a RNA/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Adenosina/metabolismo
Animais
Regulação Neoplásica da Expressão Gênica
Células HEK293
Seres Humanos
Inosina/metabolismo
Neoplasias/metabolismo
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (RNA, Double-Stranded); 0 (RNA-Binding Proteins); 5A614L51CT (Inosine); EC 3.5.4.4 (Adenosine Deaminase); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx667


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[PMID]:28833069
[Au] Autor:Anantharaman A; Gholamalamdari O; Khan A; Yoon JH; Jantsch MF; Hartner JC; Gorospe M; Prasanth SG; Prasanth KV
[Ad] Endereço:Department of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, IL, USA.
[Ti] Título:RNA-editing enzymes ADAR1 and ADAR2 coordinately regulate the editing and expression of Ctn RNA.
[So] Source:FEBS Lett;591(18):2890-2904, 2017 Sep.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adenosine deaminases acting on RNA (ADARs) are proteins that catalyse widespread A-to-I editing within RNA sequences. We recently reported that ADAR2 edits and stabilizes nuclear-retained Cat2 transcribed nuclear RNA (Ctn RNA). Here, we report that ADAR1 coordinates with ADAR2 to regulate editing and stability of Ctn RNA. We observe an RNA-dependent interaction between ADAR1 and ADAR2. Furthermore, ADAR1 negatively regulates interaction of Ctn RNA with RNA-destabilizing proteins. We also show that breast cancer (BC) cells display elevated ADAR1 but not ADAR2 levels, compared to nontumourigenic cells. Additionally, BC patients with elevated levels of ADAR1 show low survival. Our findings provide insights into overlapping substrate preferences of ADARs and potential involvement of ADAR1 in BC.
[Mh] Termos MeSH primário: Adenosina Desaminase/metabolismo
Edição de RNA/genética
Estabilidade de RNA/fisiologia
Proteínas de Ligação a RNA/metabolismo
Ribonucleoproteínas/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Adenosina Desaminase/genética
Linhagem Celular
Linhagem Celular Tumoral
Seres Humanos
Imunoprecipitação
Estabilidade de RNA/genética
Proteínas de Ligação a RNA/genética
Ribonucleoproteínas/genética
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (RNA-Binding Proteins); 0 (Ribonucleoproteins); EC 3.5.4.37 (ADAR1 protein, human); EC 3.5.4.4 (ADARB1 protein, human); EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12795


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[PMID]:28727272
[Au] Autor:Solari L; Soto A; Van der Stuyft P
[Ad] Endereço:Unit of General Epidemiology and Disease Control, Institute of Tropical Medicine of Antwerp, Antwerp, Belgium.
[Ti] Título:Performance of clinical prediction rules for diagnosis of pleural tuberculosis in a high-incidence setting.
[So] Source:Trop Med Int Health;22(10):1283-1292, 2017 Oct.
[Is] ISSN:1365-3156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Diagnosis of pleural tuberculosis (PT) is still a challenge, particularly in resource-constrained settings. Alternative diagnostic tools are needed. We aimed at evaluating the utility of Clinical Prediction Rules (CPRs) for diagnosis of pleural tuberculosis in Peru. METHODS: We identified CPRs for diagnosis of PT through a structured literature search. CPRs using high-complexity tests, as defined by the FDA, were excluded. We applied the identified CPRs to patients with pleural exudates attending two third-level hospitals in Lima, Peru, a setting with high incidence of tuberculosis. Besides pleural fluid analysis, patients underwent closed pleural biopsy for reaching a final diagnosis through combining microbiological and histopathological criteria. We evaluated the performance of the CPRs against this composite reference standard using classic indicators of diagnostic test validity. RESULTS: We found 15 eligible CPRs, of which 12 could be validated. Most included ADA, age, lymphocyte proportion and protein in pleural fluid as predictive findings. A total of 259 patients were included for their validation, of which 176 (67%) had PT and 50 (19%) malignant pleural effusion. The overall accuracy of the CPRs varied from 41% to 86%. Two had a positive likelihood ratio (LR) above 10, but none a negative LR below 0.1. ADA alone at a cut-off of ≥40 IU attained 87% diagnostic accuracy and had a positive LR of 6.6 and a negative LR of 0.2. CONCLUSION: Many CPRs for PT are available. In addition to ADA alone, none of them contributes significantly to diagnosis of PT.
[Mh] Termos MeSH primário: Adenosina Desaminase/análise
Derrame Pleural/microbiologia
Tuberculose Pleural/diagnóstico
[Mh] Termos MeSH secundário: Biomarcadores/análise
Biópsia por Agulha
Ensaios Enzimáticos Clínicos
Técnicas de Apoio para a Decisão
Seres Humanos
Incidência
Mycobacterium/isolamento & purificação
Peru/epidemiologia
Derrame Pleural/diagnóstico por imagem
Valor Preditivo dos Testes
Radiografia Torácica
Escarro/microbiologia
Toracentese/métodos
Tuberculose Pleural/enzimologia
Tuberculose Pleural/epidemiologia
Tuberculose Pleural/microbiologia
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1111/tmi.12932


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[PMID]:28714361
[Au] Autor:Zhang J; Chen Z; Tang Z; Huang J; Hu X; He J
[Ad] Endereço:1 Department of Thoracic Surgery, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
[Ti] Título:RNA editing is induced by type I interferon in esophageal squamous cell carcinoma.
[So] Source:Tumour Biol;39(7):1010428317708546, 2017 Jul.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In recent years, abnormal RNA editing has been shown to play an important role in the development of esophageal squamous cell carcinoma, as such abnormal editing is catalyzed by ADAR (adenosine deaminases acting on RNA). However, the regulatory mechanism of ADAR1 in esophageal squamous cell carcinomas remains largely unknown. In this study, we investigated ADAR1 expression and its association with RNA editing in esophageal squamous cell carcinomas. RNA sequencing applied to esophageal squamous cell carcinoma clinical samples showed that ADAR1 expression was correlated with the expression of STAT1, STAT2, and IRF9. In vitro experiments showed that the abundance of ADAR1 protein was associated with the induced activation of the JAK/STAT pathway by type I interferon. RNA sequencing results showed that treatment with type I interferon caused an increase in the number and degree of RNA editing in esophageal squamous cell carcinoma cell lines. In conclusion, the activation of the JAK/STAT pathway is a regulatory mechanism of ADAR1 expression and causes abnormal RNA editing profile in esophageal squamous cell carcinoma. This mechanism may serve as a new target for esophageal squamous cell carcinoma therapy.
[Mh] Termos MeSH primário: Adenosina Desaminase/genética
Carcinoma de Células Escamosas/genética
Neoplasias Esofágicas/genética
Interferon Tipo I/genética
Proteínas de Ligação a RNA/genética
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/patologia
Linhagem Celular Tumoral
Neoplasias Esofágicas/patologia
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Fator Gênico 3 Estimulado por Interferon, Subunidade gama/genética
Edição de RNA/genética
Fator de Transcrição STAT1/genética
Fator de Transcrição STAT2/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IRF9 protein, human); 0 (Interferon Type I); 0 (Interferon-Stimulated Gene Factor 3, gamma Subunit); 0 (RNA-Binding Proteins); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (STAT2 Transcription Factor); 0 (STAT2 protein, human); EC 3.5.4.37 (ADAR1 protein, human); EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317708546


  10 / 5936 MEDLINE  
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[PMID]:28703578
[Au] Autor:Wulff TF; Argüello RJ; Molina Jordàn M; Roura Frigolé H; Hauquier G; Filonava L; Camacho N; Gatti E; Pierre P; Ribas de Pouplana L; Torres AG
[Ad] Endereço:Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology , Parc Científic de Barcelona, C/Baldiri Reixac 10, 08028 Barcelona, Catalonia, Spain.
[Ti] Título:Detection of a Subset of Posttranscriptional Transfer RNA Modifications in Vivo with a Restriction Fragment Length Polymorphism-Based Method.
[So] Source:Biochemistry;56(31):4029-4038, 2017 Aug 08.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transfer RNAs (tRNAs) are among the most heavily modified RNA species. Posttranscriptional tRNA modifications (ptRMs) play fundamental roles in modulating tRNA structure and function and are being increasingly linked to human physiology and disease. Detection of ptRMs is often challenging, expensive, and laborious. Restriction fragment length polymorphism (RFLP) analyses study the patterns of DNA cleavage after restriction enzyme treatment and have been used for the qualitative detection of modified bases on mRNAs. It is known that some ptRMs induce specific and reproducible base "mutations" when tRNAs are reverse transcribed. For example, inosine, which derives from the deamination of adenosine, is detected as a guanosine when an inosine-containing tRNA is reverse transcribed, amplified via polymerase chain reaction (PCR), and sequenced. ptRM-dependent base changes on reverse transcription PCR amplicons generated as a consequence of the reverse transcription reaction might create or abolish endonuclease restriction sites. The suitability of RFLP for the detection and/or quantification of ptRMs has not been studied thus far. Here we show that different ptRMs can be detected at specific sites of different tRNA types by RFLP. For the examples studied, we show that this approach can reliably estimate the modification status of the sample, a feature that can be useful in the study of the regulatory role of tRNA modifications in gene expression.
[Mh] Termos MeSH primário: Adenosina Desaminase/metabolismo
Modelos Biológicos
Polimorfismo de Fragmento de Restrição
Processamento Pós-Transcricional do RNA
RNA de Transferência de Alanina/metabolismo
RNA de Transferência de Treonina/metabolismo
[Mh] Termos MeSH secundário: Adenosina/metabolismo
Adenosina Desaminase/química
Adenosina Desaminase/genética
Análise do Polimorfismo de Comprimento de Fragmentos Amplificados
Pareamento de Bases
Biologia Computacional
Desaminação
Sistemas Especialistas
Células HeLa
Seres Humanos
Concentração de Íons de Hidrogênio
Inosina/metabolismo
Interferência de RNA
RNA Interferente Pequeno/metabolismo
RNA de Transferência de Alanina/antagonistas & inibidores
RNA de Transferência de Treonina/antagonistas & inibidores
RNA de Transferência de Valina/antagonistas & inibidores
RNA de Transferência de Valina/metabolismo
Transcrição Reversa
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (RNA, Transfer, Ala); 0 (RNA, Transfer, Thr); 0 (RNA, Transfer, Val); 5A614L51CT (Inosine); EC 3.5.4.4 (ADAT2 protein, human); EC 3.5.4.4 (Adenosine Deaminase); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00324



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