Base de dados : MEDLINE Pesquisa : G05.360.340.024.340.375.500.791.365 [Categoria DeCS] Referências encontradas : 1852 [refinar] Mostrando: 1 .. 10   no formato [Detalhado]

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[PMID]: 28472120 [Au] Autor: Bwalya EC; Kim S; Fang J; Wijekoon HMS; Hosoya K; Okumura M [Ad] Endereço: Laboratory of Veterinary Surgery, Department of Veterinary Clinical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido, Japan. [Ti] Título: Pentosan polysulfate inhibits IL-1ß-induced iNOS, c-Jun and HIF-1α upregulation in canine articular chondrocytes. [So] Source: PLoS One;12(5):e0177144, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Osteoarthritic (OA) chondrocytes are shown to express inducible nitric oxide synthase (iNOS) which produces high concentrations of nitric oxide (NO), particularly when stimulated with proinflammatory cytokines. NO is involved in OA cartilage degradation. On the other hand, c-Jun N-terminal Kinase (JNK) pathway mediates the activation and transcription of c-Jun, which is required for interleukin-1 (IL-1)-induction of matrix metalloproteinases-13 (MMP-13) in OA pathogenesis. Therefore, the selective inhibition of iNOS and c-Jun is a promising target for treatment and prevention of OA. The purpose of the study was to investigate the inhibitory effects of pentosan polysulfate (PPS) on IL-1ß-induced iNOS, c-Jun and HIF-α isoforms upregulation in canine articular chondrocytes (CACs). Primary (P0) chondrocytes were isolated and cultured from femoral head cartilages of three (3) dogs. First passage (P1) chondrocytes were preincubated with 0, 1, 5, 15 and 40 µg/mL of PPS for 4 hr before treatment with 10 ng/mL rhIL-1ß for a further 8 hr. In addition, we evaluated the effects of single and multiple cytokine with or without LPS on iNOS protein induction. PPS significantly inhibited (P < 0.05) IL-1ß-induced iNOS, c-Jun and HIF-1α mRNA upregulation in a dose-dependent pattern. iNOS mRNA was significantly inhibited at 15 and 40 µg/mL whereas c-Jun and HIF-1α were significantly downregulated at 5, 15 and 40 µg/mL of PPS compared to chondrocytes treated with only rhIL-1ß. Intriguingly, CACs were recalcitrant to single IL-1ß, TNF-α or LPS-induction of iNOS protein including to a combination of IL-1ß+TNF-α, IL-1ß+LPS except to TNF-α+LPS and IL-1ß+TNF-α+LPS suggestive of a protective mechanism from iNOS detrimental effects on perpetuating OA. IL-1ß+TNF-α+LPS-induced iNOS protein expression was significantly abrogated by PPS. We demonstrate for the first time that PPS is a novel inhibitor of IL-1ß-induced iNOS, c-Jun, and HIF-1α mRNA upregulation and iNOS protein induction which may be beneficial for prevention and treatment OA. [Mh] Termos MeSH primário: Cartilagem Articular/efeitos dos fármacos Condrócitos/efeitos dos fármacos Genes jun Subunidade alfa do Fator 1 Induzível por Hipóxia/genética Interleucina-1beta/antagonistas & inibidores Óxido Nítrico Sintase Tipo II/genética Poliéster Sulfúrico de Pentosana/farmacologia Regulação para Cima/efeitos dos fármacos [Mh] Termos MeSH secundário: Animais Cartilagem Articular/citologia Cartilagem Articular/metabolismo Condrócitos/metabolismo Cães Interleucina-1beta/fisiologia RNA Mensageiro/genética Regulação para Cima/fisiologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Interleukin-1beta); 0 (RNA, Messenger); 37300-21-3 (Pentosan Sulfuric Polyester); EC 1.14.13.39 (Nitric Oxide Synthase Type II) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170915 [Lr] Data última revisão: 170915 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170505 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0177144

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[PMID]: 28196103 [Au] Autor: Wang K; Jin S; Fan D; Wang M; Xing N; Niu Y [Ad] Endereço: Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. [Ti] Título: Anti-proliferative activities of finasteride in benign prostate epithelial cells require stromal fibroblasts and c-Jun gene. [So] Source: PLoS One;12(2):e0172233, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: This study aimed to identify the role of mouse fibroblast-mediated c-Jun and IGF-1 signaling in the therapeutic effect of finasteride on benign prostatic epithelial cells. BPH-1 cells, alone or with fibroblasts (c-Jun+/+ or c-Jun-/-), were implanted subcutaneously in male nude mice who were then treated with finasteride. The degrees of cell proliferation, apoptosis, and sizes of the xenografts were determined. BPH-1 cells were grown alone or co-cultured with mouse fibroblasts in the presence of finasteride and the level of IGF-1 secreted into the medium by the fibroblasts was determined. The proliferation-associated signaling pathway in BPH-1 cells was also evaluated. Fibroblasts and c-Jun promoted xenograft growth, stimulated Ki-67 expression, and inhibited BPH-1 apoptosis. Finasteride did not induce the shrinkage of xenografts in the combined-grafted groups despite repressing Ki-67 expression and inducing cell apoptosis. The addition of c-Jun-/- fibroblasts did not promote xenograft growth. In the absence of c-Jun and fibroblasts, finasteride did not alter xenograft growth, Ki-67 expression, or cell apoptosis. The in vitro results demonstrated that when BPH-1 cells were grown in monoculture, treatment with finasteride did not induce cell death and stimulated the expression of pro-proliferative signaling molecules, while in the presence of fibroblasts containing c-Jun, finasteride treatment repressed epithelial cell proliferation, the level of IGF-1 in the medium, and the activation of downstream pro-proliferative signaling pathways. Taken together, our results suggest that fibroblasts, c-Jun, and IGF-1 play key roles in mediating stromal-epithelial interactions that are required for the therapeutic effects of finasteride in benign prostate epithelial cells. [Mh] Termos MeSH primário: Células Epiteliais Fibroblastos Finasterida/farmacologia Genes jun Neoplasias Experimentais Neoplasias da Próstata [Mh] Termos MeSH secundário: Animais Apoptose/efeitos dos fármacos Apoptose/genética Linhagem Celular Tumoral Proliferação Celular Células Epiteliais/metabolismo Células Epiteliais/patologia Fibroblastos/metabolismo Fibroblastos/patologia Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos Seres Humanos Fator de Crescimento Insulin-Like I/genética Fator de Crescimento Insulin-Like I/metabolismo Masculino Camundongos Camundongos Nus Proteínas de Neoplasias/genética Proteínas de Neoplasias/metabolismo Transplante de Neoplasias Neoplasias Experimentais/tratamento farmacológico Neoplasias Experimentais/genética Neoplasias Experimentais/metabolismo Neoplasias Experimentais/patologia Neoplasias da Próstata/tratamento farmacológico Neoplasias da Próstata/genética Neoplasias da Próstata/metabolismo Neoplasias da Próstata/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Neoplasm Proteins); 57GNO57U7G (Finasteride); 67763-96-6 (Insulin-Like Growth Factor I) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170809 [Lr] Data última revisão: 170809 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170215 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0172233

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[PMID]: 28039102 [Au] Autor: Zhang Z; Zhang S; Wang S [Ad] Endereço: Henan Institute of Science and Technology, Xinxiang 453003, China. [Ti] Título: DNAzymes Dz13 target the c-jun possess antiviral activity against influenza A viruses. [So] Source: Microb Pathog;103:155-161, 2017 Feb. [Is] ISSN: 1096-1208 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: The emergence of anti-influenza A virus drugs resistant strain highlights the need for more effective therapy. Our earlier study demonstrated that c-jun, a downstream molecule of JNK, might be important in viral infections and inflammatory responses. In the present study, we explored the function of DNAzymes Dz13 that target c-jun in influenza A virus infected mice. Dz13 displayed non-toxic side effects on A549 cells and BALB/c mice. Moreover, Dz13-treated mice had enhanced survival after influenza compared with untreated mice. Simultaneously, the pulmonary inflammatory responses and viral burden were decreased in Dz13 treated mice. Furthermore, proliferation levels of infection-induced CD4 and CD8 T cells were impaired. These data demonstrated that Dz13 could reduce viral replication and inflammatory response in vivo, suggesting that Dz13 may potentially be used to treat influenza A viral infection. [Mh] Termos MeSH primário: DNA Catalítico/genética Regulação da Expressão Gênica Genes jun Vírus da Influenza A Infecções por Orthomyxoviridae/genética Infecções por Orthomyxoviridae/virologia [Mh] Termos MeSH secundário: Animais Linhagem Celular Tumoral Citocinas/biossíntese Modelos Animais de Doenças Feminino Seres Humanos Vírus da Influenza A/genética Vírus da Influenza A/imunologia Ativação Linfocitária/imunologia Camundongos Infecções por Orthomyxoviridae/imunologia Infecções por Orthomyxoviridae/mortalidade Subpopulações de Linfócitos T/imunologia Subpopulações de Linfócitos T/metabolismo Replicação Viral [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Cytokines); 0 (DNA, Catalytic); 0 (Dz13 DNAzyme) [Em] Mês de entrada: 1704 [Cu] Atualização por classe: 170406 [Lr] Data última revisão: 170406 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170101 [St] Status: MEDLINE

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[PMID]: 27885689 [Au] Autor: Rahat B; Najar RA; Hamid A; Bagga R; Kaur J [Ad] Endereço: Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India. [Ti] Título: The role of aberrant methylation of trophoblastic stem cell origin in the pathogenesis and diagnosis of placental disorders. [So] Source: Prenat Diagn;37(2):133-143, 2017 Feb. [Is] ISSN: 1097-0223 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: OBJECTIVES: The objective of the study is to investigate the role of methylation levels at promoter regions of placental vascularization genes (VEGF, EGFR, and c-jun) in pathogenesis and diagnosis of placental disorders. METHODS: We analyzed DNA and histone methylation at promoters of VEGF, EGFR, and c-jun via methylation-sensitive high-resolution melting and chromatin immunoprecipitation assay in pregnant women with normal pregnancy in first, second, and third trimesters (n = 30 in each group) and pregnant women with pregnancy complicated with preeclampsia (n = 30) and hydatidiform mole (n = 15). RESULTS: The higher expression of VEGF, EGFR, and c-jun in early pregnancy was observed to be independent of DNA methylation, while it was associated with H3 K9/K27 trimethylations. Also, abnormally higher expression of c-jun in GTDs was associated with lower H3K9me3 level at its promoter. Under preeclampsia conditions, we observed dysregulation of both DNA methylation and H3 trimethylation and subsequent low expression of VEGF, EGFR, and c-jun. Importantly, our promoter methylation data indicated that VEGF may act as novel fetal DNA diagnostic marker for preeclampsia and molar pregnancies in maternal plasma. CONCLUSION: These findings emphasize the importance of dysregulated epigenetic phenomenon behind the pathologies of placental disorders and use of promoter region DNA methylation as an epigenetic marker for these pathological pregnancies. © 2016 John Wiley & Sons, Ltd. [Mh] Termos MeSH primário: Metilação de DNA/fisiologia Doenças Placentárias/diagnóstico Doenças Placentárias/genética Células-Tronco/metabolismo Trofoblastos/metabolismo [Mh] Termos MeSH secundário: Adulto Feminino Genes jun/genética Seres Humanos Mola Hidatiforme/diagnóstico Mola Hidatiforme/genética Doenças Placentárias/metabolismo Doenças Placentárias/patologia Pré-Eclâmpsia/diagnóstico Pré-Eclâmpsia/genética Valor Preditivo dos Testes Gravidez Diagnóstico Pré-Natal/métodos Regiões Promotoras Genéticas Receptor do Fator de Crescimento Epidérmico/genética Células-Tronco/citologia Trofoblastos/citologia Células Tumorais Cultivadas Neoplasias Uterinas/diagnóstico Neoplasias Uterinas/genética Fator A de Crescimento do Endotélio Vascular/genética Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170926 [Lr] Data última revisão: 170926 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 161126 [St] Status: MEDLINE [do] DOI: 10.1002/pd.4974

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[PMID]: 27797381 [Au] Autor: Liao YH; Chiang KH; Shieh JM; Huang CR; Shen CJ; Huang WC; Chen BK [Ad] Endereço: Institute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan, ROC. [Ti] Título: Epidermal growth factor-induced ANGPTL4 enhances anoikis resistance and tumour metastasis in head and neck squamous cell carcinoma. [So] Source: Oncogene;36(16):2228-2242, 2017 Apr 20. [Is] ISSN: 1476-5594 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Epidermal growth factor (EGF) is important for cancer cell proliferation, angiogenesis and metastasis in many types of cancer. However, the mechanisms involved in EGF-induced head and neck squamous cell carcinoma (HNSCC) metastasis remain largely unknown. In this study, we reveal that angiopoietin-like 4 (ANGPTL4) plays an important role in the regulation of EGF-induced cancer metastasis. We showed that EGF-induced ANGPTL4 expression promoted anoikis resistance and cancer cell migration and invasion in HNSCC. In addition, depletion of ANGPTL4 inhibited EGF-induced cancer cell invasion. Autocrine production of EGF-induced ANGPTL4 regulated the expression of matrix metalloproteinases (MMPs). The induction of MMP-1 gene expression by ANGPTL4-activated integrin ß1 signalling occurred through the AP-1 binding site in the MMP-1 gene promoter. Furthermore, down-regulation of MMP-1 impeded EGF- and recombinant ANGPTL4-enhanced HNSCC cell migration and invasion. Depletion of ANGPTL4 significantly blocked EGF-primed extravasation and metastatic seeding of tumour cells and MMP-1 expression in lungs. However, no effect of ANGPTL4 on tumour growth was observed. These results suggest that EGF-induced expression and autocrine production of ANGPTL4 enhances HNSCC metastasis via the up-regulation of MMP-1 expression. Inhibition of ANGPTL4 expression may be a potential strategy for the treatment of EGFR-mediated HNSCC metastasis. [Mh] Termos MeSH primário: Angiopoietinas/metabolismo Anoikis Carcinoma de Células Escamosas/metabolismo Fator de Crescimento Epidérmico/fisiologia Neoplasias de Cabeça e Pescoço/metabolismo [Mh] Termos MeSH secundário: Proteína 4 Semelhante a Angiopoietina Carcinoma de Células Escamosas/patologia Carcinoma de Células Escamosas/secundário Linhagem Celular Tumoral Genes jun Neoplasias de Cabeça e Pescoço/patologia Neoplasias de Cabeça e Pescoço/secundário Seres Humanos Integrina beta1/metabolismo Metaloproteinase 1 da Matriz/biossíntese Metástase Neoplásica Transdução de Sinais [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (ANGPTL4 protein, human); 0 (Angiopoietin-like 4 Protein); 0 (Angiopoietins); 0 (Integrin beta1); 62229-50-9 (Epidermal Growth Factor); EC 3.4.24.7 (Matrix Metalloproteinase 1) [Em] Mês de entrada: 1704 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 161101 [St] Status: MEDLINE [do] DOI: 10.1038/onc.2016.371

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[PMID]: 27495086 [Au] Autor: Chen SJ; Liao DL; Shen TW; Yang HC; Chen KC; Chen CH [Ad] Endereço: aInstitute of Medical Sciences, Tzu Chi University, Hualien bDepartment of Psychiatry, Mackay Memorial Hospital, Taitung Branch cDepartment of Health Executive Yuan, Bali Psychiatric Center dInstitute of Statistical Science, Academia Sinica, Taipei eDepartment of Psychiatry, Chang Gung Memorial Hospital at Linkou fDepartment and Graduate Institute of Biomedical Sciences, Chang Gung University, Taoyuan, Taiwan. [Ti] Título: Genetic signatures of heroin addiction. [So] Source: Medicine (Baltimore);95(31):e4473, 2016 Aug. [Is] ISSN: 1536-5964 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Heroin addiction is a complex psychiatric disorder with a chronic course and a high relapse rate, which results from the interaction between genetic and environmental factors. Heroin addiction has a substantial heritability in its etiology; hence, identification of individuals with a high genetic propensity to heroin addiction may help prevent the occurrence and relapse of heroin addiction and its complications. The study aimed to identify a small set of genetic signatures that may reliably predict the individuals with a high genetic propensity to heroin addiction. We first measured the transcript level of 13 genes (RASA1, PRKCB, PDK1, JUN, CEBPG, CD74, CEBPB, AUTS2, ENO2, IMPDH2, HAT1, MBD1, and RGS3) in lymphoblastoid cell lines in a sample of 124 male heroin addicts and 124 male control subjects using real-time quantitative PCR. Seven genes (PRKCB, PDK1, JUN, CEBPG, CEBPB, ENO2, and HAT1) showed significant differential expression between the 2 groups. Further analysis using 3 statistical methods including logistic regression analysis, support vector machine learning analysis, and a computer software BIASLESS revealed that a set of 4 genes (JUN, CEBPB, PRKCB, ENO2, or CEBPG) could predict the diagnosis of heroin addiction with the accuracy rate around 85% in our dataset. Our findings support the idea that it is possible to identify genetic signatures of heroin addiction using a small set of expressed genes. However, the study can only be considered as a proof-of-concept study. As the establishment of lymphoblastoid cell line is a laborious and lengthy process, it would be more practical in clinical settings to identify genetic signatures for heroin addiction directly from peripheral blood cells in the future study. [Mh] Termos MeSH primário: Predisposição Genética para Doença Dependência de Heroína/genética [Mh] Termos MeSH secundário: Adulto Proteína beta Intensificadora de Ligação a CCAAT/genética Proteínas Estimuladoras de Ligação a CCAAT/genética Estudos de Casos e Controles Perfilação da Expressão Gênica Genes jun/genética Seres Humanos Modelos Logísticos Linfócitos/citologia Masculino Fosfopiruvato Hidratase/genética Proteína Quinase C beta/genética RNA Ribossômico 18S/metabolismo Reação em Cadeia da Polimerase em Tempo Real Software Máquina de Vetores de Suporte [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (CCAAT-Enhancer-Binding Protein-beta); 0 (CCAAT-Enhancer-Binding Proteins); 0 (CCAAT-enhancer-binding protein-gamma); 0 (CEBPB protein, human); 0 (RNA, Ribosomal, 18S); EC 2.7.11.13 (PRKCB protein, human); EC 2.7.11.13 (Protein Kinase C beta); EC 4.2.1.11 (Phosphopyruvate Hydratase) [Em] Mês de entrada: 1702 [Cu] Atualização por classe: 170220 [Lr] Data última revisão: 170220 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 160807 [St] Status: MEDLINE [do] DOI: 10.1097/MD.0000000000004473

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[PMID]: 27462815 [Au] Autor: Lee AS; Kranzusch PJ; Doudna JA; Cate JH [Ti] Título: eIF3d is an mRNA cap-binding protein that is required for specialized translation initiation. [So] Source: Nature;536(7614):96-9, 2016 08 04. [Is] ISSN: 1476-4687 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Eukaryotic mRNAs contain a 5' cap structure that is crucial for recruitment of the translation machinery and initiation of protein synthesis. mRNA recognition is thought to require direct interactions between eukaryotic initiation factor 4E (eIF4E) and the mRNA cap. However, translation of numerous capped mRNAs remains robust during cellular stress, early development, and cell cycle progression despite inactivation of eIF4E. Here we describe a cap-dependent pathway of translation initiation in human cells that relies on a previously unknown cap-binding activity of eIF3d, a subunit of the 800-kilodalton eIF3 complex. A 1.4 Å crystal structure of the eIF3d cap-binding domain reveals unexpected homology to endonucleases involved in RNA turnover, and allows modelling of cap recognition by eIF3d. eIF3d makes specific contacts with the cap, as exemplified by cap analogue competition, and these interactions are essential for assembly of translation initiation complexes on eIF3-specialized mRNAs such as the cell proliferation regulator c-Jun (also known as JUN). The c-Jun mRNA further encodes an inhibitory RNA element that blocks eIF4E recruitment, thus enforcing alternative cap recognition by eIF3d. Our results reveal a mechanism of cap-dependent translation that is independent of eIF4E, and illustrate how modular RNA elements work together to direct specialized forms of translation initiation. [Mh] Termos MeSH primário: Fator de Iniciação 3 em Eucariotos/metabolismo Iniciação Traducional da Cadeia Peptídica Capuzes de RNA/metabolismo Proteínas de Ligação a RNA/metabolismo [Mh] Termos MeSH secundário: Ligação Competitiva Cristalografia por Raios X Fator de Iniciação 3 em Eucariotos/química Fator de Iniciação 4E em Eucariotos/antagonistas & inibidores Fator de Iniciação 4E em Eucariotos/metabolismo Fator de Iniciação 4F em Eucariotos/antagonistas & inibidores Fator de Iniciação 4F em Eucariotos/metabolismo Genes jun/genética Seres Humanos Modelos Moleculares Filogenia Ligação Proteica Estrutura Terciária de Proteína Subunidades Proteicas/química Subunidades Proteicas/metabolismo Capuzes de RNA/química Capuzes de RNA/genética Proteínas de Ligação a RNA/química [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (EIF3D protein, human); 0 (Eukaryotic Initiation Factor-3); 0 (Eukaryotic Initiation Factor-4E); 0 (Eukaryotic Initiation Factor-4F); 0 (Protein Subunits); 0 (RNA Caps); 0 (RNA-Binding Proteins) [Em] Mês de entrada: 1608 [Cu] Atualização por classe: 170324 [Lr] Data última revisão: 170324 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160728 [St] Status: MEDLINE

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[PMID]: 27317567 [Au] Autor: Zhang P; Cao L; Fan P; Mei Y; Wu M [Ad] Endereço: CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Science, Innovation Center for Cell Signaling Network, School of Life Sciences, University of Science & Technology of China, Hefei, Anhui, China. [Ti] Título: LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw7-mediated c-Myc degradation. [So] Source: EMBO Rep;17(8):1204-20, 2016 Aug. [Is] ISSN: 1469-3178 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: The c-Myc proto-oncogene is activated in more than half of all human cancers. However, the precise regulation of c-Myc protein stability is unknown. Here, we show that the lncRNA-MIF (c-Myc inhibitory factor), a c-Myc-induced long non-coding RNA, is a competing endogenous RNA for miR-586 and attenuates the inhibitory effect of miR-586 on Fbxw7, an E3 ligase for c-Myc, leading to increased Fbxw7 expression and subsequent c-Myc degradation. Our data reveal the existence of a feedback loop between c-Myc and lncRNA-MIF, through which c-Myc protein stability is finely controlled. Additionally, we show that the lncRNA-MIF inhibits aerobic glycolysis and tumorigenesis by suppressing c-Myc and miR-586. [Mh] Termos MeSH primário: Proteínas de Ciclo Celular/genética Proteínas F-Box/genética Proteínas Proto-Oncogênicas c-myc/metabolismo RNA Longo não Codificante/genética Ativação Transcricional Ubiquitina-Proteína Ligases/genética [Mh] Termos MeSH secundário: Animais Ciclo Celular/genética Proteínas de Ciclo Celular/metabolismo Proliferação Celular Proteínas F-Box/metabolismo Proteína 7 com Repetições F-Box-WD Regulação da Expressão Gênica Técnicas de Silenciamento de Genes Genes Supressores de Tumor Genes jun Glicólise/genética Masculino Camundongos MicroRNAs/genética Ligação Proteica Estabilidade Proteica Proteólise Proteínas Proto-Oncogênicas c-myc/genética Ubiquitina-Proteína Ligases/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Cell Cycle Proteins); 0 (F-Box Proteins); 0 (F-Box-WD Repeat-Containing Protein 7); 0 (FBXW7 protein, human); 0 (MIRN-586 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Long Noncoding); EC 2.3.2.27 (Ubiquitin-Protein Ligases) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160619 [St] Status: MEDLINE [do] DOI: 10.15252/embr.201642067

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[PMID]: 26805420 [Au] Autor: Xu C; Wang X; Zhu Y; Dong X; Liu C; Zhang H; Liu L; Huang S; Chen L [Ad] Endereço: Jiangsu Key Laboratory for Molecular and Medical Biotechnology, Jiangsu Key Laboratory for Microbes and Functional Genomics, College of Life Sciences, Nanjing Normal University, Nanjing 210023, PR China. [Ti] Título: Rapamycin ameliorates cadmium-induced activation of MAPK pathway and neuronal apoptosis by preventing mitochondrial ROS inactivation of PP2A. [So] Source: Neuropharmacology;105:270-284, 2016 Jun. [Is] ISSN: 1873-7064 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Cadmium (Cd) is a highly toxic metal that affects the central nervous system. Recently we have demonstrated that inhibition of mTOR by rapamycin rescues neuronal cells from Cd-poisoning. Here we show that rapamycin inhibited Cd-induced mitochondrial ROS-dependent neuronal apoptosis. Intriguingly, rapamycin remarkably blocked phosphorylation of JNK, Erk1/2 and p38 in neuronal cells induced by Cd, which was strengthened by co-treatment with Mito-TEMPO. Inhibition of JNK and Erk1/2 by SP600125 and U0126, respectively, potentiated rapamycin's prevention from Cd-induced apoptosis. Consistently, over-expression of dominant negative c-Jun or MKK1 also potently improved the inhibitory effect of rapamycin on Cd neurotoxicity. Furthermore, pretreatment with SP600125 or U0126, or expression of dominant negative c-Jun or MKK1 enhanced the inhibitory effects of rapamycin or Mito-TEMPO on Cd-induced ROS. Further investigation found that co-treatment with Mito-TEMPO/rapamycin more effectively rescued cells by preventing Cd inactivation of PP2A than treatment with rapamycin or Mito-TEMPO alone. Over-expression of wild-type PP2A reinforced rapamycin or Mito-TEMPO suppression of activated JNK and Erk1/2 pathways, as well as ROS production and apoptosis in neuronal cells in response to Cd. The findings indicate that rapamycin ameliorates Cd-evoked neuronal apoptosis by preventing mitochondrial ROS inactivation of PP2A, thereby suppressing activation of JNK and Erk1/2 pathways. Our results underline that rapamycin may have a potential in preventing Cd-induced oxidative stress and neurodegenerative diseases. [Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos Cádmio/farmacologia Sistema de Sinalização das MAP Quinases/efeitos dos fármacos Mitocôndrias/efeitos dos fármacos Proteínas Quinases Ativadas por Mitógeno/efeitos dos fármacos Neurônios/efeitos dos fármacos Proteína Fosfatase 2/efeitos dos fármacos Espécies Reativas de Oxigênio/metabolismo Sirolimo/farmacologia [Mh] Termos MeSH secundário: Animais Antracenos/farmacologia Butadienos/farmacologia Cádmio/toxicidade Genes jun/efeitos dos fármacos Genes jun/genética Mitocôndrias/metabolismo Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores Nitrilos/farmacologia Células PC12 Fosforilação Ratos Transdução de Sinais/efeitos dos fármacos [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Anthracenes); 0 (Butadienes); 0 (Nitriles); 0 (Reactive Oxygen Species); 0 (U 0126); 00BH33GNGH (Cadmium); 1TW30Y2766 (pyrazolanthrone); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.1.3.16 (Protein Phosphatase 2); W36ZG6FT64 (Sirolimus) [Em] Mês de entrada: 1706 [Cu] Atualização por classe: 170901 [Lr] Data última revisão: 170901 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160126 [St] Status: MEDLINE

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[PMID]: 26739088 [Au] Autor: Gao Y; Nai W; Yang L; Lu Z; Shi P; Jin H; Wen H; Wang G [Ad] Endereço: Department of Burns, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. [Ti] Título: Construction of an immunorelated protein-protein interaction network for clarifying the mechanism of burn. [So] Source: Burns;42(2):405-13, 2016 Mar. [Is] ISSN: 1879-1409 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: BACKGROUND AND AIM: Severe burn is known to induce a series of pathological responses resulting in increased susceptibility to systemic inflammatory response and multiple organ failure, but the underlying molecular mechanism remains unclear at present. The main aim of this study was to expand our understanding of the events leading to circulating leukocyte response after burn by subjecting the gene expression profiles to a bioinformatic analysis. MATERIALS AND METHODS: Comprehensive gene expression analysis was performed to identify differentially expressed genes (DEGs) using the expression profile GSE7404 (Mus musculus, circulating leukocyte, 25% of total body surface area (TBSA), full thickness) downloaded from the Gene Expression Omnibus, followed by the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. In addition, a postburn protein-protein interaction (PPI) network was constructed to identify potential biomarkers. RESULTS: Maximum changes in the gene expression profile were detected 1 day post burn. Separate Gene Ontology (GO) functional enrichment analysis for upregulated and downregulated DEGs revealed significant alterations of genes related to biological process such as "response to stimuli," "metabolic," "cellular and immune system processes," "biological regulation," and "death" in the leukocyte transcriptome after the burn. The KEGG pathway enrichment analysis showed that the upregulated DEGs were significantly enriched in the nodes of immunorelated and signal transduction-related pathways, and the downregulated genes were significantly enriched for the immunorelated pathways. The PPI network and module analysis revealed that, 1 day after the burn, lymphocyte-specific protein tyrosine kinase (Lck) (downregulated), Jun (upregulated), Cd19 (downregulated), Stat1 (downregulated), and Cdk1 (upregulated) were located centrally in both the PPI network and modules. CONCLUSIONS: Based on an integrated bioinformatic analysis, we concluded that Lck, Jun, Cd19, Stat1, and Cdk1 may be critical 1 day after the burn. These findings expand our understanding of the molecular mechanisms of this important pathological process. Further studies are needed to support our work, focused on identifying candidate biomarkers with sufficient predictive power to act as prognostic and therapeutic biomarkers for burn injury. [Mh] Termos MeSH primário: Queimaduras/genética Mapas de Interação de Proteínas [Mh] Termos MeSH secundário: Animais Antígenos CD19/genética Queimaduras/imunologia Queimaduras/metabolismo Biologia Computacional Quinases Ciclina-Dependentes/genética Bases de Dados Factuais Regulação para Baixo Perfilação da Expressão Gênica Regulação da Expressão Gênica/genética Regulação da Expressão Gênica/imunologia Genes jun/genética Proteína Tirosina Quinase p56(lck) Linfócito-Específica/genética Camundongos Análise em Microsséries Fator de Transcrição STAT1/genética Transdução de Sinais Transcriptoma Regulação para Cima [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antigens, CD19); 0 (CD19 antigen, mouse); 0 (STAT1 Transcription Factor); 0 (Stat1 protein, mouse); EC 2.7.10.2 (Lymphocyte Specific Protein Tyrosine Kinase p56(lck)); EC 2.7.11.22 (Cyclin-Dependent Kinases) [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: 160108 [St] Status: MEDLINE

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