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Pesquisa : G05.360.340.024.340.375.500.791.365 [Categoria DeCS]
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  1 / 1852 MEDLINE  
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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


  2 / 1852 MEDLINE  
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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


  3 / 1852 MEDLINE  
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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


  4 / 1852 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


  5 / 1852 MEDLINE  
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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


  6 / 1852 MEDLINE  
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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


  7 / 1852 MEDLINE  
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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


  8 / 1852 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


  9 / 1852 MEDLINE  
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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


  10 / 1852 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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