Base de dados : MEDLINE
Pesquisa : D12.776.260.103.937 [Categoria DeCS]
Referências encontradas : 665 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 67 ir para página                         

  1 / 665 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29233692
[Au] Autor:Tsukamoto D; Ito M; Takamatsu N
[Ad] Endereço:Laboratory of Molecular Biology, Department of Biosciences, School of Science, Kitasato University, 1-15-1 Kitasato, Minamiku, Sagamihara, 252-0373, Japan. Electronic address: tsukamot@kitasato-u.ac.jp.
[Ti] Título:Epigenetic regulation of hibernation-associated HP-20 and HP-27 gene transcription in chipmunk liver.
[So] Source:Biochem Biophys Res Commun;495(2):1758-1765, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The chipmunk hibernation-related proteins (HPs) HP-20 and HP-27 are components of a 140-kDa complex that dramatically decreases in the blood during hibernation. The HP-20 and HP-27 genes are expressed specifically in the liver and are downregulated in hibernating chipmunks. Hibernation-associated physiological changes are assumed to be under genetic control. Therefore, to elucidate the molecular mechanisms of hibernation, here we examined the mechanisms behind the altered HP-20 and HP-27 gene expression in nonhibernating versus hibernating chipmunks. Chromatin immunoprecipitation (ChIP) analyses revealed that histone H3 on the HP-20 and HP-27 gene promoters was highly acetylated at lysine (K) 9 and K14 and highly trimethylated at K4 in the liver of nonhibernating chipmunks, while these active histone modifications were nearly absent in hibernating chipmunks. Furthermore, histone acetyltransferases and a histone methyltransferase were associated with the HP-20 and HP-27 gene promoters primarily in nonhibernating chipmunks. Consistent with a previous finding that HNF-1 and USF can activate HP-20 and HP-27 gene transcription by binding to the proximal promoter region, ChIP-quantitative PCR (qPCR) analyses revealed that significantly less HNF-1 and USF were bound to these gene promoters in hibernating than in nonhibernating chipmunks. These findings collectively indicated that the hibernation-associated HP-20 and HP-27 gene expression is epigenetically regulated at the transcriptional level by the binding of HNF-1 and USF to their proximal promoters, and that histone modification has a key role in hibernation-associated transcriptional regulation.
[Mh] Termos MeSH primário: Proteínas Sanguíneas/genética
Proteínas Sanguíneas/fisiologia
Hibernação/genética
Hibernação/fisiologia
Sciuridae/genética
Sciuridae/fisiologia
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Epigênese Genética
Expressão Gênica
Fator 1 Nuclear de Hepatócito/metabolismo
Histonas/metabolismo
Masculino
Regiões Promotoras Genéticas
Ligação Proteica
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Transcrição Genética
Fatores Estimuladores Upstream/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Proteins); 0 (HP-20 protein, Tamias asiaticus); 0 (HP-27 protein, Tamias asiaticus); 0 (Histones); 0 (RNA, Messenger); 0 (Upstream Stimulatory Factors); 126548-29-6 (Hepatocyte Nuclear Factor 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE


  2 / 665 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28539359
[Au] Autor:Wang J; Zhao S; He W; Wei Y; Zhang Y; Pegg H; Shore P; Roberts SGE; Deng W
[Ad] Endereço:From the Institute of Biology and Medicine, Wuhan University of Science and Technology, Wuhan City, Hubei Province 430065, China.
[Ti] Título:A transcription factor IIA-binding site differentially regulates RNA polymerase II-mediated transcription in a promoter context-dependent manner.
[So] Source:J Biol Chem;292(28):11873-11885, 2017 Jul 14.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RNA polymerase II (pol II) is required for the transcription of all protein-coding genes and as such represents a major enzyme whose activity is tightly regulated. Transcriptional initiation therefore requires numerous general transcriptional factors and cofactors that associate with pol II at the core promoter to form a pre-initiation complex. Transcription factor IIA (TFIIA) is a general cofactor that binds TFIID and stabilizes the TFIID-DNA complex during transcription initiation. Previous studies showed that TFIIA can make contact with the DNA sequence upstream or downstream of the TATA box, and that the region bound by TFIIA could overlap with the elements recognized by another factor, TFIIB, at adenovirus major late core promoter. Whether core promoters contain a DNA motif recognized by TFIIA remains unknown. Here we have identified a core promoter element upstream of the TATA box that is recognized by TFIIA. A search of the human promoter database revealed that many natural promoters contain a TFIIA recognition element (IIARE). We show that the IIARE enhances TFIIA-promoter binding and enhances the activity of TATA-containing promoters, but represses or activates promoters that lack a TATA box. Chromatin immunoprecipitation assays revealed that the IIARE activates transcription by increasing the recruitment of pol II, TFIIA, TAF4, and P300 at TATA-dependent promoters. These findings extend our understanding of the role of TFIIA in transcription, and provide new insights into the regulatory mechanism of core promoter elements in gene transcription by pol II.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Regiões Promotoras Genéticas
RNA Polimerase II/metabolismo
Elementos de Resposta
TATA Box
Fatores Associados à Proteína de Ligação a TATA/metabolismo
Fator de Transcrição TFIIA/metabolismo
Fator de Transcrição TFIID/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Imunoprecipitação da Cromatina
DNA Recombinante
Proteína p300 Associada a E1A/química
Proteína p300 Associada a E1A/metabolismo
Genes Reporter
Células HEK293
Seres Humanos
Mutagênese Sítio-Dirigida
Mutação
Motivos de Nucleotídeos
Subunidades Proteicas/química
Subunidades Proteicas/genética
Subunidades Proteicas/metabolismo
RNA Polimerase II/química
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Fatores Associados à Proteína de Ligação a TATA/química
Proteína de Ligação a TATA-Box/química
Proteína de Ligação a TATA-Box/genética
Proteína de Ligação a TATA-Box/metabolismo
Fator de Transcrição TFIIA/química
Fator de Transcrição TFIIA/genética
Fator de Transcrição TFIID/química
Fatores Estimuladores Upstream/química
Fatores Estimuladores Upstream/genética
Fatores Estimuladores Upstream/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Recombinant); 0 (Protein Subunits); 0 (Recombinant Proteins); 0 (TAF4 protein, human); 0 (TATA-Binding Protein Associated Factors); 0 (TATA-Box Binding Protein); 0 (TBP protein, human); 0 (Transcription Factor TFIIA); 0 (Transcription Factor TFIID); 0 (USF1 protein, human); 0 (Upstream Stimulatory Factors); EC 2.3.1.48 (E1A-Associated p300 Protein); EC 2.3.1.48 (EP300 protein, human); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.770412


  3 / 665 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28011713
[Au] Autor:Ni Y; Seballos S; Fletcher B; Romigh T; Yehia L; Mester J; Senter L; Niazi F; Saji M; Ringel MD; LaFramboise T; Eng C
[Ad] Endereço:Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, OH, USA.
[Ti] Título:Germline compound heterozygous poly-glutamine deletion in USF3 may be involved in predisposition to heritable and sporadic epithelial thyroid carcinoma.
[So] Source:Hum Mol Genet;26(2):243-257, 2017 Jan 15.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cowden syndrome (CS) is an autosomal dominant disorder that predisposes to breast, thyroid, and other epithelial cancers. Differentiated thyroid carcinoma (DTC), as one of the major component cancers of CS, is the fastest rising incident cancer in the USA, and the most familial of all solid tumours. To identify additional candidate genes of CS and potentially DTC, we analysed a multi-generation CS-like family with papillary thyroid cancer (PTC), applying a combined linkage-based and whole-genome sequencing strategy and identified an in-frame germline compound heterozygous deletion, p.[Gln1478del];[Gln1476-Gln1478del] in USF3 (previously known as KIAA2018). Among 90 unrelated CS/CS-like individuals, 29% were found to have p.[Gln1478del];[Gln1476-Gln1478del]. Of 497 TCGA PTC individuals, 138 (27%) were found to carry this germline compound deletion, with somatically decreased tumour USF3 expression. We demonstrate an increased migration phenotype along with enhanced epithelial-to-mesenchymal transition (EMT) signature after USF3 knockdown or USF3 p.[Gln1478del];[Gln1476-Gln1478del] overexpression, which sensitizes cells to the endoplasmic reticulum (ER) stress. Loss of USF3 function induced cell necrosis-like features and impaired respiratory capacity while providing a glutamine-dependent cell survival advantage, strongly suggests a metabolic survival and migration-favouring microenvironment for carcinogenesis. Therefore, USF3 may be involved in the predisposition of thyroid cancer. Importantly, the results that glutamine-dependent survival and sensitivity to ER stress in USF3-deficient cells provide avenues for therapeutic and adjunct preventive interventions for both sporadic cancer as well as cancer predisposition syndromes with similar mechanisms.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Carcinoma/genética
Predisposição Genética para Doença
Síndrome do Hamartoma Múltiplo/genética
Neoplasias da Glândula Tireoide/genética
Fatores Estimuladores Upstream/genética
[Mh] Termos MeSH secundário: Carcinoma/patologia
Carcinoma Papilar
Movimento Celular
Estresse do Retículo Endoplasmático/genética
Transição Epitelial-Mesenquimal/genética
Feminino
Genoma Humano
Genótipo
Mutação em Linhagem Germinativa
Síndrome do Hamartoma Múltiplo/patologia
Heterozigoto
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Linhagem
Peptídeos/genética
Deleção de Sequência
Glândula Tireoide/patologia
Neoplasias da Glândula Tireoide/patologia
Microambiente Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Peptides); 0 (USF3 protein, human); 0 (Upstream Stimulatory Factors); 26700-71-0 (polyglutamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161225
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddw382


  4 / 665 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28003340
[Au] Autor:Hu XT; Zhu BL; Zhao LG; Wang JW; Liu L; Lai YJ; He L; Deng XJ; Chen GJ
[Ad] Endereço:Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Neurology, Chongqing, China.
[Ti] Título:Histone deacetylase inhibitor apicidin increases expression of the α-secretase ADAM10 through transcription factor USF1-mediated mechanisms.
[So] Source:FASEB J;31(4):1482-1493, 2017 Apr.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ADAM10 (a disintegrin and metalloproteinase domain-containing protein 10) is the α-secretase that is involved in APP (ß-amyloid precursor protein) processing. Enhancement of the nonamyloidogenic APP pathway by ADAM10 provides therapeutic potential for Alzheimer's disease (AD). By using high-throughput screening that targeted ADAM10, we determined that apicidin-an inhibitor of HDACs (histone deacetylases)-significantly increased mRNA and protein levels of ADAM10 in SH-SY5Y cells. A luciferase assay revealed that the nucleotides -444 to -300 in the ADAM10 promoter were sufficient to mediate this effect. In addition, knockdown of USF1 (upstream transcription factor 1) and HDAC2/3 prevented apicidin regulation of ADAM10. Moreover, USF1 acetylation was increased by apicidin, which enhanced the association of USF1 with HDAC2/3 and with the ADAM10 promoter. We further found that apicidin did not affect the phosphorylation of ERK or USF1; however, ERK inhibitor U0126 blocked the effect of apicidin on ADAM10. Finally, apicidin increased the level of α-site C-terminal fragment from APP and reduced the production of ß-amyloid peptide 1-42. Collectively, our study provides evidence that ADAM10 expression can be regulated by HDAC2/3 inhibitor apicidin USF1-dependent mechanisms in which ERK signaling plays an important role. Thus, HDAC regulation of ADAM10 might shed new light on the understanding of AD pathology.-Hu, X.-T., Zhu, B.-L., Zhao, L.-G., Wang, J.-W., Liu, L., Lai, Y.-J., He, L., Deng, X.-J., Chen, G.-J. Histone deacetylase inhibitor apicidin increases expression of the α-secretase ADAM10 through transcription factor USF1-mediated mechanisms.
[Mh] Termos MeSH primário: Proteína ADAM10/genética
Secretases da Proteína Precursora do Amiloide/genética
Inibidores de Histona Desacetilases/farmacologia
Proteínas de Membrana/genética
Peptídeos Cíclicos/farmacologia
Fatores Estimuladores Upstream/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAM10/metabolismo
Secretases da Proteína Precursora do Amiloide/metabolismo
Precursor de Proteína beta-Amiloide/genética
Precursor de Proteína beta-Amiloide/metabolismo
Animais
Linhagem Celular Tumoral
Seres Humanos
Proteínas de Membrana/metabolismo
Camundongos
Regiões Promotoras Genéticas
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ativação Transcricional/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
Fatores Estimuladores Upstream/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APP protein, human); 0 (Amyloid beta-Protein Precursor); 0 (Histone Deacetylase Inhibitors); 0 (Membrane Proteins); 0 (Peptides, Cyclic); 0 (RNA, Messenger); 0 (USF1 protein, human); 0 (Upstream Stimulatory Factors); 0 (apicidin); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201600961RR


  5 / 665 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27809618
[Au] Autor:Zang H; Li N; Pan Y; Hao J
[Ad] Endereço:a Department of Breast Surgery , Yantaishan Hospital , Yantai , China and.
[Ti] Título:Identification of upstream transcription factors (TFs) for expression signature genes in breast cancer.
[So] Source:Gynecol Endocrinol;33(3):193-198, 2017 Mar.
[Is] ISSN:1473-0766
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Breast cancer is a common malignancy among women with a rising incidence. Our intention was to detect transcription factors (TFs) for deeper understanding of the underlying mechanisms of breast cancer. Integrated analysis of gene expression datasets of breast cancer was performed. Then, functional annotation of differentially expressed genes (DEGs) was conducted, including Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. Furthermore, TFs were identified and a global transcriptional regulatory network was constructed. Seven publically available GEO datasets were obtained, and a set of 1196 DEGs were identified (460 up-regulated and 736 down-regulated). Functional annotation results showed that cell cycle was the most significantly enriched pathway, which was consistent with the fact that cell cycle is closely related to various tumors. Fifty-three differentially expressed TFs were identified, and the regulatory networks consisted of 817 TF-target interactions between 46 TFs and 602 DEGs in the context of breast cancer. Top 10 TFs covering the most downstream DEGs were SOX10, NFATC2, ZNF354C, ARID3A, BRCA1, FOXO3, GATA3, ZEB1, HOXA5 and EGR1. The transcriptional regulatory networks could enable a better understanding of regulatory mechanisms of breast cancer pathology and provide an opportunity for the development of potential therapy.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Regulação Neoplásica da Expressão Gênica
Redes Reguladoras de Genes
Proteínas de Neoplasias/metabolismo
Fatores Estimuladores Upstream/metabolismo
[Mh] Termos MeSH secundário: Adulto
Mama/metabolismo
Mama/cirurgia
Neoplasias da Mama/cirurgia
Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Curadoria de Dados
Bases de Dados Genéticas
Feminino
Perfilação da Expressão Gênica
Ontologia Genética
Seres Humanos
Meia-Idade
Proteínas de Neoplasias/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Neoplasm Proteins); 0 (Upstream Stimulatory Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE
[do] DOI:10.1080/09513590.2016.1239253


  6 / 665 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27693430
[Au] Autor:Emmerling VV; Fischer S; Kleemann M; Handrick R; Kochanek S; Otte K
[Ad] Endereço:Department of Gene Therapy, Ulm University, Helmholtz Strasse 8/1, 89081 Ulm, Germany. Electronic address: verena.fischer@sartorius-stedim.com.
[Ti] Título:miR-483 is a self-regulating microRNA and can activate its own expression via USF1 in HeLa cells.
[So] Source:Int J Biochem Cell Biol;80:81-86, 2016 Nov.
[Is] ISSN:1878-5875
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) are small non-coding RNAs that constitute a fundamental part of post-transcriptional gene regulation in mammalian cells. We have recently identified the intronic miR-483, which functions as an important regulator of protein synthesis during mild hypothermia in human and rodent cells. Since only very little is known about transcriptional regulation of intronic miRNAs and their host genes, we thoroughly investigated the regulation of miR-483 expression and its host gene IGF2 in HeLa cells. We demonstrate that miR-483 is regulated and expressed independently of its host gene IGF2 during mild hypothermia. Strikingly, we also discovered that miR-483 enhances its own transcription by up-regulation of the transcription factor USF1, which activates a promoter element upstream of the MIR483 gene. However, since the USF1 mRNA lacks binding sites for miR-483-5p and -3p, USF1 expression is likely enhanced in an indirect manner. Our results suggest that miR-483 may self-regulate its own expression independently of its host gene IGF2 in human HeLa cells. This points towards a novel feed-forward mechanism, in which selected intronic miRNAs may activate their own expression by transcriptional activation of upstream regulators.
[Mh] Termos MeSH primário: MicroRNAs/genética
Regulação para Cima
Fatores Estimuladores Upstream/genética
[Mh] Termos MeSH secundário: Células HeLa
Seres Humanos
Fator de Crescimento Insulin-Like II/genética
Íntrons/genética
Temperatura Ambiente
Transcrição Genética/genética
Ativação Transcricional/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IGF2 protein, human); 0 (MIRN483 microRNA, human); 0 (MicroRNAs); 0 (USF1 protein, human); 0 (Upstream Stimulatory Factors); 67763-97-7 (Insulin-Like Growth Factor II)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161004
[St] Status:MEDLINE


  7 / 665 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27686097
[Au] Autor:Pangou E; Befani C; Mylonis I; Samiotaki M; Panayotou G; Simos G; Liakos P
[Ad] Endereço:Laboratory of Biochemistry, Faculty of Medicine, University of Thessaly, Biopolis, Larissa 41500, Greece.
[Ti] Título:HIF-2α phosphorylation by CK1δ promotes erythropoietin secretion in liver cancer cells under hypoxia.
[So] Source:J Cell Sci;129(22):4213-4226, 2016 Nov 15.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hypoxia inducible factor 2 (HIF-2) is a transcriptional activator implicated in the cellular response to hypoxia. Regulation of its inducible subunit, HIF-2α (also known as EPAS1), involves post-translational modifications. Here, we demonstrate that casein kinase 1δ (CK1δ; also known as CSNK1D) phosphorylates HIF-2α at Ser383 and Thr528 in vitro We found that disruption of these phosphorylation sites, and silencing or chemical inhibition of CK1δ, reduced the expression of HIF-2 target genes and the secretion of erythropoietin (EPO) in two hepatic cancer cell lines, Huh7 and HepG2, without affecting the levels of HIF-2α protein expression. Furthermore, when CK1δ-dependent phosphorylation of HIF-2α was inhibited, we observed substantial cytoplasmic mislocalization of HIF-2α, which was reversed upon the addition of the nuclear protein export inhibitor leptomycin B. Taken together, these data suggest that CK1δ enhances EPO secretion from liver cancer cells under hypoxia by modifying HIF-2α and promoting its nuclear accumulation. This modification represents a new mechanism of HIF-2 regulation that might allow HIF isoforms to undertake differing functions.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Caseína Quinase Idelta/metabolismo
Eritropoetina/secreção
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas/secreção
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Sequência de Aminoácidos
Fatores de Transcrição Hélice-Alça-Hélice Básicos/química
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Hipóxia Celular
Núcleo Celular/metabolismo
Inativação Gênica
Células HeLa
Células Hep G2
Seres Humanos
Carioferinas/metabolismo
Neoplasias Hepáticas/genética
Mutação/genética
Fosforilação
Ligação Proteica
Estabilidade Proteica
Receptores Citoplasmáticos e Nucleares/metabolismo
Transcrição Genética
Fatores Estimuladores Upstream/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Karyopherins); 0 (Receptors, Cytoplasmic and Nuclear); 0 (USF2 protein, human); 0 (Upstream Stimulatory Factors); 0 (endothelial PAS domain-containing protein 1); 0 (exportin 1 protein); 11096-26-7 (Erythropoietin); EC 2.7.11.1 (Casein Kinase Idelta)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161001
[St] Status:MEDLINE


  8 / 665 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27649659
[Au] Autor:Ren YQ; Li QH; Liu LB
[Ad] Endereço:Department of Plastic Surgery, The First Affiliated Hospital of Zhengzhou University, ZhengZhou, China. liulinbo@zzu.edu.cn.
[Ti] Título:USF1 prompt melanoma through upregulating TGF-ß signaling pathway.
[So] Source:Eur Rev Med Pharmacol Sci;20(17):3592-8, 2016 Sep.
[Is] ISSN:2284-0729
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The activation of TGF-ß signaling contributes to abnormal EMT process and upstream stimulatory family1 (USF1) was recently found to activate the expression of TGF-ß. However, the specific role of USF1 in melanoma has never been explored. MATERIALS AND METHODS: The expression of USF1 was analyzed using real-time PCR and Western blot. The changes of cell morphology were observed under a microscope. Cell migration was determined using in vitro scratch test. A specific siRNA was applied to knockdown of USF1. RESULTS: The mRNA and protein levels of USF1 were significantly enhanced in melanoma cell lines, 1205-Lu, DO4, WM3211, and WM278, compared with normal human melanocytes PIG1. Overexpression of USF1 induced demonstrated an elongated and spindle-shaped morphology in the 1205-Lu cells. Meanwhile, USF1 induced the expression of α-SMA, Vimentin and Fibronectin, while the epithelial marker, E-cadherin (E-cad), was significantly decreased. Furthermore, in vitro scratch test demonstrated that overexpression of USF1 markedly enhanced 1205-Lu cell migration capacity at 24 h and 48 h. More importantly, knockdown of USF1 could partially reverse TGF-ß1-treatment-induced changes of EMT markers as well as cell morphological changes. CONCLUSIONS: We first demonstrate that overexpression of USF1 prompts the EMT process through the accumulation of TGF-ß1 production in melanoma cells.
[Mh] Termos MeSH primário: Caderinas/genética
Melanoma/genética
Neoplasias Cutâneas/genética
Fator de Crescimento Transformador beta
Fatores Estimuladores Upstream
[Mh] Termos MeSH secundário: Movimento Celular
Fibronectinas
Regulação da Expressão Gênica
Seres Humanos
Fator de Crescimento Transformador beta1/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (FN1 protein, human); 0 (Fibronectins); 0 (Transforming Growth Factor beta); 0 (Transforming Growth Factor beta1); 0 (USF1 protein, human); 0 (Upstream Stimulatory Factors)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160922
[St] Status:MEDLINE


  9 / 665 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27141965
[Au] Autor:Li Y; Schulz VP; Deng C; Li G; Shen Y; Tusi BK; Ma G; Stees J; Qiu Y; Steiner LA; Zhou L; Zhao K; Bungert J; Gallagher PG; Huang S
[Ad] Endereço:Department of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, FL 32610, USA Macau Institute for Applied Research in Medicine and Health, State Key laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Avenida Wai L
[Ti] Título:Setd1a and NURF mediate chromatin dynamics and gene regulation during erythroid lineage commitment and differentiation.
[So] Source:Nucleic Acids Res;44(15):7173-88, 2016 Sep 06.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The modulation of chromatin structure is a key step in transcription regulation in mammalian cells and eventually determines lineage commitment and differentiation. USF1/2, Setd1a and NURF complexes interact to regulate chromatin architecture in erythropoiesis, but the mechanistic basis for this regulation is hitherto unknown. Here we showed that Setd1a and NURF complexes bind to promoters to control chromatin structural alterations and gene activation in a cell context dependent manner. In human primary erythroid cells USF1/2, H3K4me3 and the NURF complex were significantly co-enriched at transcription start sites of erythroid genes, and their binding was associated with promoter/enhancer accessibility that resulted from nucleosome repositioning. Mice deficient for Setd1a, an H3K4 trimethylase, in the erythroid compartment exhibited reduced Ter119/CD71 positive erythroblasts, peripheral blood RBCs and hemoglobin levels. Loss of Setd1a led to a reduction of promoter-associated H3K4 methylation, inhibition of gene transcription and blockade of erythroid differentiation. This was associated with alterations in NURF complex occupancy at erythroid gene promoters and reduced chromatin accessibility. Setd1a deficiency caused decreased associations between enhancer and promoter looped interactions as well as reduced expression of erythroid genes such as the adult ß-globin gene. These data indicate that Setd1a and NURF complexes are specifically targeted to and coordinately regulate erythroid promoter chromatin dynamics during erythroid lineage differentiation.
[Mh] Termos MeSH primário: Linhagem da Célula
Montagem e Desmontagem da Cromatina
Eritrócitos/citologia
Eritropoese
Regulação da Expressão Gênica/genética
Histona-Lisina N-Metiltransferase/metabolismo
Complexos Multiproteicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos Nucleares/metabolismo
Linhagem da Célula/genética
Células Cultivadas
Cromatina/genética
Cromatina/metabolismo
Imunoprecipitação da Cromatina
Eritroblastos/citologia
Eritroblastos/metabolismo
Contagem de Eritrócitos
Eritrócitos/metabolismo
Eritropoese/genética
Feminino
Hemoglobinas/metabolismo
Histona-Lisina N-Metiltransferase/deficiência
Histona-Lisina N-Metiltransferase/genética
Histonas/metabolismo
Seres Humanos
Lisina/metabolismo
Masculino
Metilação
Camundongos
Camundongos Knockout
Nuclease do Micrococo/metabolismo
Complexos Multiproteicos/química
Proteínas do Tecido Nervoso/metabolismo
Regiões Promotoras Genéticas/genética
Baço/citologia
Fatores de Transcrição/metabolismo
Fatores Estimuladores Upstream/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Nuclear); 0 (Chromatin); 0 (Hemoglobins); 0 (Histones); 0 (Multiprotein Complexes); 0 (Nerve Tissue Proteins); 0 (Transcription Factors); 0 (USF1 protein, human); 0 (Upstream Stimulatory Factors); 0 (fetal Alzheimer antigen); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.1.1.43 (Nsccn1 protein, mouse); EC 2.1.1.43 (Setd1A protein, human); EC 3.1.31.1 (Micrococcal Nuclease); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160505
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkw327


  10 / 665 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27108960
[Au] Autor:Wu Y; Yu DD; Hu Y; Yan D; Chen X; Cao HX; Yu SR; Wang Z; Feng JF
[Ad] Endereço:The First Clinical School of Nanjing Medical University, Nanjing, Jiangsu 210009, P.R. China.
[Ti] Título:Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray.
[So] Source:Oncol Rep;35(6):3371-86, 2016 Jun.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Mutations in the epidermal growth factor receptor (EGFR) make lung adenocarcinoma cells sensitive to EGFR tyrosine kinase inhibitors (TKIs). Long-term cancer therapy may cause the occurrence of acquired resistance to EGFR TKIs. Long non-coding RNAs (lncRNAs) play important roles in tumor formation, tumor metastasis and the development of EGFR-TKI resistance in lung cancer. To gain insight into the molecular mechanisms of EGFR-TKI resistance, we generated an EGFR-TKI-resistant HCC827-8-1 cell line and analyzed expression patterns by lncRNA microarray and compared it with its parental HCC827 cell line. A total of 1,476 lncRNA transcripts and 1,026 mRNA transcripts were dysregulated in the HCC827­8-1 cells. The expression levels of 7 chosen lncRNAs were validated by real-time quantitative PCR. As indicated by functional analysis, several groups of lncRNAs may be involved in the bio-pathways associated with EGFR-TKI resistance through their cis- and/or trans­regulation of protein-coding genes. Thus, lncRNAs may be used as novel candidate biomarkers and potential targets in EGFR-TKI therapy in the future.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Neoplasias Pulmonares/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
RNA Longo não Codificante/análise
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Linhagem Celular Tumoral
Resistência a Medicamentos Antineoplásicos
Fator de Transcrição E2F1/fisiologia
Seres Humanos
Neoplasias Pulmonares/genética
MicroRNAs/análise
Análise de Sequência com Séries de Oligonucleotídeos
Reação em Cadeia da Polimerase em Tempo Real
Fatores Estimuladores Upstream/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (E2F1 Transcription Factor); 0 (E2F1 protein, human); 0 (MicroRNAs); 0 (Protein Kinase Inhibitors); 0 (RNA, Long Noncoding); 0 (USF1 protein, human); 0 (Upstream Stimulatory Factors); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170303
[Lr] Data última revisão:
170303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160426
[St] Status:MEDLINE
[do] DOI:10.3892/or.2016.4758



página 1 de 67 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde