Base de dados : MEDLINE
Pesquisa : G05.308.800 [Categoria DeCS]
Referências encontradas : 35621 [refinar]
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[PMID]:29295976
[Au] Autor:Liu CY; Zhang YH; Li RB; Zhou LY; An T; Zhang RC; Zhai M; Huang Y; Yan KW; Dong YH; Ponnusamy M; Shan C; Xu S; Wang Q; Zhang YH; Zhang J; Wang K
[Ad] Endereço:Center for Developmental Cardiology, Institute for Translational Medicine, College of Medicine, Qingdao University, Qingdao, 266021, China.
[Ti] Título:LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription.
[So] Source:Nat Commun;9(1):29, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H O and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases.
[Mh] Termos MeSH primário: Autofagia/genética
Infarto do Miocárdio/genética
Proteínas Nucleares/genética
RNA Longo não Codificante/genética
Transativadores/genética
Ativação Transcricional
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Células Cultivadas
Camundongos
Infarto do Miocárdio/patologia
Traumatismo por Reperfusão Miocárdica/genética
Traumatismo por Reperfusão Miocárdica/metabolismo
Miócitos Cardíacos/metabolismo
Proteínas Nucleares/metabolismo
Ligação Proteica
Interferência de RNA
RNA Longo não Codificante/metabolismo
Transativadores/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Proteins); 0 (RNA, Long Noncoding); 0 (Trans-Activators); 0 (Tumor Suppressor Protein p53); 0 (myocardin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02280-y


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[PMID]:29176792
[Au] Autor:Tai PWL; Wu H; van Wijnen AJ; Stein GS; Stein JL; Lian JB
[Ad] Endereço:Department of Biochemistry, University of Vermont College of Medicine, Burlington, Vermont, United States of America.
[Ti] Título:Genome-wide DNase hypersensitivity, and occupancy of RUNX2 and CTCF reveal a highly dynamic gene regulome during MC3T3 pre-osteoblast differentiation.
[So] Source:PLoS One;12(11):e0188056, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ability to discover regulatory sequences that control bone-related genes during development has been greatly improved by massively parallel sequencing methodologies. To expand our understanding of cis-regulatory regions critical to the control of gene expression during osteoblastogenesis, we probed the presence of open chromatin states across the osteoblast genome using global DNase hypersensitivity (DHS) mapping. Our profiling of MC3T3 mouse pre-osteoblasts during differentiation has identified more than 224,000 unique DHS sites. Approximately 65% of these sites are dynamic during temporal stages of osteoblastogenesis, and a majority of them are located within non-promoter (intergenic and intronic) regions. Nearly half of all DHS sites (both constitutive and dynamic) overlap binding events of the bone-essential RUNX2 and/or the chromatin-related CTCF transcription factors. This finding reinforces the role of these regulatory proteins as essential components of the bone gene regulome. We observe a reduction in chromatin accessibility throughout the genome between pre-osteoblast and early osteoblasts. Our analysis also defined a class of differentially expressed genes that harbor DHS peaks centered within 1 kb downstream of transcriptional end sites (TES). These DHSs at the 3'-flanks of genes exhibit dynamic changes during differentiation that may impact regulation of the osteoblast genome. Taken together, the distribution of DHS regions within non-promoter locations harboring osteoblast and chromatin related transcription factor binding motifs, reflect novel cis-regulatory requirements to support temporal gene expression in differentiating osteoblasts.
[Mh] Termos MeSH primário: Fator de Ligação a CCCTC/metabolismo
Diferenciação Celular/genética
Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo
Desoxirribonucleases/metabolismo
Regulação da Expressão Gênica
Genoma
Osteoblastos/citologia
Osteoblastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
DNA Intergênico/genética
Perfilação da Expressão Gênica
Ontologia Genética
Íntrons/genética
Camundongos
Ativação Transcricional/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCCTC-Binding Factor); 0 (Core Binding Factor Alpha 1 Subunit); 0 (DNA, Intergenic); EC 3.1.- (Deoxyribonucleases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188056


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[PMID]:29360846
[Au] Autor:Yu X; Stallone JN; Heaps CL; Han G
[Ad] Endereço:Veterinary Physiology & Pharmacology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, United States of America.
[Ti] Título:The activation of G protein-coupled estrogen receptor induces relaxation via cAMP as well as potentiates contraction via EGFR transactivation in porcine coronary arteries.
[So] Source:PLoS One;13(1):e0191418, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Estrogen exerts protective effects against cardiovascular diseases in premenopausal women, but is associated with an increased risk of both coronary heart disease and stroke in older postmenopausal women. Studies have shown that activation of the G-protein-coupled estrogen receptor 1 (GPER) can cause either relaxation or contraction of arteries. It is highly likely that these dual actions of GPER may contribute to the seemingly paradoxical effects of estrogen in regulating coronary artery function. The objective of this study was to test the hypothesis that activation of GPER enhances agonist-stimulated porcine coronary artery contraction via epidermal growth factor receptor (EGFR) transactivation and its downstream extracellular signal-regulated kinases (ERK1/2) pathway. Isometric tension studies and western blot were performed to determine the effect of GPER activation on coronary artery contraction. Our findings demonstrated that G-1 caused concentration-dependent relaxation of ET-1-induced contraction, while pretreatment of arterial rings with G-1 significantly enhanced ET-1-induced contraction. GPER antagonist, G-36, significantly inhibited both the G-1-induced relaxation effect and G-1-enhanced ET-1 contraction. Gallein, a Gßγ inhibitor, significantly increased G-1-induced relaxation, yet inhibited G-1-enhanced ET-1-mediated contraction. Similarly, inhibition of EGFR with AG1478 or inhibition of Src with phosphatase 2 further increased G-1-induced relaxation responses in coronary arteries, but decreased G-1-enhanced ET-1-induced contraction. Western blot experiments in porcine coronary artery smooth muscle cells (PCASMC) showed that G-1 increased tyrosine phosphorylation of EGFR, which was inhibited by AG-1478. Furthermore, enzyme-linked immunosorbent assays showed that the level of heparin-binding EGF (HB-EGF) released by ET-1 treatment increased two-fold; whereas pre-incubation with G-1 further increased ET-1-induced HB-EGF release to four-fold over control conditions. Lastly, the role of ERK1/2 was determined by applying the MEK inhibitor, PD98059, in isometric tension studies and detecting phospho-ERK1/2 in immunoblotting. PD98059 potentiated G-1-induced relaxation response, but blocked G-1-enhanced ET-1-induced contraction. By western blot, G-1 treatment decreased phospho-ERK1/2, however, in the presence of the adenylyl cyclase inhibitor, SQ22536, G-1 significantly increased ERK1/2 phosphorylation in PCASMC. These data demonstrate that activation of GPER induces relaxation via cAMP as well as contraction via a mechanism involving transactivation of EGFR and the phosphorylation of ERK1/2 in porcine coronary arteries.
[Mh] Termos MeSH primário: Vasos Coronários/fisiologia
Receptor do Fator de Crescimento Epidérmico/genética
Receptores Estrogênicos/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Vasos Coronários/efeitos dos fármacos
Ciclopentanos/farmacologia
Flavonoides/farmacologia
Seres Humanos
Técnicas In Vitro
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Modelos Cardiovasculares
Miócitos de Músculo Liso/metabolismo
Quinazolinas/farmacologia
Quinolinas/farmacologia
Receptores Acoplados a Proteínas-G/agonistas
Suínos
Ativação Transcricional
Tirfostinas/farmacologia
Vasodilatação/efeitos dos fármacos
Vasodilatação/genética
Vasodilatação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone); 0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Cyclopentanes); 0 (Flavonoids); 0 (Quinazolines); 0 (Quinolines); 0 (Receptors, Estrogen); 0 (Receptors, G-Protein-Coupled); 0 (Tyrphostins); 170449-18-0 (tyrphostin AG 1478); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191418


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[PMID]:28451636
[Au] Autor:Erb M; Lee B; Yeon Seo S; Lee JW; Lee S; Lee SK
[Ad] Endereço:Papé Family Pediatric Research Institute, Department of Pediatrics, Oregon Health and Science University, Portland, OR 97239.
[Ti] Título:The Isl1-Lhx3 Complex Promotes Motor Neuron Specification by Activating Transcriptional Pathways that Enhance Its Own Expression and Formation.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Motor neuron (MN) progenitor cells rapidly induce high expression of the transcription factors Islet-1 (Isl1), LIM-homeobox 3 (Lhx3), and the transcriptional regulator LMO4, as they differentiate. While these factors are critical for MN specification, the mechanisms regulating their precise temporal and spatial expression patterns are not well characterized. Isl1 and Lhx3 form the Isl1-Lhx3 complex, which induces the transcription of genes critical for MN specification and maturation. Here, we report that , , and are direct target genes of the Isl1-Lhx3 complex. Our results show that specific genomic loci associated with these genes recruit the Isl1-Lhx3 complex to activate the transcription of , , and in embryonic MNs of chick and mouse. These findings support a model in which the Isl1-Lhx3 complex amplifies its own expression through a potent autoregulatory feedback loop and simultaneously enhances the transcription of . LMO4 blocks the formation of the V2 interneuron-specifying Lhx3 complex. In developing MNs, this action inhibits the expression of V2 interneuron genes and increases the pool of unbound Lhx3 available to incorporate into the Isl1-Lhx3 complex. Identifying the pathways that regulate the expression of these key factors provides important insights into the genetic strategies utilized to promote MN differentiation and maturation.
[Mh] Termos MeSH primário: Proteínas com Homeodomínio LIM/metabolismo
Neurônios Motores/metabolismo
Fatores de Transcrição/metabolismo
Ativação Transcricional
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Proteínas Aviárias/metabolismo
Embrião de Galinha
Proteínas de Ligação a DNA/metabolismo
Proteínas com Domínio LIM/metabolismo
Camundongos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Avian Proteins); 0 (DNA-Binding Proteins); 0 (LIM Domain Proteins); 0 (LIM-Homeodomain Proteins); 0 (Lhx3 protein); 0 (Lmo4 protein, mouse); 0 (Transcription Factors); 0 (insulin gene enhancer binding protein Isl-1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:27773677
[Au] Autor:Jeronimo C; Langelier MF; Bataille AR; Pascal JM; Pugh BF; Robert F
[Ad] Endereço:Institut de recherches cliniques de Montréal, 110 Avenue des Pins Ouest, Montréal, QC H2W 1R7, Canada.
[Ti] Título:Tail and Kinase Modules Differently Regulate Core Mediator Recruitment and Function In Vivo.
[So] Source:Mol Cell;64(3):455-466, 2016 Nov 03.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mediator is a highly conserved transcriptional coactivator organized into four modules, namely Tail, Middle, Head, and Kinase (CKM). Previous work suggests regulatory roles for Tail and CKM, but an integrated model for these activities is lacking. Here, we analyzed the genome-wide distribution of Mediator subunits in wild-type and mutant yeast cells in which RNA polymerase II promoter escape is blocked, allowing detection of transient Mediator forms. We found that although all modules are recruited to upstream activated regions (UAS), assembly of Mediator within the pre-initiation complex is accompanied by the release of CKM. Interestingly, our data show that CKM regulates Mediator-UAS interaction rather than Mediator-promoter association. In addition, although Tail is required for Mediator recruitment to UAS, Tailless Mediator nevertheless interacts with core promoters. Collectively, our data suggest that the essential function of Mediator is mediated by Head and Middle at core promoters, while Tail and CKM play regulatory roles.
[Mh] Termos MeSH primário: Regulação Fúngica da Expressão Gênica
Complexo Mediador/genética
RNA Polimerase II/genética
Proteínas de Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/genética
Fator de Transcrição TFIIB/genética
[Mh] Termos MeSH secundário: Sítios de Ligação
Complexo Mediador/metabolismo
Modelos Moleculares
Regiões Promotoras Genéticas
Ligação Proteica
Conformação Proteica em alfa-Hélice
Conformação Proteica em Folha beta
Domínios e Motivos de Interação entre Proteínas
Subunidades Proteicas/genética
Subunidades Proteicas/metabolismo
RNA Polimerase II/metabolismo
Saccharomyces cerevisiae/metabolismo
Proteínas de Saccharomyces cerevisiae/metabolismo
Fator de Transcrição TFIIB/metabolismo
Iniciação da Transcrição Genética
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mediator Complex); 0 (Protein Subunits); 0 (SUA7 protein, S cerevisiae); 0 (Saccharomyces cerevisiae Proteins); 0 (Transcription Factor TFIIB); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE


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[PMID]:28450734
[Au] Autor:Woo H; Dam Ha S; Lee SB; Buratowski S; Kim T
[Ad] Endereço:Department of Life Science, Ewha Womans University, Seoul, Korea.
[Ti] Título:Modulation of gene expression dynamics by co-transcriptional histone methylations.
[So] Source:Exp Mol Med;49(4):e326, 2017 04 28.
[Is] ISSN:2092-6413
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Co-transcriptional methylations of histone H3 at lysines 4 and 36, highly conserved methyl marks from yeast to humans, have profound roles in regulation of histone acetylation. These modifications function to recruit and/or activate distinct histone acetyltransferases (HATs) or histone deacetylases (HDACs). Whereas H3K4me3 increases acetylation at promoters via multiple HATs, H3K4me2 targets Set3 HDAC to deacetylate histones in 5' transcribed regions. In 3' regions of genes, H3K36me2/3 facilitates deacetylation by Rpd3S HDAC and slows elongation. Despite their important functions in deacetylation, no strong effects on global gene expression have been seen under optimized or laboratory growth conditions. Instead, H3K4me2-Set3 HDAC and Set2-Rpd3S pathways primarily delay the kinetics of messenger RNA (mRNA) and long noncoding RNA (lncRNA) induction upon environmental changes. A majority of mRNA genes regulated by these pathways have an overlapping lncRNA transcription either from an upstream or an antisense promoter. Surprisingly, the distance between mRNA and lncRNA promoters seems to specify the repressive effects of the two pathways. Given that co-transcriptional methylations and acetylation have been linked to many cancers, studying their functions in a dynamic condition or during cancer progression will be much more important and help identify novel genes associated with cancers.
[Mh] Termos MeSH primário: Histonas/metabolismo
Processamento de Proteína Pós-Traducional
Ativação Transcricional
[Mh] Termos MeSH secundário: Acetilação
Animais
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Metilação
RNA Longo não Codificante/genética
RNA Longo não Codificante/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Histones); 0 (RNA, Long Noncoding); 0 (RNA, Messenger)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1038/emm.2017.19


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[PMID]:29277610
[Au] Autor:Liu H; Xu D; Cui M; Hou T; Zhang Q
[Ad] Endereço:Department of Ecology, Institute of Hydrobiology, School of Life Science and Technology, Key Laboratory of Eutrophication and Red Tide Prevention of Guangdong Higher Education Institutes, Engineering Research Center of Tropical and Subtropical Aquatic Ecological Engineering, Ministry of Education, J
[Ti] Título:The transcriptional factor YB-1 positively regulates Hsc70 transcription in Crassostrea hongkongensis.
[So] Source:Biochem Biophys Res Commun;495(4):2404-2409, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A Y-box binding protein ChYB-1 was discovered as a ChHsc70 promoter-associated protein in Crassostrea hongkongensis by DNA-affinity purification and mass spectrometry analysis. The overexpression of ChYB-1 in heterologous HEK293T cells led to clear enhancement of ChHsc70 promoter expression, while ChYB-1 depletion correlated with significant reduction of ChHsc70 transcription in the hemocytes of C. hongkongensis. Quantitative Real-time PCR analysis revealed that both ChHsc70 and ChYB-1 were transcriptionally responsive to external chemical or physical stressors. This indicates a plausible correlation between ChHsc70 and ChYB-1 in the genetic regulatory pathway triggered by external stresses. This study presents the first evidence of positive regulator for Hsc70 transcription and contributes to a better understanding of the regulatory mechanisms governing Hsc70 expression.
[Mh] Termos MeSH primário: Crassostrea/metabolismo
Regulação da Expressão Gênica/fisiologia
Proteínas de Choque Térmico HSC70/metabolismo
Fatores de Transcrição/metabolismo
Ativação Transcricional/fisiologia
Proteína 1 de Ligação a Y-Box/metabolismo
[Mh] Termos MeSH secundário: Animais
Estresse Oxidativo/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HSC70 Heat-Shock Proteins); 0 (Transcription Factors); 0 (Y-Box-Binding Protein 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29384939
[Au] Autor:Xing P; Dong H; Liu Q; Zhao T; Yao F; Xu Y; Chen B; Zheng X; Wu Y; Jin F; Li J
[Ad] Endereço:Breast Division, the First Hospital of China Medical University, Shenyang, Liaoning, China.
[Ti] Título:Upregulation of transmembrane 4 L6 family member 1 predicts poor prognosis in invasive breast cancer: A STROBE-compliant article.
[So] Source:Medicine (Baltimore);96(52):e9476, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transmembrane 4 L6 family member 1 (TM4SF1) belongs to the 4-transmembrane-domain family and functions as an oncogene in multiple human cancers. In this work, we aim to determine TM4SF1 expression and its prognostic impact on patients with invasive breast cancer.Overall, we enrolled 209 invasive breast cancer patients and immunohistochemically examined the expression of TM4SF1 in tumor specimens. The relationship between TM4SF1 expression and clinicopathological parameter and patient survival of breast cancer patients was analyzed.Among the 209 cases, 137 (65.6%) exhibited high expression of TM4SF1. High TM4SF1 expression was significantly associated with advanced histological grade and negative estrogen receptor and progesterone receptor status. Triple-negative breast cancer (TNBC) tumors were more likely to express high levels of TM4SF1 than non-TNBC cases. Patients with high tumoral expression of TM4SF1 had a significantly shorter disease-free survival (DFS; P = .00) and overall survival (OS; P = .01) than those with low expression of TM4SF1. When survival analysis was restricted to the 167 patients (79.9%) receiving adjuvant chemotherapy, TM4SF1 expression was also correlated with poorer DFS and OS (P = .00). In multiple Cox regression analysis TM4SF1 expression remained an independent prognostic indicator for OS and DFS.TM4SF1 is upregulated and serves as an independent poor prognostic indicator in invasive breast cancer.
[Mh] Termos MeSH primário: Antígenos de Superfície/biossíntese
Neoplasias da Mama/mortalidade
Neoplasias da Mama/patologia
Regulação Neoplásica da Expressão Gênica/fisiologia
Proteínas de Neoplasias/biossíntese
Regulação para Cima/fisiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais
Feminino
Seres Humanos
Meia-Idade
Gradação de Tumores
Invasividade Neoplásica
Prognóstico
Receptor ErbB-2/metabolismo
Receptores Estrogênicos/metabolismo
Receptores de Progesterona/metabolismo
Análise de Sobrevida
Ativação Transcricional
Neoplasias de Mama Triplo Negativas/mortalidade
Neoplasias de Mama Triplo Negativas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Surface); 0 (Biomarkers, Tumor); 0 (Neoplasm Proteins); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); 147016-68-0 (TM4SF1 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009476


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[PMID]:28467933
[Au] Autor:Koh JH; Hancock CR; Terada S; Higashida K; Holloszy JO; Han DH
[Ad] Endereço:Division of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
[Ti] Título:PPARß Is Essential for Maintaining Normal Levels of PGC-1α and Mitochondria and for the Increase in Muscle Mitochondria Induced by Exercise.
[So] Source:Cell Metab;25(5):1176-1185.e5, 2017 May 02.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The objective of this study was to evaluate the specific mechanism(s) by which PPARß regulates mitochondrial content in skeletal muscle. We discovered that PPARß increases PGC-1α by protecting it from degradation by binding to PGC-1α and limiting ubiquitination. PPARß also induces an increase in nuclear respiratory factor 1 (NRF-1) expression, resulting in increases in mitochondrial respiratory chain proteins and MEF2A, for which NRF-1 is a transcription factor. There was also an increase in AMP kinase phosphorylation mediated by an NRF-1-induced increase in CAM kinase kinase-ß (CaMKKß). Knockdown of PPARß resulted in large decreases in the levels of PGC-1α and mitochondrial proteins and a marked attenuation of the exercise-induced increase in mitochondrial biogenesis. In conclusion, PPARß induces an increase in PGC-1α protein, and PPARß is a transcription factor for NRF-1. Thus, PPARß plays essential roles in the maintenance and adaptive increase in mitochondrial enzymes in skeletal muscle by exercise.
[Mh] Termos MeSH primário: Mitocôndrias Musculares/metabolismo
PPAR beta/metabolismo
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Animais
Quinase da Proteína Quinase Dependente de Cálcio-Calmodulina/genética
Linhagem Celular
Ativação Enzimática
Técnicas de Silenciamento de Genes
Células HEK293
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Mitocôndrias Musculares/genética
Fator 1 Nuclear Respiratório/genética
PPAR beta/genética
Condicionamento Físico Animal
Proteólise
Ratos Wistar
Ativação Transcricional
Ubiquitinação
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nuclear Respiratory Factor 1); 0 (PPAR-beta); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Kinase); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29305861
[Au] Autor:Jeong B; Kim HR; Choi NS; Park BS; Eom H; Park JW; Kim JG; Lee BJ
[Ad] Endereço:Department of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan 44610, South Korea.
[Ti] Título:Role of thyroid transcription factor-1 in transcriptional regulation of heme oxygenase-1.
[So] Source:Biochem Biophys Res Commun;496(1):147-152, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Here, we report thyroid transcription factor 1 (TTF-1) as an important transcription factor for the expression of heme oxygenase-1 (HO-1). HO-1 is a well-known cytoprotective enzyme against inflammation. We observed that HO-1 co-expressed with TTF-1 in mouse hypothalamic cells. Results from luciferase and chromatin immunoprecipitation assays revealed that TTF-1 directly activated HO-1 transcription by binding to binding domains in the 5'-flanking region of the HO-1 gene. A proinflammatory cytokine, tumor necrosis factor-alpha (TNF-α), induced nuclear translocation of TTF-1 and increased binding affinity of TTF-1 to its binding sites on the HO-1 gene. HO-1 mRNA increased with TTF-1 overexpression but decreased with RNA interference of TTF-1 expression in rat astroglial C6 cells. Together with results showing involvement of TTF-1 in the TNF-α-induced increase in interleukin 1 beta and monocyte chemotactic protein 1 production, this study suggests that TTF-1 plays an important role in the mouse hypothalamus TNF-α-induced inflammatory response for regulating HO-1 gene expression.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/fisiologia
Heme Oxigenase-1/metabolismo
Hipotálamo/metabolismo
Proteínas de Membrana/metabolismo
Fator Nuclear 1 de Tireoide/metabolismo
Ativação Transcricional/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Thyroid Nuclear Factor 1); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE



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