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Pesquisa : D12.776.930.780.625.374 [Categoria DeCS]
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[PMID]:28645579
[Au] Autor:Wang H; Ding Z; Shi QM; Ge X; Wang HX; Li MX; Chen G; Wang Q; Ju Q; Zhang JP; Zhang MR; Xu LC
[Ad] Endereço:School of Public Health, Xuzhou Medical University, 209 Tong-Shan Road, Xuzhou, Jiangsu 221000, China.
[Ti] Título:Anti-androgenic mechanisms of Bisphenol A involve androgen receptor signaling pathway.
[So] Source:Toxicology;387:10-16, 2017 Jul 15.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:We have shown Bisphenol A (BPA) acts as an androgen receptor (AR) antagonist in the previous study. However, the mechanisms underlying anti-androgenic effects of BPA remain unclear. The objective of this study was to explore whether the AR signaling was involved in AR antagonism of BPA. The Cell Counting Kit-8 (CCK-8) assay and Real-Time Cell Analysis (RTCA) iCELLigence system were applied to analyze the mouse Sertoli cell TM4 proliferation. The mammalian two-hybrid assays were performed to investigate the effects of BPA on the AR amino- and carboxyl-terminal regions (N/C) interaction and the interactions of the AR with steroid receptor coactivator-1 (SRC-1), co-repressors including silencing mediator for thyroid hormone receptors (SMRT) and nuclear receptor co-repressor (NCoR). BPA exposure resulted in decreased TM4 cell proliferation. BPA inhibited the AR N/C interaction significantly. Furthermore, BPA enhanced the interactions of AR-SMRT and AR-NCoR significantly. In conclusion, these data suggest BPA inhibits Sertoli cell proliferation due to its anti-androgenic actions. The mechanisms responsible for AR antagonism of BPA involve inhibiting the AR N/C interaction and enhancing the interactions of AR-SMRT and AR-NCoR. The data uncover novel anti-androgenic mechanisms by which BPA antagonizes AR signaling, contributing to Sertoli cell proliferation suppression and male reproductive toxicology.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/toxicidade
Proliferação Celular/efeitos dos fármacos
Disruptores Endócrinos/toxicidade
Fenóis/toxicidade
Receptores Androgênicos/efeitos dos fármacos
Células de Sertoli/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Relação Dose-Resposta a Droga
Haplorrinos
Masculino
Camundongos
Correpressor 1 de Receptor Nuclear/genética
Correpressor 1 de Receptor Nuclear/metabolismo
Correpressor 2 de Receptor Nuclear/genética
Correpressor 2 de Receptor Nuclear/metabolismo
Coativador 1 de Receptor Nuclear/genética
Coativador 1 de Receptor Nuclear/metabolismo
Ligação Proteica
Receptores Androgênicos/genética
Receptores Androgênicos/metabolismo
Células de Sertoli/metabolismo
Células de Sertoli/patologia
Transdução de Sinais/efeitos dos fármacos
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AR protein, mouse); 0 (Benzhydryl Compounds); 0 (Endocrine Disruptors); 0 (Ncor1 protein, mouse); 0 (Ncor2 protein, mouse); 0 (Nuclear Receptor Co-Repressor 1); 0 (Nuclear Receptor Co-Repressor 2); 0 (Phenols); 0 (Receptors, Androgen); EC 2.3.1.48 (Ncoa1 protein, mouse); EC 2.3.1.48 (Nuclear Receptor Coactivator 1); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE


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[PMID]:28500133
[Au] Autor:Carter EL; Ramirez Y; Ragsdale SW
[Ad] Endereço:From the Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan 48109.
[Ti] Título:The heme-regulatory motif of nuclear receptor Rev-erbß is a key mediator of heme and redox signaling in circadian rhythm maintenance and metabolism.
[So] Source:J Biol Chem;292(27):11280-11299, 2017 Jul 07.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rev-erbß is a heme-responsive transcription factor that regulates genes involved in circadian rhythm maintenance and metabolism, effectively bridging these critical cellular processes. Heme binding to Rev-erbß indirectly facilitates its interaction with the nuclear receptor co-repressor (NCoR1), resulting in repression of Rev-erbß target genes. Fe -heme binds in a 6-coordinate complex with axial His and Cys ligands, the latter provided by a heme-regulatory motif (HRM). Rev-erbß was thought to be a heme sensor based on a weak value for the Rev-erbß·heme complex of 2 µm determined with isothermal titration calorimetry. However, our group demonstrated with UV-visible difference titrations that the value is in the low nanomolar range, and the Fe -heme off-rate is on the order of 10 s making Rev-erbß ineffective as a sensor of Fe -heme. In this study, we dissected the kinetics of heme binding to Rev-erbß and provided a for Fe -heme of ∼0.1 nm Loss of the HRM axial thiolate via redox processes, including oxidation to a disulfide with a neighboring cysteine or dissociation upon reduction of Fe - to Fe -heme, decreased binding affinity by >20-fold. Furthermore, as measured in a co-immunoprecipitation assay, substitution of the His or Cys heme ligands in Rev-erbß was accompanied by a significant loss of NCoR1 binding. These results demonstrate the importance of the Rev-erbß HRM in regulating interactions with heme and NCoR1 and advance our understanding of how signaling through HRMs affects the major cellular processes of circadian rhythm maintenance and metabolism.
[Mh] Termos MeSH primário: Ritmo Circadiano
Ferro/química
Receptores Citoplasmáticos e Nucleares/química
Proteínas Repressoras/química
Transdução de Sinais
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Heme
Ferro/metabolismo
Cinética
Correpressor 1 de Receptor Nuclear/química
Correpressor 1 de Receptor Nuclear/genética
Correpressor 1 de Receptor Nuclear/metabolismo
Oxirredução
Ligação Proteica
Domínios Proteicos
Receptores Citoplasmáticos e Nucleares/genética
Receptores Citoplasmáticos e Nucleares/metabolismo
Proteínas Repressoras/genética
Proteínas Repressoras/metabolismo
Espectrofotometria Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NCOR1 protein, human); 0 (NR1D2 protein, human); 0 (Nuclear Receptor Co-Repressor 1); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Repressor Proteins); 42VZT0U6YR (Heme); E1UOL152H7 (Iron)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170514
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.783118


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[PMID]:28475868
[Au] Autor:Yang F; Ma Q; Liu Z; Li W; Tan Y; Jin C; Ma W; Hu Y; Shen J; Ohgi KA; Telese F; Liu W; Rosenfeld MG
[Ad] Endereço:Howard Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
[Ti] Título:Glucocorticoid Receptor:MegaTrans Switching Mediates the Repression of an ERα-Regulated Transcriptional Program.
[So] Source:Mol Cell;66(3):321-331.e6, 2017 May 04.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The molecular mechanisms underlying the opposing functions of glucocorticoid receptors (GRs) and estrogen receptor α (ERα) in breast cancer development remain poorly understood. Here we report that, in breast cancer cells, liganded GR represses a large ERα-activated transcriptional program by binding, in trans, to ERα-occupied enhancers. This abolishes effective activation of these enhancers and their cognate target genes, and it leads to the inhibition of ERα-dependent binding of components of the MegaTrans complex. Consistent with the effects of SUMOylation on other classes of nuclear receptors, dexamethasone (Dex)-induced trans-repression of the estrogen E program appears to depend on GR SUMOylation, which leads to stable trans-recruitment of the GR-N-CoR/SMRT-HDAC3 corepressor complex on these enhancers. Together, these results uncover a mechanism by which competitive recruitment of DNA-binding nuclear receptors/transcription factors in trans to hot spot enhancers serves as an effective biological strategy for trans-repression, with clear implications for breast cancer and other diseases.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Receptor alfa de Estrogênio/metabolismo
Regulação Neoplásica da Expressão Gênica
Receptor Cross-Talk
Receptores de Glucocorticoides/metabolismo
Transcrição Genética
[Mh] Termos MeSH secundário: Sítios de Ligação
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Dexametasona/farmacologia
Regulação para Baixo
Elementos Facilitadores Genéticos
Estradiol/farmacologia
Receptor alfa de Estrogênio/agonistas
Receptor alfa de Estrogênio/genética
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Células HEK293
Histona Desacetilases/genética
Histona Desacetilases/metabolismo
Seres Humanos
Células MCF-7
Complexos Multiproteicos
Mutação
Correpressor 1 de Receptor Nuclear/genética
Correpressor 1 de Receptor Nuclear/metabolismo
Correpressor 2 de Receptor Nuclear/genética
Correpressor 2 de Receptor Nuclear/metabolismo
Ligação Proteica
Interferência de RNA
Receptor Cross-Talk/efeitos dos fármacos
Receptores de Glucocorticoides/agonistas
Receptores de Glucocorticoides/genética
Transdução de Sinais
Sumoilação
Transcrição Genética/efeitos dos fármacos
Transcriptoma
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor alpha); 0 (Multiprotein Complexes); 0 (NCOR1 protein, human); 0 (NCOR2 protein, human); 0 (Nuclear Receptor Co-Repressor 1); 0 (Nuclear Receptor Co-Repressor 2); 0 (Receptors, Glucocorticoid); 0 (estrogen receptor alpha, human); 4TI98Z838E (Estradiol); 7S5I7G3JQL (Dexamethasone); EC 3.5.1.98 (Histone Deacetylases); EC 3.5.1.98 (histone deacetylase 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE


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[PMID]:28126478
[Au] Autor:Ziv E; Yarmohammadi H; Boas FE; Petre EN; Brown KT; Solomon SB; Solit D; Reidy D; Erinjeri JP
[Ad] Endereço:Interventional Radiology Service, Department of Radiology, Memorial Sloan Kettering Cancer Center, Howard-118, 1275 York Ave., New York, NY10065. Electronic address: etay.ziv@gmail.com.
[Ti] Título:Gene Signature Associated with Upregulation of the Wnt/ß-Catenin Signaling Pathway Predicts Tumor Response to Transarterial Embolization.
[So] Source:J Vasc Interv Radiol;28(3):349-355.e1, 2017 Mar.
[Is] ISSN:1535-7732
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To identify gene mutations in tumors undergoing transarterial embolization and explore the relationship between gene mutations and tumor response to embolization. MATERIALS AND METHODS: This was a retrospective review that included 17 patients with primary or metastatic liver tumors treated with embolization and had specimens analyzed for a 341-gene panel next-generation sequence assay. Pathologic conditions included hepatocellular, carcinoid, pancreatic neuroendocrine, melanoma, medullary thyroid, and liver acinar-cell carcinoma. Disease, procedure data, and tumor response data were collected. Dimensionality reduction was performed by using principal component analysis. A linear support vector machine was used to learn a prediction rule and identify the genes most predictive of objective tumor response (partial or complete) per modified Response Evaluation Criteria In Solid Tumors. Cross-validation was used to test the prediction on the holdout set. Permutation testing was used to determine statistical significance of prediction accuracy. Recursive feature elimination was used to identify the most predictive genes. RESULTS: At 4 months after embolization, 9 tumors showed a response and 8 did not. Using the top two principal components, prediction accuracy of the gene mutation signature was 70% (±11%), which was statistically significant (P < .05). The most predictive genes were CTNNB1, MEN1, and NCOR1: three genes associated with the Wnt/ß-catenin and hypoxia signaling pathways. CONCLUSIONS: This study identifies gene mutations in tumors treated with transarterial embolization. A gene-mutation signature obtained from the mutation data suggests that upregulation of the Wnt/ß-catenin signaling pathway may be associated with sensitivity to embolization.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Quimioembolização Terapêutica
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/terapia
Transcriptoma
Via de Sinalização Wnt/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Quimioembolização Terapêutica/efeitos adversos
Feminino
Perfilação da Expressão Gênica/métodos
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Modelos Lineares
Neoplasias Hepáticas/patologia
Neoplasias Hepáticas/secundário
Masculino
Meia-Idade
Mutação
Correpressor 1 de Receptor Nuclear/genética
Valor Preditivo dos Testes
Análise de Componente Principal
Proteínas Proto-Oncogênicas/genética
Reprodutibilidade dos Testes
Estudos Retrospectivos
Máquina de Vetores de Suporte
Fatores de Tempo
Resultado do Tratamento
Regulação para Cima
beta Catenina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CTNNB1 protein, human); 0 (MEN1 protein, human); 0 (NCOR1 protein, human); 0 (Nuclear Receptor Co-Repressor 1); 0 (Proto-Oncogene Proteins); 0 (beta Catenin)
[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:170128
[St] Status:MEDLINE


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[PMID]:28057584
[Au] Autor:Schnyder S; Kupr B; Handschin C
[Ad] Endereço:Biozentrum, University of Basel, Klingelbergstrasse 50/70, CH-4056 Basel, Switzerland.
[Ti] Título:Coregulator-mediated control of skeletal muscle plasticity - A mini-review.
[So] Source:Biochimie;136:49-54, 2017 May.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Skeletal muscle plasticity is a complex process entailing massive transcriptional programs. These changes are mediated by the action of nuclear receptors and other transcription factors. In addition, coregulator proteins have emerged as important players in this process by linking transcription factors to the RNA polymerase II complex and inducing changes in the chromatic structure. An accumulating body of work highlights the pleiotropic functions of coregulator proteins in the control of tissue-specific and whole body metabolism. In skeletal muscle, several coregulators have been identified as potent modulators of metabolic and myofibrillar plasticity. In this mini-review, we will discuss the control, function and physiological significance of these coregulators in skeletal muscle biology.
[Mh] Termos MeSH primário: Músculo Esquelético/fisiologia
Coativadores de Receptor Nuclear/fisiologia
[Mh] Termos MeSH secundário: Animais
Histona Acetiltransferases/metabolismo
Histona Desacetilases/metabolismo
Seres Humanos
Correpressor 1 de Receptor Nuclear/fisiologia
Proteína-Arginina N-Metiltransferases/metabolismo
Proteína do Retinoblastoma/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Nuclear Receptor Co-Repressor 1); 0 (Nuclear Receptor Coactivators); 0 (Retinoblastoma Protein); EC 2.1.1.319 (Protein-Arginine N-Methyltransferases); EC 2.3.1.48 (Histone Acetyltransferases); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE


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[PMID]:27925185
[Au] Autor:Pace E; Di Vincenzo S; Ferraro M; Siena L; Chiappara G; Dino P; Vitulo P; Bertani A; Saibene F; Lanata L; Gjomarkaj M
[Ad] Endereço:Institute of Biomedicine and Molecular Immunology, Consiglio Nazionale delle Ricerche, Palermo, Italy.
[Ti] Título:Effects of Carbocysteine and Beclomethasone on Histone Acetylation/Deacetylation Processes in Cigarette Smoke Exposed Bronchial Epithelial Cells.
[So] Source:J Cell Physiol;232(10):2851-2859, 2017 Oct.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Histone deacetylase expression/activity may control inflammation, cell senescence, and responses to corticosteroids. Cigarette smoke exposure, increasing oxidative stress, may negatively affect deacetylase expression/activity. The effects of cigarette smoke extracts (CSE), carbocysteine, and beclomethasone dipropionate on chromatin remodeling processes in human bronchial epithelial cells are largely unknown. The present study was aimed to assess the effects of cigarette smoke, carbocysteine, and beclomethasone dipropionate on histone deacetylase 3 (HDAC3) expression/activity, N-CoR (nuclear receptor corepressor) expression, histone acetyltransferases (HAT) (p300/CBP) expression, p-CREB and IL-1 m-RNA expression, neutrophil chemotaxis. Increased p-CREB expression was observed in the bronchial epithelium of smokers. CSE increased p-CREB expression and decreased HDAC3 expression and activity and N-CoR m-RNA and protein expression. At the same time, CSE increased the expression of the HAT, p300/CBP. All these events increased acetylation processes within the cells and were associated to increased IL-1 m-RNA expression and neutrophil chemotaxis. The incubation of CSE exposed cells with carbocysteine and beclomethasone counteracted the effects of cigarette smoke on HDAC3 and N-CoR but not on p300/CBP. The increased deacetylation processes due to carbocysteine and beclomethasone dipropionate incubation is associated to reduced p-CREB, IL-1 m-RNA expression, neutrophil chemotaxis. These findings suggest a new role of combination therapy with carbocysteine and beclomethasone dipropionate in restoring deacetylation processes compromised by cigarette smoke exposure. J. Cell. Physiol. 232: 2851-2859, 2017. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Beclometasona/farmacologia
Brônquios/efeitos dos fármacos
Carbocisteína/farmacologia
Proteína p300 Associada a E1A/metabolismo
Células Epiteliais/efeitos dos fármacos
Histona Desacetilases/metabolismo
Histonas/metabolismo
Processamento de Proteína Pós-Traducional
Fumaça/efeitos adversos
Fumar/efeitos adversos
[Mh] Termos MeSH secundário: Acetilação
Brônquios/enzimologia
Brônquios/patologia
Linhagem Celular
Quimiotaxia de Leucócito/efeitos dos fármacos
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Citoproteção
Células Epiteliais/enzimologia
Células Epiteliais/patologia
Seres Humanos
Interleucina-1/genética
Interleucina-1/metabolismo
Neutrófilos/efeitos dos fármacos
Neutrófilos/metabolismo
Correpressor 1 de Receptor Nuclear/genética
Correpressor 1 de Receptor Nuclear/metabolismo
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CREB1 protein, human); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Histones); 0 (Interleukin-1); 0 (NCOR1 protein, human); 0 (Nuclear Receptor Co-Repressor 1); 0 (Smoke); 740J2QX53R (Carbocysteine); EC 2.3.1.48 (E1A-Associated p300 Protein); EC 2.3.1.48 (EP300 protein, human); EC 3.5.1.98 (Histone Deacetylases); EC 3.5.1.98 (histone deacetylase 3); KGZ1SLC28Z (Beclomethasone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25710


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[PMID]:27918994
[Au] Autor:Obermoser V; Mauersberger R; Schuster D; Czifersky M; Lipova M; Siegl M; Kintscher U; Gust R
[Ad] Endereço:Department of Pharmaceutical Chemistry, Institute of Pharmacy, Center for Molecular Biosciences Innsbruck, University of Innsbruck, CCB - Centrum for Chemistry and Biomedicine, Innrain 80-82, 6020 Innsbruck, Austria.
[Ti] Título:Importance of 5/6-aryl substitution on the pharmacological profile of 4'-((2-propyl-1H-benzo[d]imidazol-1-yl)methyl)-[1,1'-biphenyl]-2-carboxylic acid derived PPARγ agonists.
[So] Source:Eur J Med Chem;126:590-603, 2017 Jan 27.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:In this structure-activity relationship study, the influence of aryl substituents at position 5 or 6 on the pharmacological profile of the partial PPARγ agonist 4'-((2-propyl-1H-benzo[d]imidazol-1-yl)methyl)-[1,1'-biphenyl]-2-carboxylic acid was investigated. This lead was previously identified as the essential part of telmisartan to induce PPARγ activation. Para-OCH -phenyl substitution strongly increased potency and efficacy independent of the position. Both compounds represent full agonists because of strong hydrophobic contacts with the amino acid Phe363 in the ligand binding domain. Partial agonists with higher potency than telmisartan or the lead were obtained with OH or Cl substituents at the phenyl ring. Molecular modeling suggested additional hydrogen or halogen bonds with Phe360 located at helix 7. It is assumed that these interactions fix helix 7, thereby promoting a partial agonist conformation of the receptor. The theoretical considerations correlate very well with the results from the luciferase transactivation assay using hPPARγ-LBD as well as those from a time-resolved fluorescent resonance energy transfer (TR-FRET) assay in which the coactivator (TRAP220, PGC-1α) recruitment and corepressor (NCoR1) release pattern was investigated.
[Mh] Termos MeSH primário: Benzimidazóis/farmacologia
Benzoatos/farmacologia
PPAR gama/agonistas
[Mh] Termos MeSH secundário: Benzimidazóis/química
Seres Humanos
Modelos Moleculares
Correpressor 1 de Receptor Nuclear/efeitos dos fármacos
Correpressor 1 de Receptor Nuclear/metabolismo
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo
Ligação Proteica
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzimidazoles); 0 (Benzoates); 0 (NCOR1 protein, human); 0 (Nuclear Receptor Co-Repressor 1); 0 (PPAR gamma); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); U5SYW473RQ (telmisartan)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170221
[Lr] Data última revisão:
170221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161206
[St] Status:MEDLINE


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[PMID]:27639592
[Au] Autor:Chen Y; Chen S; Yue Z; Zhang Y; Zhou C; Cao W; Chen X; Zhang L; Liu P
[Ad] Endereço:Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, People's Republic of China; Department of Pharmacy, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, People's Republic of China; National and Local United Engine
[Ti] Título:Receptor-interacting protein 140 overexpression impairs cardiac mitochondrial function and accelerates the transition to heart failure in chronically infarcted rats.
[So] Source:Transl Res;180:91-102.e1, 2017 Feb.
[Is] ISSN:1878-1810
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heart failure (HF) is associated with myocardial energy metabolic abnormality. Receptor-interacting protein 140 (RIP140) is an important transcriptional cofactor for maintaining energy balance in high-oxygen consumption tissues. However, the role of RIP140 in the pathologic processes of HF remains to be elucidated. In this study, we investigated the role of RIP140 in mitochondrial and cardiac functions in rodent hearts under myocardial infarction (MI) stress. MI was created by a permanent ligation of left anterior descending coronary artery and exogenous expression of RIP140 by adenovirus (Ad) vector delivery. Four weeks after MI or Ad-RIP140 treatment, cardiac function was assessed by echocardiographic and hemodynamics analyses, and the mitochondrial function was determined by mitochondrial genes expression, biogenesis, and respiration rates. In Ad-RIP140 or MI group, a subset of metabolic genes changed, accompanied with slight reductions in mitochondrial biogenesis and respiration rates but no change in adenosine triphosphate (ATP) content. Cardiac malfunction was compensated. However, under MI stress, rats overexpressing RIP140 exhibited greater repressions in mitochondrial genes, state 3 respiration rates, respiration control ratio, and ATP content and had further deteriorated cardiac malfunction. In conclusion, RIP140 overexpression leads to comparable cardiac function as resulted from MI, but RIP140 aggravates metabolic repression, mitochondrial malfunction, and further accelerates the transition to HF in response to MI stress.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/complicações
Insuficiência Cardíaca/metabolismo
Mitocôndrias Cardíacas/metabolismo
Infarto do Miocárdio/metabolismo
Miocárdio/metabolismo
Correpressor 1 de Receptor Nuclear/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Adenoviridae/metabolismo
Animais
Respiração Celular
Doença Crônica
Eletrocardiografia
Regulação da Expressão Gênica
Redes Reguladoras de Genes
Vetores Genéticos/metabolismo
Insuficiência Cardíaca/genética
Insuficiência Cardíaca/fisiopatologia
Hemodinâmica
Masculino
Mitocôndrias Cardíacas/ultraestrutura
Infarto do Miocárdio/diagnóstico por imagem
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Miocárdio/patologia
Miocárdio/ultraestrutura
Biogênese de Organelas
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos Sprague-Dawley
Disfunção Ventricular Esquerda
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nuclear Receptor Co-Repressor 1); 0 (RNA, Messenger); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160919
[St] Status:MEDLINE


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[PMID]:27756201
[Au] Autor:Privalsky ML; Snyder CA; Goodson ML
[Ad] Endereço:Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California at Davis, One Shields Avenue, Davis, CA, 95616, USA. mlprivalsky@ucdavis.edu.
[Ti] Título:Corepressor diversification by alternative mRNA splicing is species specific.
[So] Source:BMC Evol Biol;16(1):221, 2016 Oct 19.
[Is] ISSN:1471-2148
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: SMRT and NCoR are corepressor paralogs that help mediate transcriptional repression by a variety of transcription factors, including the nuclear hormone receptors. The functions of both corepressors are extensively diversified in mice by alternative mRNA splicing, generating a series of protein variants that differ in different tissues and that exert different, even diametrically opposite, biochemical and biological effects from one another. RESULTS: We report here that the alternative splicing previously reported for SMRT appears to be a relatively recent evolutionary phenomenon, with only one of these previously identified sites utilized in a teleost fish and a limited additional number of the additional known sites utilized in a bird, reptile, and marsupial. In contrast, extensive SMRT alternative splicing at these sites was detected among the placental mammals. The alternative splicing of NCoR previously identified in mice (and shown to regulate lipid and carbohydrate metabolism) is likely to have arisen separately and after that of SMRT, and includes an example of convergent evolution. CONCLUSIONS: We propose that the functions of both SMRT and NCoR have been diversified by alternative splicing during evolution to allow customization for different purposes in different tissues and different species.
[Mh] Termos MeSH primário: Processamento Alternativo/genética
Proteínas Correpressoras/genética
Evolução Molecular
[Mh] Termos MeSH secundário: Animais
Proteínas Correpressoras/metabolismo
Seres Humanos
Fígado/metabolismo
Camundongos
Correpressor 1 de Receptor Nuclear/genética
Correpressor 1 de Receptor Nuclear/metabolismo
Correpressor 2 de Receptor Nuclear/genética
Correpressor 2 de Receptor Nuclear/metabolismo
Gambás/genética
Sítios de Splice de RNA/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ovinos/genética
Especificidade da Espécie
Xenopus/genética
Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Co-Repressor Proteins); 0 (Nuclear Receptor Co-Repressor 1); 0 (Nuclear Receptor Co-Repressor 2); 0 (RNA Splice Sites); 0 (RNA, Messenger)
[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:161021
[St] Status:MEDLINE


  10 / 495 MEDLINE  
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Texto completo
[PMID]:27545894
[Au] Autor:Takeuchi Y; Yahagi N; Aita Y; Murayama Y; Sawada Y; Piao X; Toya N; Oya Y; Shikama A; Takarada A; Masuda Y; Nishi M; Kubota M; Izumida Y; Yamamoto T; Sekiya M; Matsuzaka T; Nakagawa Y; Urayama O; Kawakami Y; Iizuka Y; Gotoda T; Itaka K; Kataoka K; Nagai R; Kadowaki T; Yamada N; Lu Y; Jain MK; Shimano H
[Ad] Endereço:Nutrigenomics Research Group, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
[Ti] Título:KLF15 Enables Rapid Switching between Lipogenesis and Gluconeogenesis during Fasting.
[So] Source:Cell Rep;16(9):2373-86, 2016 Aug 30.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatic lipogenesis is nutritionally regulated (i.e., downregulated during fasting and upregulated during the postprandial state) as an adaptation to the nutritional environment. While alterations in the expression level of the transcription factor SREBP-1c are known to be critical for nutritionally regulated lipogenesis, upstream mechanisms governing Srebf1 expression remain unclear. Here, we show that the fasting-induced transcription factor KLF15, a key regulator of gluconeogenesis, forms a complex with LXR/RXR, specifically on the Srebf1 promoter. This complex recruits the corepressor RIP140 instead of the coactivator SRC1, resulting in reduced Srebf1 and thus downstream lipogenic enzyme expression during the early and euglycemic period of fasting prior to hypoglycemia and PKA activation. Through this mechanism, KLF15 overexpression specifically ameliorates hypertriglyceridemia without affecting LXR-mediated cholesterol metabolism. These findings reveal a key molecular link between glucose and lipid metabolism and have therapeutic implications for the treatment of hyperlipidemia.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/genética
Genoma
Gluconeogênese/genética
Hepatócitos/metabolismo
Lipogênese/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Animais
Proteínas Quinases Dependentes de AMP Cíclico/genética
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Proteínas de Ligação a DNA/metabolismo
Jejum
Genes Reporter
Hepatócitos/citologia
Fígado/citologia
Fígado/metabolismo
Receptores X do Fígado/genética
Receptores X do Fígado/metabolismo
Luciferases/genética
Luciferases/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos ICR
Camundongos Knockout
Correpressor 1 de Receptor Nuclear/genética
Correpressor 1 de Receptor Nuclear/metabolismo
Cultura Primária de Células
Regiões Promotoras Genéticas
Ligação Proteica
Receptores X Retinoide/genética
Receptores X Retinoide/metabolismo
Transdução de Sinais
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
Fatores de Transcrição/metabolismo
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Klf15 protein, mouse); 0 (Liver X Receptors); 0 (Nuclear Receptor Co-Repressor 1); 0 (Retinoid X Receptors); 0 (Srebf1 protein, mouse); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Transcription Factors); EC 1.13.12.- (Luciferases); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160823
[St] Status:MEDLINE



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