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Pesquisa : D12.776.260.643.039 [Categoria DeCS]
Referências encontradas : 201 [refinar]
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  1 / 201 MEDLINE  
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[PMID]:27714695
[Au] Autor:Sandoval-Hernández A; Contreras MJ; Jaramillo J; Arboleda G
[Ad] Endereço:Grupo de Neurociencias y Muerte Celular, Facultad de Medicina e Instituto de Genética, Universidad Nacional de Colombia, Bogotá, Colombia.
[Ti] Título:Regulation of Oligodendrocyte Differentiation and Myelination by Nuclear Receptors: Role in Neurodegenerative Disorders.
[So] Source:Adv Exp Med Biol;949:287-310, 2016.
[Is] ISSN:0065-2598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During development and through adulthood, differentiation of diverse cell types is controlled by specific genetic and molecular programs for which transcription factors are master regulators of gene expression. Here, we present an overview of the role of nuclear receptors and their selective pharmacological modulators in oligodendrocytes linage, their role in myelination and remyelination and their potential use as a therapeutic strategy for demyelinating diseases. We discuss several aspects of nuclear receptors including: (1) the biochemistry of nuclear receptors superfamily; (2) their role on stem cells physiology, focusing in differentiation and cell removal; (3) the role of nuclear receptor in the oligodendrocytes cell linage, from oligodendrocyte progenitors cells to mature myelinating cells; and (4) the therapeutics opportunities of nuclear receptors for specific demyelinating diseases.
[Mh] Termos MeSH primário: Adrenoleucodistrofia/genética
Doença de Alzheimer/genética
Oligodendroglia/metabolismo
Receptores do Ácido Retinoico/genética
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Adrenoleucodistrofia/tratamento farmacológico
Adrenoleucodistrofia/metabolismo
Adrenoleucodistrofia/patologia
Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/metabolismo
Doença de Alzheimer/patologia
Animais
Fatores de Transcrição COUP/agonistas
Fatores de Transcrição COUP/genética
Fatores de Transcrição COUP/metabolismo
Diferenciação Celular
Linhagem da Célula
Drogas em Investigação/uso terapêutico
Regulação da Expressão Gênica
Seres Humanos
Receptores X do Fígado/agonistas
Receptores X do Fígado/genética
Receptores X do Fígado/metabolismo
Fármacos Neuroprotetores/uso terapêutico
Oligodendroglia/efeitos dos fármacos
Oligodendroglia/patologia
Receptores Ativados por Proliferador de Peroxissomo/agonistas
Receptores Ativados por Proliferador de Peroxissomo/genética
Receptores Ativados por Proliferador de Peroxissomo/metabolismo
Receptores Citoplasmáticos e Nucleares/agonistas
Receptores Citoplasmáticos e Nucleares/genética
Receptores Citoplasmáticos e Nucleares/metabolismo
Receptores do Ácido Retinoico/agonistas
Receptores do Ácido Retinoico/metabolismo
Células-Tronco/efeitos dos fármacos
Células-Tronco/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (COUP Transcription Factors); 0 (Drugs, Investigational); 0 (Liver X Receptors); 0 (NR2E1 protein, human); 0 (Neuroprotective Agents); 0 (Peroxisome Proliferator-Activated Receptors); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Receptors, Retinoic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161008
[St] Status:MEDLINE


  2 / 201 MEDLINE  
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[PMID]:26658017
[Au] Autor:Wu SP; Yu CT; Tsai SY; Tsai MJ
[Ad] Endereço:Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130, USA.
[Ti] Título:Choose your destiny: Make a cell fate decision with COUP-TFII.
[So] Source:J Steroid Biochem Mol Biol;157:7-12, 2016 Mar.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cell fate specification is a critical process to generate cells with a wide range of characteristics from stem and progenitor cells. Emerging evidence demonstrates that the orphan nuclear receptor COUP-TFII serves as a key regulator in determining the cell identity during embryonic development. The present review summarizes our current knowledge on molecular mechanisms by which COUP-TFII employs to define the cell fates, with special emphasis on cardiovascular and renal systems. These novel insights pave the road for future studies of regenerative medicine.
[Mh] Termos MeSH primário: Vasos Sanguíneos/citologia
Fatores de Transcrição COUP/metabolismo
Rim/citologia
Miocárdio/citologia
Células-Tronco/citologia
Células-Tronco/fisiologia
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição COUP/genética
Diferenciação Celular
Regulação da Expressão Gênica no Desenvolvimento
Coração/embriologia
Átrios do Coração/citologia
Átrios do Coração/embriologia
Seres Humanos
Rim/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (COUP Transcription Factors)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170301
[Lr] Data última revisão:
170301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[St] Status:MEDLINE


  3 / 201 MEDLINE  
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[PMID]:26387951
[Au] Autor:Hermann-Kleiter N; Klepsch V; Wallner S; Siegmund K; Klepsch S; Tuzlak S; Villunger A; Kaminski S; Pfeifhofer-Obermair C; Gruber T; Wolf D; Baier G
[Ad] Endereço:Translational Cell Genetics, Department for Pharmacology and Genetics, Medical University of Innsbruck, 6020 Innsbruck, Austria. Electronic address: natascha.kleiter@i-med.ac.at.
[Ti] Título:The Nuclear Orphan Receptor NR2F6 Is a Central Checkpoint for Cancer Immune Surveillance.
[So] Source:Cell Rep;12(12):2072-85, 2015 Sep 29.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nuclear receptor subfamily 2, group F, member 6 (NR2F6) is an orphan member of the nuclear receptor superfamily. Here, we show that genetic ablation of Nr2f6 significantly improves survival in the murine transgenic TRAMP prostate cancer model. Furthermore, Nr2f6(-/-) mice spontaneously reject implanted tumors and develop host-protective immunological memory against tumor rechallenge. This is paralleled by increased frequencies of both CD4(+) and CD8(+) T cells and higher expression levels of interleukin 2 and interferon γ at the tumor site. Mechanistically, CD4(+) and CD8(+) T cell-intrinsic NR2F6 acts as a direct repressor of the NFAT/AP-1 complex on both the interleukin 2 and the interferon γ cytokine promoters, attenuating their transcriptional thresholds. Adoptive transfer of Nr2f6-deficient T cells into tumor-bearing immunocompetent mice is sufficient to delay tumor outgrowth. Altogether, this defines NR2F6 as an intracellular immune checkpoint in effector T cells, governing the amplitude of anti-cancer immunity.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Fatores de Transcrição COUP/genética
Vigilância Imunológica
Imunoterapia Adotiva/métodos
Neoplasias da Próstata/terapia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/citologia
Linfócitos T CD4-Positivos/transplante
Linfócitos T CD8-Positivos/citologia
Linfócitos T CD8-Positivos/transplante
Fatores de Transcrição COUP/deficiência
Fatores de Transcrição COUP/imunologia
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Memória Imunológica
Interferon gama/agonistas
Interferon gama/genética
Interferon gama/imunologia
Interleucina-2/agonistas
Interleucina-2/genética
Interleucina-2/imunologia
Ativação Linfocitária
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Transplante de Neoplasias
Neoplasias da Próstata/genética
Neoplasias da Próstata/imunologia
Neoplasias da Próstata/mortalidade
Transdução de Sinais
Análise de Sobrevida
Fator de Necrose Tumoral alfa/agonistas
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COUP Transcription Factors); 0 (Interleukin-2); 0 (Nr2f6 protein, mouse); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:151029
[Lr] Data última revisão:
151029
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150922
[St] Status:MEDLINE


  4 / 201 MEDLINE  
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[PMID]:25505127
[Au] Autor:Peláez-García A; Barderas R; Batlle R; Viñas-Castells R; Bartolomé RA; Torres S; Mendes M; Lopez-Lucendo M; Mazzolini R; Bonilla F; García de Herreros A; Casal JI
[Ad] Endereço:From the ‡Department of Cellular and Molecular Medicine, Centro de Investigaciones Biológicas (CIB-CSIC), Madrid, Spain;
[Ti] Título:A proteomic analysis reveals that Snail regulates the expression of the nuclear orphan receptor Nuclear Receptor Subfamily 2 Group F Member 6 (Nr2f6) and interleukin 17 (IL-17) to inhibit adipocyte differentiation.
[So] Source:Mol Cell Proteomics;14(2):303-15, 2015 Feb.
[Is] ISSN:1535-9484
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adipogenesis requires a differentiation program driven by multiple transcription factors, where PPARγ and C/EBPα play a central role. Recent findings indicate that Snail inhibits adipocyte differentiation in 3T3-L1 and murine mesenchymal stem cells (mMSC). An in-depth quantitative SILAC analysis of the nuclear fraction of Snail-induced alterations of 3T3-L1 cells was carried out. In total, 2251 overlapping proteins were simultaneously quantified in forward and reverse experiments. We observed 574 proteins deregulated by Snail1 using a fold-change ≥1.5, with 111 up- and 463 down-regulated proteins, respectively. Among other proteins, multiple transcription factors such as Trip4, OsmR, Nr2f6, Cbx6, and Prrx1 were down-regulated. Results were validated in 3T3-L1 cells and mMSC cells by Western blot and quantitative PCR. Knock-down experiments in 3T3-L1 cells demonstrated that only Nr2f6 (and Trip4 at minor extent) was required for adipocyte differentiation. Ectopic expression of Nr2f6 reversed the effects of Snail1 and promoted adipogenesis. Because Nr2f6 inhibits the expression of IL-17, we tested the effect of Snail on IL-17 expression. IL-17 and TNFα were among the most up-regulated pro-inflammatory cytokines in Snail-transfected 3T3-L1 and mMSC cells. Furthermore, the blocking of IL-17 activity in Snail-transfected cells promoted adipocyte differentiation, reverting Snail inhibition. In summary, Snail inhibits adipogenesis through a down-regulation of Nr2f6, which in turn facilitates the expression of IL-17, an anti-adipogenic cytokine. These results would support a novel and important role for Snail and Nr2f6 in obesity control.
[Mh] Termos MeSH primário: Adipócitos/citologia
Adipócitos/metabolismo
Fatores de Transcrição COUP/metabolismo
Diferenciação Celular
Interleucina-17/metabolismo
Proteômica/métodos
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipogenia
Animais
Extratos Celulares
Núcleo Celular/metabolismo
Regulação para Baixo
Células Mesenquimais Estromais/metabolismo
Camundongos
Modelos Biológicos
Reprodutibilidade dos Testes
Transdução de Sinais
Fatores de Transcrição da Família Snail
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COUP Transcription Factors); 0 (Cell Extracts); 0 (Interleukin-17); 0 (Nr2f6 protein, mouse); 0 (Snai1 protein, mouse); 0 (Snail Family Transcription Factors); 0 (Transcription Factors)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141216
[St] Status:MEDLINE
[do] DOI:10.1074/mcp.M114.045328


  5 / 201 MEDLINE  
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[PMID]:24878540
[Au] Autor:Tang K; Tsai SY; Tsai MJ
[Ad] Endereço:Institute of Life Science, Nanchang University, Nanchang, Jiangxi 330031, China; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: ktang.sc@gmail.com.
[Ti] Título:COUP-TFs and eye development.
[So] Source:Biochim Biophys Acta;1849(2):201-9, 2015 Feb.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Recent studies reveal that COUP-TF genes are essential for neural development, cardiovascular development, energy metabolism and adipogenesis, as well as for organogenesis of multiple systems. In this review, we mainly describe the COUP-TF genes, molecular mechanisms of COUP-TF action, and their crucial functions in the morphogenesis of the murine eye. Mutations of COUP-TF genes lead to the congenital coloboma and/or optic atrophy in both mouse and human, indicating that the study on COUP-TFs and the eye will benefit our understanding of the etiology of human ocular diseases. This article is part of a Special Issue entitled: Nuclear receptors in animal development.
[Mh] Termos MeSH primário: Fatores de Transcrição COUP/fisiologia
Olho/embriologia
Organogênese/genética
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição COUP/genética
Drosophila/embriologia
Drosophila/genética
Olho/metabolismo
Oftalmopatias/genética
Seres Humanos
Camundongos/embriologia
Camundongos/genética
Xenopus/embriologia
Xenopus/genética
Peixe-Zebra/embriologia
Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (COUP Transcription Factors)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140601
[St] Status:MEDLINE


  6 / 201 MEDLINE  
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[PMID]:25455729
[Au] Autor:Roshan-Moniri M; Hsing M; Butler MS; Cherkasov A; Rennie PS
[Ti] Título:Orphan nuclear receptors as drug targets for the treatment of prostate and breast cancers.
[So] Source:Cancer Treat Rev;40(10):1137-52, 2014 Dec.
[Is] ISSN:1532-1967
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Nuclear receptors (NRs), a family of 48 transcriptional factors, have been studied intensively for their roles in cancer development and progression. The presence of distinctive ligand binding sites capable of interacting with small molecules has made NRs attractive targets for developing cancer therapeutics. In particular, a number of drugs have been developed over the years to target human androgen- and estrogen receptors for the treatment of prostate cancer and breast cancer. In contrast, orphan nuclear receptors (ONRs), which in many cases lack known biological functions or ligands, are still largely under investigated. This review is a summary on ONRs that have been implicated in prostate and breast cancers, specifically retinoic acid-receptor-related orphan receptors (RORs), liver X receptors (LXRs), chicken ovalbumin upstream promoter transcription factors (COUP-TFs), estrogen related receptors (ERRs), nerve growth factor 1B-like receptors, and ''dosage-sensitive sex reversal, adrenal hypoplasia critical region, on chromosome X, gene 1'' (DAX1). Discovery and development of small molecules that can bind at various functional sites on these ONRs will help determine their biological functions. In addition, these molecules have the potential to act as prototypes for future drug development. Ultimately, the therapeutic value of targeting the ONRs may go well beyond prostate and breast cancers.
[Mh] Termos MeSH primário: Neoplasias da Mama/tratamento farmacológico
Terapia de Alvo Molecular/métodos
Receptores Nucleares Órfãos/metabolismo
Neoplasias da Próstata/tratamento farmacológico
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Neoplasias da Mama/metabolismo
Fator I de Transcrição COUP/metabolismo
Fatores de Transcrição COUP/metabolismo
Receptor Nuclear Órfão DAX-1/metabolismo
Feminino
Seres Humanos
Receptores X do Fígado
Masculino
Proteínas de Membrana Transportadoras/metabolismo
Membro 1 do Grupo F da Subfamília 1 de Receptores Nucleares/metabolismo
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Neoplasias da Próstata/metabolismo
Bibliotecas de Moléculas Pequenas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (COUP Transcription Factor I); 0 (COUP Transcription Factors); 0 (DAX-1 Orphan Nuclear Receptor); 0 (Liver X Receptors); 0 (Membrane Transport Proteins); 0 (NR0B1 protein, human); 0 (NR2F1 protein, human); 0 (NR4A2 protein, human); 0 (Nuclear Receptor Subfamily 1, Group F, Member 1); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (OSCP1 protein, human); 0 (Orphan Nuclear Receptors); 0 (RORA protein, human); 0 (Small Molecule Libraries)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141203
[St] Status:MEDLINE
[do] DOI:10.1016/j.ctrv.2014.10.005


  7 / 201 MEDLINE  
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[PMID]:25386650
[Au] Autor:Kalampoki LG; Flytzanis CN
[Ad] Endereço:Department of Biology, University of Patras, Patras 26504, Greece.
[Ti] Título:Cis-regulatory control of the nuclear receptor Coup-TF gene in the sea urchin Paracentrotus lividus embryo.
[So] Source:PLoS One;9(11):e109274, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Coup-TF, an orphan member of the nuclear receptor super family, has a fundamental role in the development of metazoan embryos. The study of the gene's regulatory circuit in the sea urchin embryo will facilitate the placement of this transcription factor in the well-studied embryonic Gene Regulatory Network (GRN). The Paracentrotus lividus Coup-TF gene (PlCoup-TF) is expressed throughout embryonic development preferentially in the oral ectoderm of the gastrula and the ciliary band of the pluteus stage. Two overlapping λ genomic clones, containing three exons and upstream sequences of PlCoup-TF, were isolated from a genomic library. The transcription initiation site was determined and 5' deletions and individual segments of a 1930 bp upstream region were placed ahead of a GFP reporter cassette and injected into fertilized P.lividus eggs. Module a (-532 to -232), was necessary and sufficient to confer ciliary band expression to the reporter. Comparison of P.lividus and Strongylocentrotus purpuratus upstream Coup-TF sequences, revealed considerable conservation, but none within module a. 5' and internal deletions into module a, defined a smaller region that confers ciliary band specific expression. Putative regulatory cis-acting elements (RE1, RE2 and RE3) within module a, were specifically bound by proteins in sea urchin embryonic nuclear extracts. Site-specific mutagenesis of these elements resulted in loss of reporter activity (RE1) or ectopic expression (RE2, RE3). It is proposed that sea urchin transcription factors, which bind these three regulatory sites, are necessary for spatial and quantitative regulation of the PlCoup-TF gene at pluteus stage sea urchin embryos. These findings lead to the future identification of these factors and to the hierarchical positioning of PlCoup-TF within the embryonic GRN.
[Mh] Termos MeSH primário: Fatores de Transcrição COUP/genética
Regulação da Expressão Gênica no Desenvolvimento/genética
Paracentrotus/genética
Sequências Reguladoras de Ácido Nucleico/genética
Sítio de Iniciação de Transcrição
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Clonagem Molecular
Proteínas de Ligação a DNA/genética
Ensaio de Desvio de Mobilidade Eletroforética
Embrião não Mamífero
Paracentrotus/embriologia
Receptores Citoplasmáticos e Nucleares/genética
Deleção de Sequência/genética
Strongylocentrotus purpuratus/genética
Iniciação da Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COUP Transcription Factors); 0 (DNA-Binding Proteins); 0 (Receptors, Cytoplasmic and Nuclear)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:141112
[Lr] Data última revisão:
141112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0109274


  8 / 201 MEDLINE  
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[PMID]:24919548
[Au] Autor:Hermann-Kleiter N; Baier G
[Ad] Endereço:Department for Pharmacology and Genetics, Translational Cell Genetics, Medical University of Innsbruck, Peter Mayr Str, 1a, A-6020, Innsbruck, Austria. natascha.kleiter@i-med.ac.at.
[Ti] Título:Orphan nuclear receptor NR2F6 acts as an essential gatekeeper of Th17 CD4+ T cell effector functions.
[So] Source:Cell Commun Signal;12:38, 2014 Jun 12.
[Is] ISSN:1478-811X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Members of the evolutionarily conserved family of the chicken ovalbumin upstream promoter transcription factor NR2F/COUP-TF orphan receptors have been implicated in lymphocyte biology, ranging from activation to differentiation and elicitation of immune effector functions. In particular, a CD4+ T cell intrinsic and non-redundant function of NR2F6 as a potent and selective repressor of the transcription of the pro-inflammatory cytokines interleukin (Il) 2, interferon y (ifng) and consequently of T helper (Th)17 CD4+ T cell-mediated autoimmune disorders has been discovered. NR2F6 serves as an antigen receptor signaling threshold-regulated barrier against autoimmunity where NR2F6 is part of a negative feedback loop that limits inflammatory tissue damage induced by weakly immunogenic antigens such as self-antigens. Under such low affinity antigen receptor stimulation, NR2F6 appears as a prototypical repressor that functions to "lock out" harmful Th17 lineage effector transcription. Mechanistically, only sustained high affinity antigen receptor-induced protein kinase C (PKC)-mediated phosphorylation has been shown to inactivate NR2F6, thereby displacing pre-bound NR2F6 from the DNA and, subsequently, allowing for robust NFAT/AP-1- and RORγt-mediated cytokine transcription. The NR2F6 target gene repertoire thus identifies a general anti-inflammatory gatekeeper role for this orphan receptor. Investigating these signaling pathway(s) will enable a greater knowledge of the genetic, immune, and environmental mechanisms that lead to chronic inflammation and of certain autoimmune disorders in a given individual.
[Mh] Termos MeSH primário: Fatores de Transcrição COUP/metabolismo
Células Th17/metabolismo
[Mh] Termos MeSH secundário: Animais
Autoimunidade
Fatores de Transcrição COUP/química
Fatores de Transcrição COUP/genética
Citocinas/genética
Citocinas/metabolismo
Seres Humanos
Inflamação/imunologia
Inflamação/metabolismo
Células Th17/imunologia
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (COUP Transcription Factors); 0 (Cytokines)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140613
[St] Status:MEDLINE
[do] DOI:10.1186/1478-811X-12-38


  9 / 201 MEDLINE  
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[PMID]:24465611
[Au] Autor:Ogawa D; Eguchi J; Wada J; Terami N; Hatanaka T; Tachibana H; Nakatsuka A; Horiguchi CS; Nishii N; Makino H
[Ad] Endereço:Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan ; Department of Diabetic Nephropathy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
[Ti] Título:Nuclear hormone receptor expression in mouse kidney and renal cell lines.
[So] Source:PLoS One;9(1):e85594, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nuclear hormone receptors (NHRs) are transcription factors that regulate carbohydrate and lipid metabolism, immune responses, and inflammation. Although several NHRs, including peroxisome proliferator-activated receptor-γ (PPARγ) and PPARα, demonstrate a renoprotective effect in the context of diabetic nephropathy (DN), the expression and role of other NHRs in the kidney are still unrecognized. To investigate potential roles of NHRs in the biology of the kidney, we used quantitative real-time polymerase chain reaction to profile the expression of all 49 members of the mouse NHR superfamily in mouse kidney tissue (C57BL/6 and db/m), and cell lines of mesangial (MES13), podocyte (MPC), proximal tubular epithelial (mProx24) and collecting duct (mIMCD3) origins in both normal and high-glucose conditions. In C57BL/6 mouse kidney cells, hepatocyte nuclear factor 4α, chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) and COUP-TFIII were highly expressed. During hyperglycemia, the expression of the NHR 4A subgroup including neuron-derived clone 77 (Nur77), nuclear receptor-related factor 1, and neuron-derived orphan receptor 1 significantly increased in diabetic C57BL/6 and db/db mice. In renal cell lines, PPARδ was highly expressed in mesangial and proximal tubular epithelial cells, while COUP-TFs were highly expressed in podocytes, proximal tubular epithelial cells, and collecting duct cells. High-glucose conditions increased the expression of Nur77 in mesangial and collecting duct cells, and liver x receptor α in podocytes. These data demonstrate NHR expression in mouse kidney cells and cultured renal cell lines and suggest potential therapeutic targets in the kidney for the treatment of DN.
[Mh] Termos MeSH primário: Nefropatias Diabéticas/genética
Expressão Gênica
Rim/metabolismo
Receptores Citoplasmáticos e Nucleares/genética
[Mh] Termos MeSH secundário: Animais
Fator II de Transcrição COUP/genética
Fator II de Transcrição COUP/metabolismo
Fatores de Transcrição COUP/genética
Fatores de Transcrição COUP/metabolismo
Linhagem Celular
Células Cultivadas
Nefropatias Diabéticas/metabolismo
Rim/citologia
Túbulos Renais/citologia
Túbulos Renais/metabolismo
Masculino
Células Mesangiais/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Microscopia de Fluorescência
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Podócitos/metabolismo
Receptores Citoplasmáticos e Nucleares/classificação
Receptores Citoplasmáticos e Nucleares/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COUP Transcription Factor II); 0 (COUP Transcription Factors); 0 (Nr2f6 protein, mouse); 0 (Nr4a1 protein, mouse); 0 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Receptors, Cytoplasmic and Nuclear)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:150515
[Lr] Data última revisão:
150515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0085594


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[PMID]:24096122
[Au] Autor:Ichim CV; Dervovic DD; Zúñiga-Pflücker JC; Wells RA
[Ad] Endereço:Department of Medical Biophysics, University of Toronto, Toronto, Canada; Biological Sciences, Sunnybrook Research Institute, Toronto, Canada; Salk Institute for Biological Studies, La Jolla, CA, USA.
[Ti] Título:The orphan nuclear receptor Ear-2 (Nr2f6) is a novel negative regulator of T cell development.
[So] Source:Exp Hematol;42(1):46-58, 2014 Jan.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We describe a novel role for the orphan nuclear receptor Ear-2 in regulating T cell development. Retrovirus-mediated overexpression of Ear-2 (EAR-2++) in a bone marrow (BM) transplantation assay resulted in limited T cell development and a greater than tenfold decrease in thymus size and cellularity relative to controls. Ear-2-transduced murine BM hematopoietic stem cells (HSCs) in OP9-DL1 cultures showed a proliferation deficit during days 1-5 after induction of differentiation, which corresponded to increased expression of the cell cycle regulators p21 (cdkn1a) and p27 (cdkn1b), as well as increased expression of Hes1, Notch3, Egr1, and Scl (Tal1) and decreased expression of Gli1, Gfi-1, HoxA9, PU.1, Nrarp, and Tcf1. In addition, there was a block in differentiation at the DN4 to double-positive (DP) transition accompanied by an increase in apoptosis, similar to the deficit seen in the RORγt null mouse. Gene expression profiling revealed that, like the RORγt-deficient mouse, EAR-2++ DP cells had decreased expression of BclXL and increased expression of the proapoptosis gene Bad. In addition, EAR-2++ DP cells had decreased expression of Bcl11b, PU.1, and HoxA9, and increased expression of Id2. Based on these findings, we conclude that EAR-2++ cells were able to migrate to, but not fully repopulate, the thymus because of a cell-intrinsic defect in the proliferation of DN1 cells followed by a block in differentiation from the DN4 to DP stage of T cell development. We conclude that Ear-2 is a novel negative regulator of T-cell development and that downregulation of Ear-2 is indispensable for the proliferation of DN1 cells and the survival of DN4-DP cells.
[Mh] Termos MeSH primário: Fatores de Transcrição COUP/fisiologia
Linfócitos T/fisiologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Diferenciação Celular
Regulação da Expressão Gênica
Células-Tronco Hematopoéticas/citologia
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COUP Transcription Factors); 0 (Nr2f6 protein, mouse)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:131216
[Lr] Data última revisão:
131216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131008
[St] Status:MEDLINE



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