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Pesquisa : D12.776.260.643.430 [Categoria DeCS]
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  1 / 13 MEDLINE  
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[PMID]:28808448
[Au] Autor:Malhotra SS; Gupta SK
[Ad] Endereço:Reproductive Cell Biology Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, -110 067 India.
[Ti] Título:Relevance of the NR4A sub-family of nuclear orphan receptors in trophoblastic BeWo cell differentiation.
[So] Source:Cell Mol Biol Lett;22:15, 2017.
[Is] ISSN:1689-1392
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nur-77, a member of the NR4A sub-family of nuclear orphan receptors, is downregulated in the placentae of pre-eclamptic women. Here, we investigate the relevance of Nor-1, Nurr-1 and Nur-77 in trophoblastic cell differentiation. Their transcript levels were found to be significantly upregulated in BeWo cells treated with forskolin. The maximum increase was observed after 2 h, with a second peak in the expression levels after 48 h. The expression of NR4A sub-family members was also found to be upregulated in BeWo cells after treatment with hCG and GnRH. A similar significant increase was observed at the respective protein levels after 2 and 48 h of treatment with forskolin, hCG or GnRH. Silencing Nor-1, Nurr-1 or Nur-77 individually did not show any effect on forskolin-, hCG- and/or GnRH-mediated BeWo cell fusion and/or hCG secretion. After silencing any one member of the NR4A sub-family, an increase in the transcript levels of the other sub-family members was observed, indicating a compensatory effect due to their functional redundancy. Simultaneously silencing all three NR4A sub-family members significantly downregulated forskolin- and hCG-mediated BeWo cell fusion and/or hCG secretion. However, a considerable amount of cell death occurred after forskolin or hCG treatment as compared to the control siRNA-transfected cells. These results suggest that the NR4A sub-family of nuclear orphan receptors has a role in trophoblastic cell differentiation.
[Mh] Termos MeSH primário: Diferenciação Celular
Receptores Nucleares Órfãos/fisiologia
Trofoblastos/metabolismo
[Mh] Termos MeSH secundário: Gonadotropina Coriônica Humana Subunidade beta/farmacologia
Colforsina/farmacologia
Regulação da Expressão Gênica no Desenvolvimento
Hormônio Liberador de Gonadotropina/farmacologia
Seres Humanos
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/fisiologia
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/fisiologia
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/fisiologia
Receptores Nucleares Órfãos/genética
Trofoblastos/efeitos dos fármacos
Trofoblastos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chorionic Gonadotropin, beta Subunit, Human); 0 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3); 0 (Orphan Nuclear Receptors); 1F7A44V6OU (Colforsin); 33515-09-2 (Gonadotropin-Releasing Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1186/s11658-017-0046-0


  2 / 13 MEDLINE  
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[PMID]:28637666
[Au] Autor:Prince LR; Prosseda SD; Higgins K; Carlring J; Prestwich EC; Ogryzko NV; Rahman A; Basran A; Falciani F; Taylor P; Renshaw SA; Whyte MKB; Sabroe I
[Ad] Endereço:Department of Infection, Immunity and Cardiovascular Disease and.
[Ti] Título:NR4A orphan nuclear receptor family members, NR4A2 and NR4A3, regulate neutrophil number and survival.
[So] Source:Blood;130(8):1014-1025, 2017 Aug 24.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The lifespan of neutrophils is plastic and highly responsive to factors that regulate cellular survival. Defects in neutrophil number and survival are common to both hematologic disorders and chronic inflammatory diseases. At sites of inflammation, neutrophils respond to multiple signals that activate protein kinase A (PKA) signaling, which positively regulates neutrophil survival. The aim of this study was to define transcriptional responses to PKA activation and to delineate the roles of these factors in neutrophil function and survival. In human neutrophil gene array studies, we show that PKA activation upregulates a significant number of apoptosis-related genes, the most highly regulated of these being and Direct PKA activation by the site-selective PKA agonist pair N6/8-AHA (8-AHA-cAMP and N6-MB-cAMP) and treatment with endogenous activators of PKA, including adenosine and prostaglandin E2, results in a profound delay of neutrophil apoptosis and concomitant upregulation of NR4A2/3 in a PKA-dependent manner. NR4A3 expression is also increased at sites of neutrophilic inflammation in a human model of intradermal inflammation. PKA activation also promotes survival of murine neutrophil progenitor cells, and small interfering RNA to decreases neutrophil production in this model. Antisense knockdown of and homologs in zebrafish larvae significantly reduces the absolute neutrophil number without affecting cellular migration. In summary, we show that NR4A2 and NR4A3 are components of a downstream transcriptional response to PKA activation in the neutrophil, and that they positively regulate neutrophil survival and homeostasis.
[Mh] Termos MeSH primário: Neutrófilos/citologia
Neutrófilos/metabolismo
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Contagem de Células
Proliferação Celular
Sobrevivência Celular
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Dinoprostona/metabolismo
Ativação Enzimática
Deleção de Genes
Técnicas de Silenciamento de Genes
Seres Humanos
Inflamação/patologia
Larva/metabolismo
Camundongos
Família Multigênica
Análise de Sequência com Séries de Oligonucleotídeos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reprodutibilidade dos Testes
Transdução de Sinais
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3); 0 (RNA, Messenger); 0 (RNA, Small Interfering); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-03-770164


  3 / 13 MEDLINE  
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[PMID]:26600038
[Au] Autor:Sambri I; Crespo J; Aguiló S; Ingrosso D; Rodríguez C; Martínez González J
[Ad] Endereço:Centro de Investigación Cardiovascular (CSIC-ICCC), IIB-Sant Pau, Barcelona, Spain.
[Ti] Título:miR-17 and -20a Target the Neuron-Derived Orphan Receptor-1 (NOR-1) in Vascular Endothelial Cells.
[So] Source:PLoS One;10(11):e0141932, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuron-derived orphan receptor-1 (NOR-1) plays a major role in vascular biology by controlling fibroproliferative and inflammatory responses. Because microRNAs (miRNAs) have recently emerged as key players in the regulation of gene expression in the vasculature, here we have investigated the regulation of NOR-1 by miRNAs in endothelial cells. Computational algorithms suggest that NOR-1 could be targeted by members of the miR-17 family. Accordingly, ectopic over-expression of miR-17 or miR-20a in endothelial cells using synthetic premiRNAs attenuated the up-regulation of NOR-1 expression induced by VEGF (as evidenced by real time PCR, Western blot and immunocitochemistry). Conversely, the antagonism of these miRNAs by specific antagomirs prevented the down-regulation of NOR-1 promoted by miR-17 or miR-20a in VEGF-stimulated cells. Disruption of the miRNA-NOR-1 mRNA interaction using a custom designed target protector evidenced the selectivity of these responses. Further, luciferase reporter assays and seed-sequence mutagenesis confirmed that miR-17 and -20a bind to NOR-1 3'-UTR. Finally, miR-17 and -20a ameliorated the up-regulation of VCAM-1 mediated by NOR-1 in VEGF-stimulated cells. Therefore, miR-17 and -20a target NOR-1 thereby regulating NOR-1-dependent gene expression.
[Mh] Termos MeSH primário: Células Endoteliais da Veia Umbilical Humana/metabolismo
MicroRNAs/metabolismo
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Sequência de Bases
Sítios de Ligação
Biologia Computacional
Regulação para Baixo/genética
Seres Humanos
MicroRNAs/genética
Dados de Sequência Molecular
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MIRN17 microRNA, human); 0 (MIRN20 microRNA, human); 0 (MicroRNAs); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3); 0 (RNA, Messenger)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:151203
[Lr] Data última revisão:
151203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0141932


  4 / 13 MEDLINE  
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[PMID]:26150530
[Au] Autor:Crean D; Cummins EP; Bahar B; Mohan H; McMorrow JP; Murphy EP
[Ad] Endereço:UCD Veterinary Sciences Centre, University College Dublin, Belfield, Dublin 4, Ireland; and Conway Institute for Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland.
[Ti] Título:Adenosine Modulates NR4A Orphan Nuclear Receptors To Attenuate Hyperinflammatory Responses in Monocytic Cells.
[So] Source:J Immunol;195(4):1436-48, 2015 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adenosine receptor-mediated regulation of monocyte/macrophage inflammatory responses is critical in the maintenance of tissue homeostasis. In this study, we reveal that adenosine potently modulates the expression of NR4A1, 2, and 3 orphan nuclear receptors in myeloid cells, and this modulation is primarily through the adenosine A2a receptor subtype. We demonstrate that A2a receptor activation of NR4A1-3 receptor synthesis is further enhanced in TLR4-stimulated monocytes. After TLR4 stimulation, NR4A receptor-depleted monocyte/macrophage cells display significantly altered expression of cell-surface markers and produce increased inflammatory cytokine and chemokine secretion rendering the cells an enhanced proinflammatory phenotype. Exposure of TLR4 or TNF-α-stimulated monocytes to adenosine analogs directs changes in the expression of MIP-3α and IL-23p19, with NR4A2 depletion leading to significantly enhanced expression of these factors. Furthermore, we establish that nuclear levels of NF-κB/p65 are increased in TLR/adenosine-stimulated NR4A2-depleted cells. We show that, after TLR/adenosine receptor stimulation, NR4A2 depletion promotes significant binding of NF-κB/p65 to a κB consensus binding motif within the MIP-3α proximal promoter leading to increased protein secretion, confirming a pivotal role for NF-κB activity in controlling cellular responses and gene expression outcomes in response to these mediators. Thus, these data demonstrate that during an inflammatory response, adenosine modulation of NR4A receptor activity acts to limit NF-κB-mediated effects and that loss of NR4A2 expression leads to enhanced NF-κB activity and hyperinflammatory responses in myeloid cells.
[Mh] Termos MeSH primário: Adenosina/metabolismo
Monócitos/imunologia
Monócitos/metabolismo
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Quimiocina CCL20/genética
Proteínas de Ligação a DNA/genética
Regulação da Expressão Gênica
Seres Humanos
Hipersensibilidade/genética
Hipersensibilidade/imunologia
Hipersensibilidade/metabolismo
Inflamação/genética
Inflamação/imunologia
Inflamação/metabolismo
Subunidade p19 da Interleucina-23/metabolismo
Macrófagos/imunologia
Macrófagos/metabolismo
Camundongos
Modelos Biológicos
NF-kappa B/metabolismo
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Receptores Nucleares Órfãos
Receptor A2A de Adenosina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CCL20); 0 (DNA-Binding Proteins); 0 (Interleukin-23 Subunit p19); 0 (NF-kappa B); 0 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3); 0 (Orphan Nuclear Receptors); 0 (Receptor, Adenosine A2A); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:150808
[Lr] Data última revisão:
150808
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150708
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1402039


  5 / 13 MEDLINE  
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[PMID]:24056879
[Au] Autor:Ariës IM; van den Dungen ES; Pieters R; den Boer ML
[Ad] Endereço:Department of Pediatric Oncology/Hematology, Erasmus Medical Center-Sophia Children's Hospital, Rotterdam, The Netherlands.
[Ti] Título:The NR4A orphan nuclear receptors do not confer prednisolone resistance in pediatric acute lymphoblastic leukemia.
[So] Source:Leukemia;28(2):422-5, 2014 Feb.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Resistência a Medicamentos Antineoplásicos/genética
Receptores Nucleares Órfãos/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
[Mh] Termos MeSH secundário: Animais
Criança
Técnicas de Silenciamento de Genes
Seres Humanos
Camundongos
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Transcriptoma
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3); 0 (Orphan Nuclear Receptors)
[Em] Mês de entrada:1404
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130924
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2013.275


  6 / 13 MEDLINE  
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[PMID]:23104421
[Au] Autor:Zhu X; Walton RG; Tian L; Luo N; Ho SR; Fu Y; Garvey WT
[Ad] Endereço:Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294-3360, USA. xiaolin@uab.edu
[Ti] Título:Prostaglandin A2 enhances cellular insulin sensitivity via a mechanism that involves the orphan nuclear receptor NR4A3.
[So] Source:Horm Metab Res;45(3):213-20, 2013 Mar.
[Is] ISSN:1439-4286
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:We have previously reported that members of the NR4A family of orphan nuclear receptors can augment insulin's ability to stimulate glucose transport in adipocytes. In the current study, we endeavored to test for an insulin-sensitizing effect in muscle cells and to identify a potential transactivator. Lentiviral constructs were used to engineer both hyperexpression and shRNA silencing of NR4A3 in C2C12 myocytes. The NR4A3 hyper-expression construct led to a significant increase in glucose transport rates in the presence of maximal insulin while the NR4A3 knock-down exhibited a significant reduction in insulin-stimulated glucose transport rates. Consistently, insulin-mediated AKT phosphorylation was increased by NR4A3 hyperexpression and decreased following shRNA NR4A3 suppression. Then, we examined effects of prostaglandin A2 (PGA2) on insulin action and NR4A3 transactivation. PGA2 augmented insulin-stimulated glucose uptake in C2C12 myocytes and AKT phosphorylation after 12-h treatment, without significant effects on basal transport or basal AKT phosphorylation. More importantly, we demonstrated that PGA2 led to a greater improvement in insulin-stimulated glucose rates in NR4A3 overexpressing C2C12 myocytes, when compared with Lac-Z controls stimulated with insulin and PGA2. Moreover, the sensitizing effect of PGA2 was significantly diminished in NR4A3 knockdown myocytes compared to scramble controls. These results show for the first time that: (i) PGA2 augments insulin action in myocytes as manifested by enhanced stimulation of glucose transport and AKT phosphorylation; and (ii) the insulin sensitizing effect is dependent upon the orphan nuclear receptor NR4A3.
[Mh] Termos MeSH primário: Resistência à Insulina
Insulina/farmacologia
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Prostaglandinas A/farmacologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Inativação Gênica/efeitos dos fármacos
Células HEK293
Seres Humanos
Lentivirus/efeitos dos fármacos
Lentivirus/metabolismo
Camundongos
Células Musculares/citologia
Células Musculares/efeitos dos fármacos
Células Musculares/metabolismo
Fatores de Tempo
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Insulin); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3); 0 (Prostaglandins A); K6VT5BDY9E (prostaglandin A2)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121030
[St] Status:MEDLINE
[do] DOI:10.1055/s-0032-1327619


  7 / 13 MEDLINE  
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[PMID]:22583411
[Au] Autor:Deutsch AJ; Angerer H; Fuchs TE; Neumeister P
[Ad] Endereço:Division of Hematology, Department of Internal Medicine, Medical University Graz, Austria. alexander.deutsch@medunigraz.at
[Ti] Título:The nuclear orphan receptors NR4A as therapeutic target in cancer therapy.
[So] Source:Anticancer Agents Med Chem;12(9):1001-14, 2012 Nov.
[Is] ISSN:1875-5992
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:NR4A1 (Nur77), NR4A2 (Nurr1) and NR4A3 (Nor-1) are three members of the orphan nuclear receptor (NR) family referred to as NR4A family. This subgroup activates gene expression in a constitutive ligand-independent manner. These nuclear receptors are classified as early response genes that are induced by a diverse range of signals. These orphan NRs have been implicated in cell cycle regulation, apoptosis, inflammation, metabolism and more recently in carcinogenesis. The ultimate growth of a tumor depends not only on the rate of tumor cell proliferation, but also the rate of apoptosis and NR4A1 controls both, survival and death of cancer cells. It has been demonstrated that NR4A1 activities are regulated through its subcellular localisation. In the nucleus, NR4A1 can function in a context dependent manner either as an oncogenic survival factor, promoting cancer cell growth or as the opposite through the activation of apoptosis. Additionally, in an atypical fashion, it is a potent killer when migrating to the mitochondria, where it binds to Bcl-2 and converts its survival phenotype, triggering cytochrome c release and apoptosis. The most convincing evidence that nuclear orphan receptors function as critical tumor suppressors is the observation that the NR4A1 and NR4A3 double knock out mouse develops rapidly acute myeloid leukemia. Down regulation of NR4A1 and NR4A3 was a common feature in leukemic blasts from human AML patients. In particular, the recent identification of pro-apoptotic agents inducing NR4A expression or acting as agonists suggests that these members could serve as potential targets for cancer therapy.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Terapia de Alvo Molecular/métodos
Neoplasias/tratamento farmacológico
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Neoplasias/genética
Neoplasias/metabolismo
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3)
[Em] Mês de entrada:1305
[Cu] Atualização por classe:121205
[Lr] Data última revisão:
121205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120516
[St] Status:MEDLINE


  8 / 13 MEDLINE  
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[PMID]:22282471
[Au] Autor:Pearen MA; Eriksson NA; Fitzsimmons RL; Goode JM; Martel N; Andrikopoulos S; Muscat GE
[Ad] Endereço:Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4072, Australia.
[Ti] Título:The nuclear receptor, Nor-1, markedly increases type II oxidative muscle fibers and resistance to fatigue.
[So] Source:Mol Endocrinol;26(3):372-84, 2012 Mar.
[Is] ISSN:1944-9917
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nuclear hormone receptors (NR) have been implicated as regulators of lipid and carbohydrate metabolism. The orphan NR4A subgroup has emerged as regulators of metabolic function. Targeted silencing of neuron-derived orphan receptor 1 (Nor-1)/NR4A3 in skeletal muscle cells suggested that this NR was necessary for oxidative metabolism in vitro. To investigate the in vivo role of Nor-1, we have developed a mouse model with preferential expression of activated Nor-1 in skeletal muscle. In skeletal muscle, this resulted in a marked increase in: 1) myoglobin expression, 2) mitochondrial DNA and density, 3) oxidative enzyme staining, and 4) genes/proteins encoding subunits of electron transport chain complexes. This was associated with significantly increased type IIA and IIX myosin heavy chain mRNA and proteins and decreased type IIB myosin heavy chain mRNA and protein. The contractile protein/fiber type remodeling driving the acquisition of the oxidative type II phenotype was associated with 1) the significantly increased expression of myocyte-specific enhancer factor 2C, and phospho-histone deacetylase 5, and 2) predominantly cytoplasmic HDAC5 staining in the Tg-Nor-1 mice. Moreover, the Nor-1 transgenic line displayed significant improvements in glucose tolerance, oxygen consumption, and running endurance (in the absence of increased insulin sensitivity), consistent with increased oxidative capacity of skeletal muscle. We conclude that skeletal muscle fiber type is not only regulated by exercise-sensitive calcineurin-induced signaling cascade but also by NR signaling pathways that operate at the nexus that coordinates muscle performance and metabolic capacity in this major mass tissue.
[Mh] Termos MeSH primário: Fibras Musculares de Contração Rápida/fisiologia
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/fisiologia
[Mh] Termos MeSH secundário: Animais
Glicemia
Genes Mitocondriais
Histona Desacetilases/genética
Histona Desacetilases/metabolismo
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Mitocôndrias/metabolismo
Fibras Musculares de Contração Rápida/enzimologia
Fibras Musculares de Contração Rápida/metabolismo
Mioglobina/genética
Mioglobina/metabolismo
Cadeias Pesadas de Miosina/genética
Cadeias Pesadas de Miosina/metabolismo
NAD/metabolismo
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Oxirredução
Fosforilação
Resistência Física/genética
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Succinato Desidrogenase/genética
Succinato Desidrogenase/metabolismo
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Myoglobin); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3); 0 (Protein Isoforms); 0U46U6E8UK (NAD); EC 1.3.99.1 (Succinate Dehydrogenase); EC 3.5.1.98 (Hdac5 protein, mouse); EC 3.5.1.98 (Histone Deacetylases); EC 3.6.4.1 (Myosin Heavy Chains)
[Em] Mês de entrada:1206
[Cu] Atualização por classe:170514
[Lr] Data última revisão:
170514
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120128
[St] Status:MEDLINE
[do] DOI:10.1210/me.2011-1274


  9 / 13 MEDLINE  
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[PMID]:21277978
[Au] Autor:van Tiel CM; de Vries CJ
[Ad] Endereço:Academic Medical Center, K1-113, University of Amsterdam, Meibergdreef 15, 1105AZ Amsterdam, The Netherlands.
[Ti] Título:NR4All in the vessel wall.
[So] Source:J Steroid Biochem Mol Biol;130(3-5):186-93, 2012 Jul.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A number of nuclear receptors are involved in maintenance of normal vessel wall physiology as well as in pathophysiological processes such as atherosclerosis, restenosis and remodelling. Recent studies revealed a previously unrecognized function of the NR4A subfamily of nuclear receptors as key regulatory proteins in vascular disease. The NR4A subfamily comprises the members Nur77, Nurr1 and NOR-1 and in the current review a comprehensive overview is given of the data supporting functional involvement of these nuclear receptors in three major cell types in vascular (patho)physiology; endothelial cells, smooth muscle cells and monocytes-macrophages.
[Mh] Termos MeSH primário: Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Doenças Vasculares/metabolismo
[Mh] Termos MeSH secundário: Animais
Endotélio Vascular/metabolismo
Seres Humanos
Macrófagos/metabolismo
Camundongos
Músculo Liso Vascular/metabolismo
Ratos
Doenças Vasculares/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3)
[Em] Mês de entrada:1207
[Cu] Atualização por classe:120514
[Lr] Data última revisão:
120514
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110201
[St] Status:MEDLINE
[do] DOI:10.1016/j.jsbmb.2011.01.010


  10 / 13 MEDLINE  
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[PMID]:21621845
[Au] Autor:Lundequist A; Calounova G; Wensman H; Rönnberg E; Pejler G
[Ad] Endereço:Swedish University of Agricultural Sciences, Dept of Anatomy, Physiology and Biochemistry, BMC, Box 575, 75123 Uppsala, Sweden. Anders.Lundequist@afb.slu.se
[Ti] Título:Differential regulation of Nr4a subfamily nuclear receptors following mast cell activation.
[So] Source:Mol Immunol;48(15-16):1753-61, 2011 Sep.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The biological function of the Nr4a subfamily of nuclear receptors is only partially understood. Here we show for the fist time that mast cell (MC) activation processes involve the regulation of Nr4a factors. Exposure of murine bone marrow-derived MCs (BMMCs) to live bacteria causes a robust and selective upregulation of all Nr4a members (Nr4a1-Nr4a3). In response to purified LPS, strong upregulation of Nr4a3, but not of Nr4a1 or Nr4a2 was seen. Nr4a3 expression was also induced after the activation of BMMCs by IgE receptor cross-linking. Moreover, Nr4a expression was induced in activated human MCs. As shown by Western blot analysis, Nr4a phosphorylation was induced by IgE receptor cross-linking and calcium ionophore stimulation of BMMCs and LAD2 cells, respectively. By using various inhibitors of signaling pathways, Nr4a3 induction in BMMCs was shown to be strongly dependent on Gö6976-sensitive kinases and partially dependent on the nuclear factor of activated T-cells (NFAT) pathway, while nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) inhibition failed to inhibit Nr4a3 expression in BMMCs. Together, these data reveal selective induction of Nr4a family members in activated MCs and implicate Nr4a family nuclear receptors in the regulation of MC function.
[Mh] Termos MeSH primário: Mastócitos/metabolismo
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Transdução de Sinais/imunologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Imunofluorescência
Regulação da Expressão Gênica/imunologia
Seres Humanos
Mastócitos/imunologia
Camundongos
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/imunologia
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/imunologia
Membro 3 do Grupo A da Subfamília 4 de Receptores Nucleares/imunologia
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 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (Nuclear Receptor Subfamily 4, Group A, Member 3)
[Em] Mês de entrada:1110
[Cu] Atualização por classe:110829
[Lr] Data última revisão:
110829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110531
[St] Status:MEDLINE
[do] DOI:10.1016/j.molimm.2011.04.017



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