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Pesquisa : D12.776.260.643.327 [Categoria DeCS]
Referências encontradas : 26 [refinar]
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  1 / 26 MEDLINE  
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[PMID]:28623141
[Au] Autor:Karim MF; Yoshizawa T; Sobuz SU; Sato Y; Yamagata K
[Ad] Endereço:Department of Medical Biochemistry, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
[Ti] Título:Sirtuin 7-dependent deacetylation of DDB1 regulates the expression of nuclear receptor TR4.
[So] Source:Biochem Biophys Res Commun;490(2):423-428, 2017 Aug 19.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sirtuin 7 (SIRT7) is an NAD -dependent deacetylase/deacylase, but only a limited number of SIRT7 substrates have been identified. Recently, we found that Sirt7 knockout mice are resistant to high-fat diet-induced fatty liver, and that SIRT7 positively regulates the protein level of TR4, a nuclear receptor involved in lipid metabolism, by inhibiting the CUL4B/DDB1/DCAF1 E3 ubiquitin ligase complex. However, the mechanism by which SIRT7 inhibits the E3 ubiquitin ligase complex was not identified. Here, we demonstrate that SIRT7 binds directly to DDB1 and deacetylates DDB1 at Lys1121. K1121R-DDB1 (a deacetylation-mimicking mutant) displayed reduced binding with DCAF1. The expression of TR4 protein and TR4 target genes, including Cd36, Cidea, Cidec and Pparg1, was increased in K1121R-DDB1-overexpressing Hepa1-6 cells compared to WT-DDB1-overexpressing cells. Our results indicate that the SIRT7-mediated deacetylation of K1121 attenuates the activity of the CUL4B/DDB1/DCAF1 E3 ubiquitin ligase complex by reducing binding between DDB1 and DCAF1, leading to the increased expression of TR4.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/metabolismo
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/metabolismo
Sirtuínas/metabolismo
[Mh] Termos MeSH secundário: Acetilação
Animais
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Camundongos
Camundongos Knockout
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/genética
Ligação Proteica
Mapas de Interação de Proteínas
Proteólise
Sirtuínas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DDB1 protein, human); 0 (DNA-Binding Proteins); 0 (Ddb1 protein, mouse); 0 (Nuclear Receptor Subfamily 2, Group C, Member 2); 0 (SIRT7 protein, human); 0 (Sirt7 protein, mouse); EC 3.5.1.- (Sirtuins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170618
[St] Status:MEDLINE


  2 / 26 MEDLINE  
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[PMID]:27497262
[Au] Autor:Shinohara H; Yasuda T; Kurosaki T
[Ad] Endereço:Laboratory for Integrated Cellular Systems, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Kanagawa, Japan. hisaaki.shinohara@riken.jp.
[Ti] Título:TAK1 adaptor proteins, TAB2 and TAB3, link the signalosome to B-cell receptor-induced IKK activation.
[So] Source:FEBS Lett;590(18):3264-9, 2016 Sep.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Transforming growth factor-ß-activated kinase (TAK)1-binding proteins (TAB) activate nuclear factor-κB by linking TAK1 to signaling molecules. We investigated the mechanisms underlying B-cell receptor (BCR) signaling in TAB2- and TAB3-deficient and TAB3 domain deletion mutant DT40 B cell lines. Loss of TAB2 and TAB3 abolished BCR-induced inhibitor of κB kinase (IKK) activation and TAK1 binding to caspase recruitment domain membrane-associated guanylate kinase protein (CARMA)1. Deletion of TAB3, coupling of ubiquitin conjugation to ER degradation, coiled-coil, and zinc finger domains blocked IKK activation and association with CARMA1. Thus, TAB2 and TAB3 connect signaling molecules that activate IKK in BCR signaling.
[Mh] Termos MeSH primário: Quinase I-kappa B/metabolismo
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/metabolismo
Receptores de Antígenos de Linfócitos B/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Proteínas Adaptadoras de Sinalização CARD/metabolismo
Linhagem Celular
Galinhas
Guanilato Ciclase/metabolismo
Ligação Proteica
Ubiquitina/metabolismo
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (CARD Signaling Adaptor Proteins); 0 (Nuclear Receptor Subfamily 2, Group C, Member 2); 0 (Receptors, Antigen, B-Cell); 0 (Ubiquitin); EC 2.7.11.10 (I-kappa B Kinase); EC 4.6.1.2 (Guanylate Cyclase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160807
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12342


  3 / 26 MEDLINE  
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[PMID]:27253665
[Au] Autor:Zhang D; Du L; Heaney AP
[Ad] Endereço:Departments of Medicine (D.Z., L.D., A.P.H.) and Neurosurgery (A.P.H.), David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095; and Beckman Research Institute, City of Hope (L.D.), Duarte, California 91010.
[Ti] Título:Testicular Receptor-4: Novel Regulator of Glucocorticoid Resistance.
[So] Source:J Clin Endocrinol Metab;101(8):3123-33, 2016 Aug.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Glucocorticoids are powerful steroid hormones that regulate development, metabolism, and immune response. However, glucocorticoid unresponsiveness or resistance is observed in the treatment of inflammatory, autoimmune, and lymphoproliferative diseases and significantly limits their efficacy. OBJECTIVE: In Cushing's disease, although some glucocorticoid-mediated suppression of pituitary-derived ACTH is seen, corticotroph tumors exhibit relative resistance to glucocorticoid action. We previously demonstrated that testicular orphan receptor 4 (TR4) binds to the pro-opiomelanocortin (POMC) promoter to induce corticotroph tumor POMC expression and ACTH secretion, and we hypothesized that TR4 may interact with glucocorticoid signaling to modulate POMC expression and action. RESULTS: Here we demonstrate that TR4 abrogates glucocorticoid receptor (GR)- or dexamethasone-mediated POMC and activator protein-1 transrepression in both murine and human pituitary corticotroph tumor cells. Co-immunoprecipitation studies indicate that TR4 and GR interact directly with each other, resulting in TR4-mediated disruption of GR binding to the POMC promoter. CONCLUSION: These results demonstrate that TR4 binds GR to play an important role in glucocorticoid-directed corticotroph tumor POMC regulation in addition to modulating glucocorticoid actions on other GR targets. Characterization of this pathway may offer important insights into glucocorticoid resistance and may identify a novel approach for the treatment of Cushing's disease and the glucocorticoid-resistant states.
[Mh] Termos MeSH primário: Erros Inatos do Metabolismo/genética
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/fisiologia
Receptores de Glucocorticoides/deficiência
[Mh] Termos MeSH secundário: Animais
Dexametasona/farmacologia
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Camundongos
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/metabolismo
Pró-Opiomelanocortina/genética
Regiões Promotoras Genéticas
Ligação Proteica
Receptores de Glucocorticoides/genética
Receptores de Glucocorticoides/metabolismo
Fator de Transcrição AP-1/metabolismo
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nuclear Receptor Subfamily 2, Group C, Member 2); 0 (Receptors, Glucocorticoid); 0 (Transcription Factor AP-1); 66796-54-1 (Pro-Opiomelanocortin); 7S5I7G3JQL (Dexamethasone)
[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:160603
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-1379


  4 / 26 MEDLINE  
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[PMID]:27109382
[Au] Autor:Peng XP; Huang L; Liu ZH
[Ad] Endereço:Department of Cardiovascular Medicine, First Affiliated Hospital of Hunan Traditional Chinese Medical College, Zhuzhou, Hunan 412000, China.
[Ti] Título:miRNA-133a attenuates lipid accumulation via TR4-CD36 pathway in macrophages.
[So] Source:Biochimie;127:79-85, 2016 Aug.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:lipid metabolism is the major causes of atherosclerosis. There is increasing evidence that miR-133a plays an important role in atherosclerosis. However, the regulatory mechanism of miR-133a in macrophages is still unclear. Several lines of evidence indicate that loss of TR4 leads to reduce lipid accumulation in liver and adipose tissues, etc, and lesional macrophages-derived TR4 can greatly increase the foam cell formation through increasing the CD36-mediated the uptake of ox-LDL. Interestingly, computational analysis suggests that TR4 may be a target gene of miR-133a. Here, we examined whether miR-133a regulates TR4 expression in ox-LDL-induced mouse RAW 264.7 macrophages, thereby affecting lipid accumulation. Using ox-LDL-treatment RAW 264.7 macrophages transfected with miR-133a mimics or inhibitors, we have showed that miR-133a can directly regulate the expression of TR4 in RAW 264.7 cells, thereby attenuates CD36-medide lipid accumulation. Furthermore, our studies suggest an additional explanation for the regulatory mechanism of miR-133a regulation to its functional target, TR4 in RAW 264.7 macrophages. Thus, our findings suggest that miR-133a may regulate lipid accumulation in ox-LDL-stimulated RAW 264.7 macrophages via TR4-CD36 pathway.
[Mh] Termos MeSH primário: Antígenos CD36/metabolismo
Metabolismo dos Lipídeos/genética
Macrófagos/citologia
Macrófagos/metabolismo
MicroRNAs/genética
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/metabolismo
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Metabolismo dos Lipídeos/efeitos dos fármacos
Lipoproteínas LDL/farmacologia
Macrófagos/efeitos dos fármacos
Camundongos
Células RAW 264.7
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (Lipoproteins, LDL); 0 (MicroRNAs); 0 (Mirn133 microRNA, mouse); 0 (Nuclear Receptor Subfamily 2, Group C, Member 2); 0 (oxidized low density lipoprotein)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160426
[St] Status:MEDLINE


  5 / 26 MEDLINE  
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[PMID]:27084994
[Au] Autor:Zhu L; Lu J; Tang X; Fu G; Duan P; Quan C; Zhang L; Zhang Z; Chang W; Shi Y
[Ad] Endereço:School of Public Health, Medical College, Wuhan University of Science and Technology, 947Heping Avenue, Wuhan 430081, PR China.
[Ti] Título:Di-(2-ethylhexyl) phthalate induces apoptosis of GC-2spd cells via TR4/Bcl-2 pathway.
[So] Source:Environ Toxicol Pharmacol;44:18-24, 2016 Jun.
[Is] ISSN:1872-7077
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Di-(2-ethylhexyl) phthalate (DEHP) is a widely used environmental endocrine disruptor. Many studies have reported that DEHP exposure causes reproductive toxicity and cells apoptosis. However, the mechanism by which DEHP exposure causes male reproductive toxicity remains unknown. This study investigated the role of the testicular orphan nuclear receptor4 (TR4)/Bcl-2 pathway in apoptosis induced by DEHP, which resulted in reproductive damage. To elucidate the mechanism underpinning the male reproductive toxicity of DEHP, we sought to investigate apoptotic effects, expression levels of TR4/Bcl-2 pathway in GC-2spd cells, including TR4, Bcl-2 and caspase-3. GC-2spd cells were exposed to various concentrations of DEHP (0, 50, 100, or 200µM). The results indicated that, with the increase of the concentrations of DEHP, the survival rate of cell decreased gradually. DEHP exposure at over 100µM significantly induced apoptotic cell death. DEHP decreased SOD and GSH-Px activity in 200µM group. Compared to the control group, the mRNA levels of caspase-3 increased significantly, however, Bcl-2 mRNA decreased (P<0.05). In addition, there was a significant reduction in TR4, Bcl-2 and procaspase-3 protein levels. Taken together, these results lead us to speculate that in vitro exposure to DEHP might induce apoptosis in GC-2spd cells through the TR4/Bcl-2 pathway.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Dietilexilftalato/toxicidade
Disruptores Endócrinos/toxicidade
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/metabolismo
Plastificantes/toxicidade
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Caspase 3/genética
Caspase 3/metabolismo
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Glutationa Peroxidase/metabolismo
Malondialdeído/metabolismo
Camundongos
Proteínas Proto-Oncogênicas c-bcl-2/genética
RNA Mensageiro/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endocrine Disruptors); 0 (Nuclear Receptor Subfamily 2, Group C, Member 2); 0 (Plasticizers); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (RNA, Messenger); 4Y8F71G49Q (Malondialdehyde); C42K0PH13C (Diethylhexyl Phthalate); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160417
[St] Status:MEDLINE


  6 / 26 MEDLINE  
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[PMID]:26677977
[Au] Autor:Zimmerman EI; Gibson AA; Hu S; Vasilyeva A; Orwick SJ; Du G; Mascara GP; Ong SS; Chen T; Vogel P; Inaba H; Maitland ML; Sparreboom A; Baker SD
[Ad] Endereço:Department of Pharmaceutical Sciences, St. Jude Children's Research Hospital, Memphis, Tennessee.
[Ti] Título:Multikinase Inhibitors Induce Cutaneous Toxicity through OAT6-Mediated Uptake and MAP3K7-Driven Cell Death.
[So] Source:Cancer Res;76(1):117-26, 2016 Jan 01.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The use of multikinase inhibitors (MKI) in oncology, such as sorafenib, is associated with a cutaneous adverse event called hand-foot skin reaction (HFSR), in which sites of pressure or friction become inflamed and painful, thus significantly impacting quality of life. The pathogenesis of MKI-induced HFSR is unknown, and the only available treatment options involve dose reduction or discontinuation of therapy, which have negative effects on primary disease management. To investigate the underlying mechanisms by which sorafenib promotes keratinocyte cytotoxicity and subsequent HFSR induction, we performed a transporter-directed RNAi screen in human epidermal keratinocytes and identified SLC22A20 (OAT6) as an uptake carrier of sorafenib. Further investigations into the intracellular mechanism of sorafenib activity through in situ kinome profiling identified the mitogen-activated protein kinase MAP3K7 (TAK1) as a target of sorafenib that induces cell death. Finally, we demonstrate that sorafenib induced keratinocyte injury in vivo and that this effect could be reversed by cotreatment with the OAT6 inhibitor probenecid. Collectively, our findings reveal a novel pathway that regulates the entry of some MKIs into keratinocytes and explains the basis underlying sorafenib-induced skin toxicity, with important implications for the therapeutic management of HFSR.
[Mh] Termos MeSH primário: MAP Quinase Quinase Quinases/metabolismo
Niacinamida/análogos & derivados
Transportadores de Ânions Orgânicos/metabolismo
Compostos de Fenilureia/toxicidade
Inibidores de Proteínas Quinases/toxicidade
Dermatopatias/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Morte Celular/efeitos dos fármacos
Morte Celular/fisiologia
Linhagem Celular Tumoral
Feminino
Células Hep G2
Seres Humanos
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
MAP Quinase Quinase Quinases/genética
Camundongos
Camundongos Endogâmicos C57BL
Niacinamida/farmacocinética
Niacinamida/toxicidade
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/metabolismo
Transportadores de Ânions Orgânicos/genética
Compostos de Fenilureia/farmacocinética
Inibidores de Proteínas Quinases/farmacocinética
Distribuição Aleatória
Pele/efeitos dos fármacos
Pele/metabolismo
Pele/patologia
Dermatopatias/metabolismo
Dermatopatias/patologia
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Receptor Subfamily 2, Group C, Member 2); 0 (OAT6 protein, mouse); 0 (Organic Anion Transporters); 0 (Phenylurea Compounds); 0 (Protein Kinase Inhibitors); 25X51I8RD4 (Niacinamide); 9ZOQ3TZI87 (sorafenib); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (MAP kinase kinase kinase 7)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170101
[Lr] Data última revisão:
170101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151219
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-15-0694


  7 / 26 MEDLINE  
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[PMID]:26159912
[Au] Autor:Zhi X; Zhou XE; Melcher K; Xu HE
[Ad] Endereço:Laboratory of Structural Sciences, Van Andel Research Institute, 333 Bostwick Ave., N.E., Grand Rapids, MI 49503, USA; Autophagy Research Center, University of Texas Southwestern Medical Center, 6000Harry Hines Blvd., Dallas, TX 75390, USA. Electronic address: Xiaoyong.Zhi@UTsouthwestern.edu.
[Ti] Título:Structures and regulation of non-X orphan nuclear receptors: A retinoid hypothesis.
[So] Source:J Steroid Biochem Mol Biol;157:27-40, 2016 Mar.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nuclear receptors are defined as a family of ligand regulated transcription factors [1-6]. While this definition reflects that ligand binding is a key property of nuclear receptors, it is still a heated subject of debate if all the nuclear receptors (48 human members) can bind ligands (ligands referred here to both physiological and synthetic ligands). Recent studies in nuclear receptor structure biology and pharmacology have undoubtedly increased our knowledge of nuclear receptor functions and their regulation. As a result, they point to new avenues for the discovery and development of nuclear receptor regulators, including nuclear receptor ligands. Here we review the recent literature on orphan nuclear receptor structural analysis and ligand identification, particularly on the orphan nuclear receptors that do not heterodimerize with retinoid X receptors, which we term as non-X orphan receptors. We also propose a speculative "retinoid hypothesis" for a subset of non-X orphan nuclear receptors, which we hope to help shed light on orphan nuclear receptor biology and drug discovery. This article is part of a Special Issue entitled 'Orphan Nuclear Receptors'.
[Mh] Termos MeSH primário: Receptores Nucleares Órfãos/química
Receptores Nucleares Órfãos/metabolismo
Retinoides/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Fator II de Transcrição COUP/química
Fator II de Transcrição COUP/metabolismo
Receptor Nuclear Órfão DAX-1/química
Receptor Nuclear Órfão DAX-1/metabolismo
Seres Humanos
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/química
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/metabolismo
Conformação Proteica
Receptores Citoplasmáticos e Nucleares/química
Receptores Citoplasmáticos e Nucleares/metabolismo
Retinoides/química
Fator Esteroidogênico 1/química
Fator Esteroidogênico 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (COUP Transcription Factor II); 0 (DAX-1 Orphan Nuclear Receptor); 0 (NR0B1 protein, human); 0 (NR2E3 protein, human); 0 (NR5A2 protein, human); 0 (Nuclear Receptor Subfamily 2, Group C, Member 2); 0 (Orphan Nuclear Receptors); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Retinoids); 0 (Steroidogenic Factor 1); 0 (nuclear receptor subfamily 0, group B, member 2)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:160121
[Lr] Data última revisão:
160121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150711
[St] Status:MEDLINE


  8 / 26 MEDLINE  
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[PMID]:26460253
[Au] Autor:White JC; Pawar A; Fu G; Cui S; Tavernier F; Hamid M; Harro D; Giacherio D; Campbell AD; Hines PC
[Ad] Endereço:Wayne State University School of Medicine, Department of Pediatrics, United States.
[Ti] Título:TR2/TR4 overexpression in a humanized sickle cell disease mouse model decreases RBC adhesion to VCAM-1.
[So] Source:Blood Cells Mol Dis;55(4):316-7, 2015 Dec.
[Is] ISSN:1096-0961
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Anemia Falciforme/genética
Anemia Falciforme/metabolismo
Eritrócitos/metabolismo
Expressão Gênica
Membro 1 do Grupo C da Subfamília 2 de Receptores Nucleares/genética
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/genética
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Seres Humanos
Camundongos
Camundongos Transgênicos
[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 2, Group C, Member 1); 0 (Nuclear Receptor Subfamily 2, Group C, Member 2); 0 (Vascular Cell Adhesion Molecule-1)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151014
[St] Status:MEDLINE


  9 / 26 MEDLINE  
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[PMID]:26144287
[Au] Autor:Zhang L; Zhang J; Ma Y; Chen J; Dong B; Zhao W; Wang X; Zheng Q; Fang F; Yang Y
[Ad] Endereço:Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Beijing, People's Republic of China.
[Ti] Título:Testicular orphan receptor 4 (TR4) is a marker for metastasis and poor prognosis in non-small cell lung cancer that drives the EMT phenotype.
[So] Source:Lung Cancer;89(3):320-8, 2015 Sep.
[Is] ISSN:1872-8332
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Aberrant expression of testicular orphan receptor 4 (TR4) has been shown to regulate biological processes near solid tumors. However, the role of TR4 in non-small cell lung cancer (NSCLC) patient prognosis and the development of NSCLC cancer cells are unclear. METHODS: Immunohistochemical analysis was used to evaluate the correlation between TR4 expression and clinicopathological characteristics in 291 cases of NSCLC specimens. A knockdown and overexpression of TR4 was performed to assess the role of TR4. Transwell and colony formation assays were completed to investigate the metastatic and proliferative abilities. Quantitative real-time PCR, Western blotting and immunofluorescence staining were carried out to analyze the epithelial-to-mesenchymal transition (EMT) phenotype. RESULTS: Immunohistochemical evaluation of clinical samples revealed that most of the lung cancer tissues were strongly positive for TR4, whereas the tissues that stained weakly positive or negative for TR4 expression were shown in the paired normal tissues. Moreover, higher levels of TR4 expression were significantly associated with higher lymph node metastases, TNM stages, tumor thrombus in vena and poor prognosis. We observed that downregulation and up-regulation of TR4 with stable cell transfection significantly influence the proliferation, invasive and metastatic abilities of NSCLC lines. In addition, aberrant TR4 expression could modulate the expression levels of several EMT related markers. CONCLUSIONS: Collectively, our results show TR4 expression in NSCLC samples is significantly associated with poor clinicopathological features, and TR4 plays an important role in the metastatic capacity of NSCLC cells by EMT regulation.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/mortalidade
Transição Epitelial-Mesenquimal/genética
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/mortalidade
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Movimento Celular/genética
Feminino
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Gradação de Tumores
Metástase Neoplásica
Estadiamento de Neoplasias
Fenótipo
Prognóstico
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nuclear Receptor Subfamily 2, Group C, Member 2)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:150811
[Lr] Data última revisão:
150811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150707
[St] Status:MEDLINE


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[PMID]:25840044
[Au] Autor:Zhu F; Shi L; Engel JD; Guan Y
[Ad] Endereço:Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI 48109, USA.
[Ti] Título:Regulatory network inferred using expression data of small sample size: application and validation in erythroid system.
[So] Source:Bioinformatics;31(15):2537-44, 2015 Aug 01.
[Is] ISSN:1367-4811
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:MOTIVATION: Modeling regulatory networks using expression data observed in a differentiation process may help identify context-specific interactions. The outcome of the current algorithms highly depends on the quality and quantity of a single time-course dataset, and the performance may be compromised for datasets with a limited number of samples. RESULTS: In this work, we report a multi-layer graphical model that is capable of leveraging many publicly available time-course datasets, as well as a cell lineage-specific data with small sample size, to model regulatory networks specific to a differentiation process. First, a collection of network inference methods are used to predict the regulatory relationships in individual public datasets. Then, the inferred directional relationships are weighted and integrated together by evaluating against the cell lineage-specific dataset. To test the accuracy of this algorithm, we collected a time-course RNA-Seq dataset during human erythropoiesis to infer regulatory relationships specific to this differentiation process. The resulting erythroid-specific regulatory network reveals novel regulatory relationships activated in erythropoiesis, which were further validated by genome-wide TR4 binding studies using ChIP-seq. These erythropoiesis-specific regulatory relationships were not identifiable by single dataset-based methods or context-independent integrations. Analysis of the predicted targets reveals that they are all closely associated with hematopoietic lineage differentiation.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Linhagem da Célula/genética
Células Eritroides/metabolismo
Eritropoese/genética
Regulação da Expressão Gênica
Redes Reguladoras de Genes
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Algoritmos
Células Cultivadas
Imunoprecipitação da Cromatina
Células Eritroides/citologia
Genoma Humano
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Seres Humanos
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/genética
Membro 2 do Grupo C da Subfamília 2 de Receptores Nucleares/metabolismo
Príons/genética
Príons/metabolismo
Curva ROC
Tamanho da Amostra
Células-Tronco/citologia
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[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 (Nuclear Receptor Subfamily 2, Group C, Member 2); 0 (Prions); 0 (Transcription Factors)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150404
[St] Status:MEDLINE
[do] DOI:10.1093/bioinformatics/btv186



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