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Pesquisa : G02.111.570.080.689.330.700.800 [Categoria DeCS]
Referências encontradas : 192 [refinar]
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  1 / 192 MEDLINE  
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[PMID]:28407230
[Au] Autor:Xu H; Luo J; Ma G; Zhang X; Yao D; Li M; Loor JJ
[Ad] Endereço:Shaanxi Key Laboratory of Molecular Biology for Agriculture, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, P. R. China.
[Ti] Título:Acyl-CoA synthetase short-chain family member 2 (ACSS2) is regulated by SREBP-1 and plays a role in fatty acid synthesis in caprine mammary epithelial cells.
[So] Source:J Cell Physiol;233(2):1005-1016, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sterol regulatory element binding protein 1 (SREBP-1) is well-known as the master regulator of lipogenesis in rodents. Acyl-CoA synthetase short-chain family member 2 (ACSS2) plays a key role in lipogenesis by synthesizing acetyl-CoA from acetate for lipogenesis. ATP citrate lyase (ACLY) catalyzes the conversion of citrate and coenzyme A to acetyl-CoA, hence, it is also important for lipogenesis. Although ACSS2 function in cancer cells has been elucidated, its essentiality in ruminant mammary lipogenesis is unknown. Furthermore, ACSS2 gene promoter and its regulatory mechanisms have not known. Expression of ACSS2 was high in lipid synthesizing tissues, and its expression increased during lactation compared with non-lactating period. Simultaneous knockdown of both ACSS2 and ACLY by siRNA in primary goat mammary epithelial cells decreased (p < 0.05) the mRNA abundance of genes associated with de novo fatty acid synthesis (FASN, ACACA, SCD1) and triacylglycerol (TAG) synthesis (DGAT1, DGAT2, GPAM, and AGPAT6). Genes responsible for lipid droplet formation and secretion (PLIN2 and PLIN3) and fatty acid oxidation (ATGL, HSL, ACOX, and CPT1A) all decreased (p < 0.05) after ACSS2 and ACLY knockdown. Total cellular TAG content and lipid droplet formation also decreased. Use of a luciferase reporter assay revealed a direct regulation of ACSS2 by SREBP-1. Furthermore, SREBP-1 interacted with an SRE (SREBP response element) spanning at -475 to -483 bp on the ACSS2 promoter. Taken together, our results revealed a novel pathway that SREBP-1 may regulate fatty acid and TAG synthesis by regulating the expression of ACSS2.
[Mh] Termos MeSH primário: Acetato-CoA Ligase/metabolismo
Células Epiteliais/enzimologia
Ácidos Graxos/biossíntese
Lactação
Glândulas Mamárias Animais/enzimologia
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
[Mh] Termos MeSH secundário: ATP Citrato (pro-S)-Liase/genética
ATP Citrato (pro-S)-Liase/metabolismo
Acetato-CoA Ligase/genética
Animais
Células Cultivadas
Feminino
Regulação Enzimológica da Expressão Gênica
Cabras
Gotículas Lipídicas/metabolismo
Lipogênese/genética
Glândulas Mamárias Animais/citologia
Mutagênese Sítio-Dirigida
Mutação
Regiões Promotoras Genéticas
Interferência de RNA
Elemento de Resposta Sérica
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Transfecção
Triglicerídeos/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Triglycerides); EC 2.3.3.8 (ATP Citrate (pro-S)-Lyase); EC 6.2.1.1 (Acetate-CoA Ligase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25954


  2 / 192 MEDLINE  
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[PMID]:28285914
[Au] Autor:Hutchings KM; Lisabeth EM; Rajeswaran W; Wilson MW; Sorenson RJ; Campbell PL; Ruth JH; Amin A; Tsou PS; Leipprandt JR; Olson SR; Wen B; Zhao T; Sun D; Khanna D; Fox DA; Neubig RR; Larsen SD
[Ad] Endereço:Vahlteich Medicinal Chemistry Core, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA.
[Ti] Título:Pharmacokinetic optimitzation of CCG-203971: Novel inhibitors of the Rho/MRTF/SRF transcriptional pathway as potential antifibrotic therapeutics for systemic scleroderma.
[So] Source:Bioorg Med Chem Lett;27(8):1744-1749, 2017 04 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We recently reported the development of a novel inhibitor of Rho-mediated gene transcription (1, CCG-203971) that is efficacious in multiple animal models of acute fibrosis, including scleroderma, when given intraperitoneally. The modest in vivo potency and poor pharmacokinetics (PK) of this lead, however, make it unsuitable for long term efficacy studies. We therefore undertook a systematic medicinal chemistry effort to improve both the metabolic stability and the solubility of 1, resulting in the identification of two analogs achieving over 10-fold increases in plasma exposures in mice. We subsequently showed that one of these analogs (8f, CCG-232601) could inhibit the development of bleomycin-induced dermal fibrosis in mice when administered orally at 50mg/kg, an effect that was comparable to what we had observed earlier with 1 at a 4-fold higher IP dose.
[Mh] Termos MeSH primário: Ácidos Nipecóticos/farmacocinética
Ácidos Nipecóticos/uso terapêutico
Fator Rho/antagonistas & inibidores
Escleroderma Sistêmico/tratamento farmacológico
Pele/efeitos dos fármacos
Ativação Transcricional/efeitos dos fármacos
[Mh] Termos MeSH secundário: Administração Oral
Animais
Modelos Animais de Doenças
Fibrose
Células HEK293
Seres Humanos
Camundongos
Ácidos Nipecóticos/administração & dosagem
Ácidos Nipecóticos/química
Fator Rho/metabolismo
Escleroderma Sistêmico/genética
Escleroderma Sistêmico/metabolismo
Escleroderma Sistêmico/patologia
Elemento de Resposta Sérica/efeitos dos fármacos
Pele/metabolismo
Pele/patologia
Transativadores/antagonistas & inibidores
Transativadores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (MKL1 protein, human); 0 (N-(4-chlorophenyl)-1-((3-(furan-2-yl)phenyl)carbonyl)piperidine-3-carboxamide); 0 (Nipecotic Acids); 0 (Rho Factor); 0 (Trans-Activators)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE


  3 / 192 MEDLINE  
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[PMID]:28157379
[Au] Autor:Dou Q; Hao F; Sun L; Xu X; Cui MZ
[Ad] Endereço:a Department of Biomedical & Diagnostic Sciences, University of Tennessee, Knoxville, Tennessee, USA.
[Ti] Título:CRE and SRE mediate LPA-induced CCN1 transcription in mouse aortic smooth muscle cells.
[So] Source:Can J Physiol Pharmacol;95(3):275-280, 2017 Mar.
[Is] ISSN:1205-7541
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:Lysophosphatidic acid (LPA), one component of oxidized low-density lipoprotein (ox-LDL), is a potent bioactive phospholipid. Our recent data reveal that LPA induces matricellular protein CCN1 (also known as Cyr61) expression in aortic smooth muscle cells (SMCs) and that CCN1 bridges LPA and integrin signaling pathways leading to SMC migration. Whether and how LPA regulates the transcriptional machinery of the CCN1 gene are unknown. In this study, we found that LPA markedly induces CCN1 mRNA expression in SMCs. Using deleting mutation and reporter gene strategies, we demonstrated regions from -2038 to -1787 and from -101 to +63 of the CCN1 promoter contain the essential regulatory elements. The serum response element (SRE) and cyclic AMP-response element (CRE) are located in these regions. LPA induced time-dependent phosphorylation of serum response factor (SRF) and CRE-binding protein (CREB) in mouse SMCs. Luciferase assays of a series of deleted, mutated CCN1 promoter-reporter gene constructs and dominant negative construct revealed the distal SRE and the proximal CRE in the CCN1 promoter are required for LPA-induced CCN1 gene expression. Our results imply that elevated LPA levels may trigger SMC migration and exacerbate restenosis and atherosclerotic lesions through the induced CCN1, which communicates with a set of plasma membrane proteins and intracellular kinases.
[Mh] Termos MeSH primário: Proteína Rica em Cisteína 61/genética
Lisofosfolipídeos/farmacologia
Músculo Liso Vascular/efeitos dos fármacos
Miócitos de Músculo Liso/efeitos dos fármacos
Elemento de Resposta Sérica/efeitos dos fármacos
Transcrição Genética/efeitos dos fármacos
Ativação Transcricional/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aorta/efeitos dos fármacos
Aorta/metabolismo
Sítios de Ligação
Células Cultivadas
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Proteína Rica em Cisteína 61/metabolismo
Genes Reporter
Camundongos
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Fosforilação
Ligação Proteica
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Fator de Resposta Sérica/metabolismo
Fatores de Tempo
Transfecção
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Creb1 protein, mouse); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Cyr61 protein, mouse); 0 (Cysteine-Rich Protein 61); 0 (Lysophospholipids); 0 (RNA, Messenger); 0 (Serum Response Factor); PG6M3969SG (lysophosphatidic acid)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1139/cjpp-2016-0559


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[PMID]:28005346
[Au] Autor:Lingerfelt MA; Zhao P; Sharir HP; Hurst DP; Reggio PH; Abood ME
[Ad] Endereço:Department of Chemistry and Biochemistry, University of North Carolina-Greensboro , Greensboro, North Carolina 27402, United States.
[Ti] Título:Identification of Crucial Amino Acid Residues Involved in Agonist Signaling at the GPR55 Receptor.
[So] Source:Biochemistry;56(3):473-486, 2017 Jan 24.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:GPR55 is a newly deorphanized class A G-protein-coupled receptor that has been implicated in inflammatory pain, neuropathic pain, metabolic disorder, bone development, and cancer. Few potent GPR55 ligands have been identified to date. This is largely due to an absence of information about salient features of GPR55, such as residues important for signaling and residues implicated in the GPR55 signaling cascade. The goal of this work was to identify residues that are key for the signaling of the GPR55 endogenous ligand, l-α-lysophosphatidylinositol (LPI), as well as the signaling of the GPR55 agonist, ML184 {CID 2440433, 3-[4-(2,3-dimethylphenyl)piperazine-1-carbonyl]-N,N-dimethyl-4-pyrrolidin-1-ylbenzenesulfonamide}. Serum response element (SRE) and serum response factor (SRF) luciferase assays were used as readouts for studying LPI and ML184 signaling at the GPR55 mutants. A GPR55 R* model based on the recent δ-opioid receptor (DOR) crystal structure was used to interpret the resultant mutation data. Two residues were found to be crucial for agonist signaling at GPR55, K2.60 and E3.29, suggesting that these residues form the primary interaction site for ML184 and LPI at GPR55. Y3.32F, H(170)F, and F6.55A/L mutation results suggested that these residues are part of the orthosteric binding site for ML184, while Y3.32F and H(170)F mutation results suggest that these two residues are part of the LPI binding pocket. Y3.32L, M3.36A, and F6.48A mutation results suggest the importance of a Y3.32/M3.36/F6.48 cluster in the GPR55 signaling cascade. C(10)A and C(260)A mutations suggest that these residues form a second disulfide bridge in the extracellular domain of GPR55, occluding ligand extracellular entry in the TMH1-TMH7 region of GPR55. Taken together, these results provide the first set of discrete information about GPR55 residues important for LPI and ML184 signaling and for GPR55 activation. This information should aid in the rational design of next-generation GPR55 ligands and the creation of the first high-affinity GPR55 radioligand, a tool that is sorely needed in the field.
[Mh] Termos MeSH primário: Lisofosfolipídeos/química
Piperazinas/química
Pirrolidinas/química
Receptores Acoplados a Proteínas-G/química
Proteínas Recombinantes de Fusão/química
Elemento de Resposta Sérica
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Sítios de Ligação
Cristalografia por Raios X
Expressão Gênica
Células HEK293
Seres Humanos
Cinética
Ligantes
Lisofosfolipídeos/farmacologia
Simulação de Acoplamento Molecular
Mutação
Piperazinas/farmacologia
Ligação Proteica
Pirrolidinas/farmacologia
Receptores Acoplados a Proteínas-G/agonistas
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/metabolismo
Receptores Opioides delta/química
Receptores Opioides delta/genética
Receptores Opioides delta/metabolismo
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/metabolismo
Fator de Resposta Sérica/química
Fator de Resposta Sérica/genética
Fator de Resposta Sérica/metabolismo
Transdução de Sinais
Feijão de Soja
Homologia Estrutural de Proteína
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPR55 protein, human); 0 (Ligands); 0 (Lysophospholipids); 0 (Piperazines); 0 (Pyrrolidines); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Opioid, delta); 0 (Recombinant Fusion Proteins); 0 (Serum Response Factor); 0 (lysophosphatidylinositol)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.6b01013


  5 / 192 MEDLINE  
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[PMID]:27765816
[Au] Autor:Sato K; Kimura M; Sugiyama K; Nishikawa M; Okano Y; Nagaoka H; Nagase T; Kitade Y; Ueda H
[Ad] Endereço:From the United Graduate School of Drug Discovery and Medical Information Sciences and.
[Ti] Título:Four-and-a-half LIM Domains 1 (FHL1) Protein Interacts with the Rho Guanine Nucleotide Exchange Factor PLEKHG2/FLJ00018 and Regulates Cell Morphogenesis.
[So] Source:J Biol Chem;291(48):25227-25238, 2016 Nov 25.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PLEKHG2/FLJ00018 is a Gßγ-dependent guanine nucleotide exchange factor for the small GTPases Rac and Cdc42 and has been shown to mediate the signaling pathways leading to actin cytoskeleton reorganization. Here we showed that the zinc finger domain-containing protein four-and-a-half LIM domains 1 (FHL1) acts as a novel interaction partner of PLEKHG2 by the yeast two-hybrid system. Among the isoforms of FHL1 (i.e. FHL1A, FHL1B, and FHL1C), FHL1A and FHL1B interacted with PLEKHG2. We found that there was an FHL1-binding region at amino acids 58-150 of PLEKHG2. The overexpression of FHL1A but not FHL1B enhanced the PLEKHG2-induced serum response element-dependent gene transcription. The co-expression of FHL1A and Gßγ synergistically enhanced the PLEKHG2-induced serum response element-dependent gene transcription. Increased transcription activity was decreased by FHL1A knock-out with the CRISPR/Cas9 system. Compared with PLEKHG2-expressing cells, the number and length of finger-like protrusions were increased in PLEKHG2-, Gßγ-, and FHL1A-expressing cells. Our results provide evidence that FHL1A interacts with PLEKHG2 and regulates cell morphological change through the activity of PLEKHG2.
[Mh] Termos MeSH primário: Fatores de Troca do Nucleotídeo Guanina/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteínas com Domínio LIM/metabolismo
Proteínas Musculares/metabolismo
Elemento de Resposta Sérica/fisiologia
Transcrição Genética/fisiologia
[Mh] Termos MeSH secundário: Fatores de Troca do Nucleotídeo Guanina/genética
Células HEK293
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/genética
Proteínas com Domínio LIM/genética
Proteínas Musculares/genética
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FHL1 protein, human); 0 (Guanine Nucleotide Exchange Factors); 0 (Intracellular Signaling Peptides and Proteins); 0 (LIM Domain Proteins); 0 (Muscle Proteins); 0 (PLEKHG2 protein, human); 0 (Protein Isoforms)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161022
[St] Status:MEDLINE


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[PMID]:26515162
[Au] Autor:Ronnekleiv-Kelly SM; Nukaya M; Díaz-Díaz CJ; Megna BW; Carney PR; Geiger PG; Kennedy GD
[Ad] Endereço:Department of Surgery, School of Medicine and Public Health, University of Wisconsin, 600 Highland Avenue, G4/701A CSC, Madison, WI 53792, USA.
[Ti] Título:Aryl hydrocarbon receptor-dependent apoptotic cell death induced by the flavonoid chrysin in human colorectal cancer cells.
[So] Source:Cancer Lett;370(1):91-9, 2016 Jan 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The polyphenolic flavone chrysin has been evaluated as a natural chemopreventive agent due to its anti-cancer effects in a variety of cancer cell lines. However, the mechanism of the chemopreventive effect has been not well established, especially in human colorectal cancer cells. We evaluated the chemopreventive effect of chrysin in three different human colorectal cancer cell lines. We found that chrysin treatment consequently reduced cell viability via induction of apoptosis. We identified that the involvement of up-regulation of pro-apoptotic cytokines tumor necrosis factor (Tnf) α and ß genes and consequent activation of the TNF-mediated transcriptional pathway in chrysin-induced apoptosis. Using our generated AHR siRNA expressing colorectal cancer cells, we demonstrated that the chrysin-induced up-regulation of Tnfα and ß gene expression was dependent on the aryl hydrocarbon receptor (AHR), which is a ligand-receptor for chrysin. Subsequently, we found that the AHR siRNA expressing colorectal cancer cells were resistant to chrysin-induced apoptosis. Therefore, we concluded that AHR is required for the chrysin-induced apoptosis and the up-regulation of Tnfα and ß gene expression in human colorectal cancer cells.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Neoplasias Colorretais/tratamento farmacológico
Flavonoides/farmacologia
Receptores de Hidrocarboneto Arílico/fisiologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Neoplasias Colorretais/patologia
Citocromo P-450 CYP1A1/genética
Citocromo P-450 CYP1A2/genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Linfotoxina-alfa/genética
Elemento de Resposta Sérica/fisiologia
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Flavonoids); 0 (Lymphotoxin-alpha); 0 (Receptors, Aryl Hydrocarbon); 0 (Tumor Necrosis Factor-alpha); 3CN01F5ZJ5 (chrysin); EC 1.14.14.1 (CYP1A1 protein, human); EC 1.14.14.1 (CYP1A2 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP1A1); EC 1.14.14.1 (Cytochrome P-450 CYP1A2)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:170101
[Lr] Data última revisão:
170101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151031
[St] Status:MEDLINE


  7 / 192 MEDLINE  
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[PMID]:26691724
[Au] Autor:Buffet C; Catelli MG; Hecale-Perlemoine K; Bricaire L; Garcia C; Gallet-Dierick A; Rodriguez S; Cormier F; Groussin L
[Ad] Endereço:Endocrinology-Metabolism-Diabetes Department, Institut Cochin, Université Paris Descartes, CNRS (UMR8104), INSERM U1016, Paris, France.
[Ti] Título:Dual Specificity Phosphatase 5, a Specific Negative Regulator of ERK Signaling, Is Induced by Serum Response Factor and Elk-1 Transcription Factor.
[So] Source:PLoS One;10(12):e0145484, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Serum stimulation of mammalian cells induces, via the MAPK pathway, the nuclear protein DUSP5 (dual-specificity phosphatase 5), which specifically interacts with and inactivates the ERK1/2 MAP kinases. However, molecular mechanisms underlying DUSP5 induction are not well known. Here, we found that the DUSP5 mRNA induction depends on a transcriptional regulation by the MAPK pathway, without any modification of the mRNA stability. Two contiguous CArG boxes that bind serum response factor (SRF) were found in a 1 Kb promoter region, as well as several E twenty-six transcription factor family binding sites (EBS). These sites potentially bind Elk-1, a transcription factor activated by ERK1/2. Using wild type or mutated DUSP5 promoter reporters, we demonstrated that SRF plays a crucial role in serum induction of DUSP5 promoter activity, the proximal CArG box being important for SRF binding in vitro and in living cells. Moreover, in vitro and in vivo binding data of Elk-1 to the same promoter region further demonstrate a role for Elk-1 in the transcriptional regulation of DUSP5. SRF and Elk-1 form a ternary complex (Elk-1-SRF-DNA) on DUSP5 promoter, consequently providing a link to an important negative feedback tightly regulating phosphorylated ERK levels.
[Mh] Termos MeSH primário: Fosfatases de Especificidade Dupla/genética
Fosfatases de Especificidade Dupla/metabolismo
Sistema de Sinalização das MAP Quinases/fisiologia
Fator de Resposta Sérica/metabolismo
Proteínas Elk-1 do Domínio ets/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Regulação Enzimológica da Expressão Gênica
Meia-Vida
Camundongos
Mutação
Células NIH 3T3
Regiões Promotoras Genéticas
RNA Mensageiro/metabolismo
Elemento de Resposta Sérica
Fator de Resposta Sérica/genética
Transdução de Sinais
Proteínas Elk-1 do Domínio ets/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Elk1 protein, mouse); 0 (RNA, Messenger); 0 (Serum Response Factor); 0 (ets-Domain Protein Elk-1); EC 3.1.3.48 (Dual-Specificity Phosphatases); EC 3.1.3.48 (Dusp5 protein, mouse)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160108
[Lr] Data última revisão:
160108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151223
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0145484


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[PMID]:26241044
[Au] Autor:Lee MY; Park C; Berent RM; Park PJ; Fuchs R; Syn H; Chin A; Townsend J; Benson CC; Redelman D; Shen TW; Park JK; Miano JM; Sanders KM; Ro S
[Ad] Endereço:Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America; Department of Physiology, Wonkwang Digestive Disease Research Institute and Institute of Wonkwang Medical Science, School of Medicine, Wonkwang University, Iksan, Jeollabuk-do,
[Ti] Título:Smooth Muscle Cell Genome Browser: Enabling the Identification of Novel Serum Response Factor Target Genes.
[So] Source:PLoS One;10(8):e0133751, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genome-scale expression data on the absolute numbers of gene isoforms offers essential clues in cellular functions and biological processes. Smooth muscle cells (SMCs) perform a unique contractile function through expression of specific genes controlled by serum response factor (SRF), a transcription factor that binds to DNA sites known as the CArG boxes. To identify SRF-regulated genes specifically expressed in SMCs, we isolated SMC populations from mouse small intestine and colon, obtained their transcriptomes, and constructed an interactive SMC genome and CArGome browser. To our knowledge, this is the first online resource that provides a comprehensive library of all genetic transcripts expressed in primary SMCs. The browser also serves as the first genome-wide map of SRF binding sites. The browser analysis revealed novel SMC-specific transcriptional variants and SRF target genes, which provided new and unique insights into the cellular and biological functions of the cells in gastrointestinal (GI) physiology. The SRF target genes in SMCs, which were discovered in silico, were confirmed by proteomic analysis of SMC-specific Srf knockout mice. Our genome browser offers a new perspective into the alternative expression of genes in the context of SRF binding sites in SMCs and provides a valuable reference for future functional studies.
[Mh] Termos MeSH primário: Proteínas Musculares/genética
Miócitos de Músculo Liso/metabolismo
RNA Mensageiro/genética
Elemento de Resposta Sérica/genética
Fator de Resposta Sérica/metabolismo
Navegador
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Proteínas de Transporte/genética
Colo/citologia
Simulação por Computador
Biblioteca Gênica
Genes Reporter
Proteínas de Fluorescência Verde
Código das Histonas
Histonas/metabolismo
Canais Iônicos/genética
Jejuno/citologia
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Especificidade de Órgãos
Proteômica
Fator de Resposta Sérica/deficiência
Transcriptoma
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Histones); 0 (Ion Channels); 0 (Muscle Proteins); 0 (RNA, Messenger); 0 (Serum Response Factor); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150805
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0133751


  9 / 192 MEDLINE  
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[PMID]:25923532
[Au] Autor:Stepánek J; Kopecký V; Turpin PY; Li Z; Alpert B; Zentz C
[Ad] Endereço:Laboratoire Jean Perrin, UPMC Université Paris 06, CNRS FRE 3231, Paris, France; ER12, UPMC Université Paris 06, Paris, France; Institute of Physics, Faculty of Mathematics and Physics, Charles University in Prague, Prague, Czech Republic.
[Ti] Título:DNA Electric Charge Oscillations Govern Protein-DNA Recognition.
[So] Source:PLoS One;10(4):e0124444, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transcriptional activity of the serum response factor (SRF) protein is triggered by its binding to a 10-base-pair DNA consensus sequence designated the CArG box, which is the core sequence of the serum response element (SRE). Sequence-specific recognition of the CArG box by a core domain of 100 amino acid residues of SRF (core-SRF) was asserted to depend almost exclusively on the intrinsic SRE conformation and on the degree of protein-induced SRE bending. Nevertheless, this paradigm was invalidated by a temperature-dependent Raman spectroscopy study of 20-mer oligonucleotides involved in bonding interactions with core-SRF that reproduced both wild type and mutated c-fos SREs. Indeed, the SRE moieties that are complexed with core-SRF exhibit permanent interconversion dynamics between bent and linear conformers. Thus, sequence-specific recognition of the CArG box by core-SRF cannot be explained only in terms of the three-dimensional structure of the SRE. A particular dynamic pairing process discriminates between the wild type and mutated complexes. Specific oscillations of the phosphate charge network of the SRE govern the recognition between both partners rather than an intrinsic set of conformations of the SRE.
[Mh] Termos MeSH primário: DNA/química
Oligonucleotídeos/química
Fosfatos/química
Elemento de Resposta Sérica/genética
Fator de Resposta Sérica/química
[Mh] Termos MeSH secundário: Sítios de Ligação
Seres Humanos
Simulação de Dinâmica Molecular
Dados de Sequência Molecular
Conformação de Ácido Nucleico
Motivos de Nucleotídeos
Ligação Proteica
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Fator de Resposta Sérica/genética
Análise Espectral Raman
Eletricidade Estática
Termodinâmica
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Oligonucleotides); 0 (Phosphates); 0 (Recombinant Proteins); 0 (SRF protein, human); 0 (Serum Response Factor); 9007-49-2 (DNA)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150430
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0124444


  10 / 192 MEDLINE  
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[PMID]:25722434
[Au] Autor:Zhao H; Wen G; Wen G; Huang Y; Yu X; Chen Q; Afzal TA; Luong le A; Zhu J; Ye S; Shu Y; Zhang L; Xiao Q
[Ad] Endereço:From the Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom (H.Z., G.W., Y.H., X.Y., Q.C., T.A.A., L.A.L., Y.S., Q.X.); and Department of Cardiology, the First Affiliated
[Ti] Título:MicroRNA-22 regulates smooth muscle cell differentiation from stem cells by targeting methyl CpG-binding protein 2.
[So] Source:Arterioscler Thromb Vasc Biol;35(4):918-29, 2015 Apr.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: In this study, we attempted to uncover the functional impact of microRNA-22 (miR-22) and its target gene in smooth muscle cell (SMC) differentiation and delineate the molecular mechanism involved. APPROACH AND RESULTS: miR-22 was found to be significantly upregulated during SMC differentiation from embryonic stem cells and adventitia stem/progenitor cells. Enforced expression of miR-22 by its mimic, while knockdown of miR-22 by its antagomiR, promotes or inhibits SMC differentiation from embryonic stem cells and adventitia stem/progenitor cells, respectively. Expectedly, miR-22 overexpression in stem cells promoted SMC differentiation in vivo. Methyl CpG-binding protein 2 (MECP2) was predicted as one of the top targets of miR-22. Interestingly, the gene expression levels of MECP2 were significantly decreased during SMC differentiation, and MECP2 was dramatically decreased in miR-22 overexpressing cells but significantly increased when miR-22 was knockdown in the differentiating stem cells. Importantly, luciferase assay showed that miR-22 substantially inhibited wild-type, but not mutant MECP2-3' untranslated region-luciferase activity. In addition, modulation of MECP2 expression levels affects multiple SMC-specific gene expression in differentiated embryonic stem cells. Mechanistically, our data showed that MECP2 could transcriptionally repress SMC gene expression through modulating various SMC transcription factors, as well as several proven SMC differentiation regulators. Evidence also revealed that enrichment of H3K9 trimethylation around the promoter regions of the SMC differentiation regulators genes were significantly increased by MECP2 overexpression. Finally, miR-22 was upregulated by platelet-derived growth factor-BB and transforming growth factor-ß through a transcriptional mechanism during SMC differentiation. CONCLUSIONS: miR-22 plays an important role in SMC differentiation, and epigenetic regulation through MECP2 is required for miR-22 mediated SMC differentiation.
[Mh] Termos MeSH primário: Diferenciação Celular
Células-Tronco Embrionárias/metabolismo
Proteína 2 de Ligação a Metil-CpG/metabolismo
MicroRNAs/metabolismo
Miócitos de Músculo Liso/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Sítios de Ligação
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Células-Tronco Embrionárias/efeitos dos fármacos
Epigênese Genética
Regulação da Expressão Gênica
Histonas/metabolismo
Proteína 2 de Ligação a Metil-CpG/genética
Metilação
Camundongos
MicroRNAs/genética
Mutação
Miócitos de Músculo Liso/efeitos dos fármacos
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Oligonucleotídeos/metabolismo
Fosfolipases A2/genética
Fosfolipases A2/metabolismo
Proteínas Proto-Oncogênicas c-sis/farmacologia
Interferência de RNA
Elemento de Resposta Sérica
Fator de Resposta Sérica/genética
Fator de Resposta Sérica/metabolismo
Transdução de Sinais
Fatores de Tempo
Transativadores/genética
Transativadores/metabolismo
Transcrição Genética
Transfecção
Fator de Crescimento Transformador beta/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Histones); 0 (Mecp2 protein, mouse); 0 (Methyl-CpG-Binding Protein 2); 0 (MicroRNAs); 0 (Mirn22 microRNA, mouse); 0 (Nuclear Proteins); 0 (Oligonucleotides); 0 (Proto-Oncogene Proteins c-sis); 0 (Serum Response Factor); 0 (Trans-Activators); 0 (Transforming Growth Factor beta); 0 (myocardin); 1B56C968OA (becaplermin); EC 3.1.1.4 (Phospholipases A2); EC 3.1.1.4 (Pla2g7 protein, mouse)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150228
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.114.305212



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