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Pesquisa : E05.196.401.133 [Categoria DeCS]
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[PMID]:26404144
[Au] Autor:Jia Y; Nagore L; Jarrett H
[Ad] Endereço:Department of Chemistry, University of Texas at San Antonio, One UTSA Circle, San Antonio, TX, 78249, USA.
[Ti] Título:Southwestern Blotting Assay.
[So] Source:Methods Mol Biol;1334:85-99, 2015.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Southwestern blotting is a technique used to study DNA-protein interactions. This method detects specific DNA-binding proteins by incubating radiolabeled DNA with a gel blot, washing, and visualizing through autoradiography. A blot resulting from 1-dimensional SDS-PAGE reveals the molecular weight of the binding proteins. To increase separation and determine isoelectric point a 2-dimensional gel can be blotted. Additional dimensions of electrophoresis, such as a gel shift (EMSA), can precede isoelectric focusing and SDS-PAGE to further improve separation. Combined with other techniques, such as mass spectrometry, the DNA-binding protein can be identified.
[Mh] Termos MeSH primário: Southwestern Blotting/métodos
Proteínas de Ligação a DNA/química
DNA/química
Ensaio de Desvio de Mobilidade Eletroforética/métodos
[Mh] Termos MeSH secundário: DNA/genética
Proteínas de Ligação a DNA/genética
Eletroforese em Gel Bidimensional
Espectrometria de Massas
Fatores de Transcrição/química
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Transcription Factors); 9007-49-2 (DNA)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150926
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-2877-4_5


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[PMID]:26139255
[Au] Autor:Franke C; Gräfe D; Bartsch H; Bachmann MP
[Ad] Endereço:Institut für Immunologie, Carl Gustav Carus Technische Universität Dresden, Germany, Fetscherstrasse 74, Dresden, 01307, Germany.
[Ti] Título:Use of Nonradioactive Detection Method for North- and South-Western Blot.
[So] Source:Methods Mol Biol;1314:63-71, 2015.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many proteins bind to nucleic acids. For the first characterization of novel proteins, a fast and simple technique for testing their nucleic acid binding capabilities is desirable. Here we describe the use of a North-western and South-western blot protocol for the evaluation of the DNA and RNA binding abilities of a novel putative methyl transferase HSPC133 (METTL5).
[Mh] Termos MeSH primário: Northern Blotting/métodos
Southwestern Blotting/métodos
Western Blotting/métodos
DNA/metabolismo
Metiltransferases/metabolismo
RNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Sondas de DNA/metabolismo
Seres Humanos
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA Probes); 63231-63-0 (RNA); 9007-49-2 (DNA); EC 2.1.1.- (Methyltransferases)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150703
[Lr] Data última revisão:
150703
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150704
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-2718-0_8


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[PMID]:25813524
[Au] Autor:Shukla S; Khan S; Kumar S; Sinha S; Farhan M; Bora HK; Maurya R; Meeran SM
[Ad] Endereço:Laboratory of Cancer Epigenetics, Division of Endocrinology, CSIR-Central Drug Research Institute, Lucknow, India.
[Ti] Título:Cucurbitacin B Alters the Expression of Tumor-Related Genes by Epigenetic Modifications in NSCLC and Inhibits NNK-Induced Lung Tumorigenesis.
[So] Source:Cancer Prev Res (Phila);8(6):552-62, 2015 Jun.
[Is] ISSN:1940-6215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Non-small cell lung cancer (NSCLC) represents almost 85% of total diagnosed lung cancer. Studies have shown that combination of DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors is effective against various cancers, including lung cancer. However, optimizing the synergistic dose regime is very difficult and involves adverse side effects. Therefore, in this study, we have shown that cucurbitacin B (CuB), a single bioactive triterpenoid compound, inhibits both DNMTs and HDACs starting at a very low dose of 60 nmol/L in NSCLC H1299 cells. The CuB-mediated inhibition of DNMTs and HDACs in H1299 cells leads to the reactivation of key tumor suppressor genes (TSG) such as CDKN1A and CDKN2A, as well as downregulation of oncogenes c-MYC and K-RAS and key tumor promoter gene (TPG), human telomerase reverse transcriptase (hTERT). The upregulation of TSGs and downregulation of TPG were consistently correlated with the alterations in their promoter methylation and histone modifications. This altered expression of TPG and TSGs is, at least in part, responsible for the inhibition of cellular proliferation and induction of cellular apoptosis in NSCLC. Furthermore, CuB treatment significantly inhibited the tumor incidence and multiplicity in 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice, which was associated with the induction of apoptosis and inhibition of hyperproliferation in the lung tissues. Together, our study provides new insight into the CuB-mediated epigenetic alterations and its chemotherapeutic effects on lung cancer.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/prevenção & controle
Transformação Celular Neoplásica/efeitos dos fármacos
Epigênese Genética
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Neoplasias Pulmonares/prevenção & controle
Nitrosaminas/toxicidade
Triterpenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Southwestern Blotting
Western Blotting
Carcinógenos/toxicidade
Carcinoma Pulmonar de Células não Pequenas/induzido quimicamente
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/patologia
Imunoprecipitação da Cromatina
Metilação de DNA/efeitos dos fármacos
Feminino
Genes Neoplásicos
Histona Desacetilases/química
Seres Humanos
Técnicas Imunoenzimáticas
Neoplasias Pulmonares/induzido quimicamente
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Camundongos
Camundongos Endogâmicos A
Regiões Promotoras Genéticas
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carcinogens); 0 (Nitrosamines); 0 (RNA, Messenger); 0 (Triterpenes); 0115W5MABF (cucurbitacin B); 7S395EDO61 (4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150328
[St] Status:MEDLINE
[do] DOI:10.1158/1940-6207.CAPR-14-0286


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[PMID]:25151354
[Au] Autor:Cole F; Baudat F; Grey C; Keeney S; de Massy B; Jasin M
[Ad] Endereço:1] Developmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA. [2] Department of Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Smithville, Texas, USA. [3].
[Ti] Título:Mouse tetrad analysis provides insights into recombination mechanisms and hotspot evolutionary dynamics.
[So] Source:Nat Genet;46(10):1072-80, 2014 Oct.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ability to examine all chromatids from a single meiosis in yeast tetrads has been indispensable for defining the mechanisms of homologous recombination initiated by DNA double-strand breaks (DSBs). Using a broadly applicable strategy for the analysis of chromatids from a single meiosis at two recombination hotspots in mouse oocytes and spermatocytes, we demonstrate here the unidirectional transfer of information-gene conversion-in both crossovers and noncrossovers. Whereas gene conversion in crossovers is associated with reciprocal exchange, the unbroken chromatid is not altered in noncrossover gene conversion events, providing strong evidence that noncrossovers arise from a distinct pathway. Gene conversion frequently spares the binding site of the hotspot-specifying protein PRDM9, with the result that erosion of the hotspot is slowed. Thus, mouse tetrad analysis demonstrates how unique aspects of mammalian recombination mechanisms shape hotspot evolutionary dynamics.
[Mh] Termos MeSH primário: Evolução Molecular
Meiose/genética
Oócitos/metabolismo
Recombinação Genética/genética
Espermatócitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Southwestern Blotting
Cromossomos de Mamíferos/genética
Cromossomos de Mamíferos/metabolismo
Troca Genética
Feminino
Conversão Gênica
Histona-Lisina N-Metiltransferase/genética
Histona-Lisina N-Metiltransferase/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos DBA
Camundongos Endogâmicos
Modelos Genéticos
Oócitos/citologia
Espermatócitos/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.1.1.43 (prdm9 protein, mouse)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:170604
[Lr] Data última revisão:
170604
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140825
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3068


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[PMID]:25099485
[Au] Autor:Szeberényi J
[Ad] Endereço:Department of Medical Biology, Medical School, University of Pécs, H-7624, Pécs, Hungary.
[Ti] Título:Problem-solving test: Southwestern blotting.
[So] Source:Biochem Mol Biol Educ;42(5):443-5, 2014 Sep-Oct.
[Is] ISSN:1539-3429
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Terms to be familiar with before you start to solve the test: Southern blotting, Western blotting, restriction endonucleases, agarose gel electrophoresis, nitrocellulose filter, molecular hybridization, polyacrylamide gel electrophoresis, proto-oncogene, c-abl, Src-homology domains, tyrosine protein kinase, nuclear localization signal, cDNA, deletion mutants, expression plasmid, transfection, RNA polymerase II, promoter, Shine-Dalgarno sequence, polyadenylation element, affinity chromatography, Northern blotting, immunoprecipitation, sodium dodecylsulfate, autoradiography, tandem repeats.
[Mh] Termos MeSH primário: Southwestern Blotting/métodos
Biologia Molecular/métodos
Resolução de Problemas
Inquéritos e Questionários
[Mh] Termos MeSH secundário: Southern Blotting/métodos
Western Blotting/métodos
Enzimas de Restrição do DNA/metabolismo
Eletroforese em Gel de Poliacrilamida/métodos
Imunoprecipitação/métodos
Biologia Molecular/educação
Aprendizagem Baseada em Problemas/métodos
RNA Polimerase II/metabolismo
Terminologia como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.7.- (RNA Polymerase II); EC 3.1.21.- (DNA Restriction Enzymes)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140808
[St] Status:MEDLINE
[do] DOI:10.1002/bmb.20816


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[PMID]:24218554
[Au] Autor:Pohjoismäki JL; Williams SL; Boettger T; Goffart S; Kim J; Suomalainen A; Moraes CT; Braun T
[Ad] Endereço:Department of Cardiac Development and Remodelling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
[Ti] Título:Overexpression of Twinkle-helicase protects cardiomyocytes from genotoxic stress caused by reactive oxygen species.
[So] Source:Proc Natl Acad Sci U S A;110(48):19408-13, 2013 Nov 26.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial DNA (mtDNA) in adult human heart is characterized by complex molecular forms held together by junctional molecules of unknown biological significance. These junctions are not present in mouse hearts and emerge in humans during postnatal development, concomitant with increased demand for oxidative metabolism. To analyze the role of mtDNA organization during oxidative stress in cardiomyocytes, we used a mouse model, which recapitulates the complex mtDNA organization of human hearts by overexpression of the mitochondrial helicase, TWINKLE. Overexpression of TWINKLE rescued the oxidative damage induced replication stalling of mtDNA, reduced mtDNA point mutation load, and modified mtDNA rearrangements in heterozygous mitochondrial superoxide dismutase knockout hearts, as well as ameliorated cardiomyopathy in mice superoxide dismutase knockout in a p21-dependent manner. We conclude that mtDNA integrity influences cell survival and reason that tissue specific modes of mtDNA maintenance represent an adaptation to oxidative stress.
[Mh] Termos MeSH primário: Adaptação Biológica/fisiologia
DNA Helicases/metabolismo
DNA Mitocondrial/metabolismo
Proteínas Mitocondriais/metabolismo
Miócitos Cardíacos/metabolismo
Estresse Oxidativo/fisiologia
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Southwestern Blotting
Western Blotting
DNA Helicases/farmacologia
Replicação do DNA/efeitos dos fármacos
DNA Mitocondrial/fisiologia
Eletroforese em Gel Bidimensional
Perfilação da Expressão Gênica
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Imuno-Histoquímica
Imagem por Ressonância Magnética
Camundongos
Camundongos Knockout
Proteínas Mitocondriais/farmacologia
Dados de Sequência Molecular
Miócitos Cardíacos/fisiologia
Superóxido Dismutase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Mitochondrial); 0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (superoxide dismutase 2); EC 3.6.1.- (Peo1 protein, mouse); EC 3.6.4.- (DNA Helicases)
[Em] Mês de entrada:1401
[Cu] Atualização por classe:150422
[Lr] Data última revisão:
150422
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131113
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1303046110


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[PMID]:24086737
[Au] Autor:Brozovic A; Vukovic L; Polancac DS; Arany I; Köberle B; Fritz G; Fiket Z; Majhen D; Ambriovic-Ristov A; Osmak M
[Ad] Endereço:Division Of Molecular Biology, Ruder Boskovic Institute, Zagreb, Croatia.
[Ti] Título:Endoplasmic reticulum stress is involved in the response of human laryngeal carcinoma cells to Carboplatin but is absent in Carboplatin-resistant cells.
[So] Source:PLoS One;8(9):e76397, 2013.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The major obstacle of successful tumor treatment with carboplatin (CBP) is the development of drug resistance. In the present study, we found that following treatment with CBP the amount of platinum which enters the human laryngeal carcinoma (HEp2)-derived CBP-resistant (7T) cells is reduced relative to the parental HEp2. As a consequence, the formation of reactive oxidative species (ROS) is reduced, the induction of endoplasmic reticulum (ER) stress is diminished, the amount of inter- and intrastrand cross-links is lower, and the induction of apoptosis is depressed. In HEp2 cells, ROS scavenger tempol, inhibitor of ER stress salubrinal, as well as gene silencing of ER stress marker CCAAT/enhancer-binding protein (CHOP) increases their survival and renders them as resistant to CBP as 7T cell subline but did not influence the survival of 7T cells. Our results suggest that in HEp2 cells CBP-induced ROS is a stimulus for ER stress. To the contrary, despite the ability of CBP to induce formation of ROS and activate ER stress in 7T cells, the cell death mechanism in 7T cells is independent of ROS induction and activation of ER stress. The novel signaling pathway of CBP-driven toxicity that was found in the HEp2 cell line, i.e. increased ROS formation and induction of ER stress, may be predictive for therapeutic response of epithelial cancer cells to CBP-based therapy.
[Mh] Termos MeSH primário: Carboplatina/uso terapêutico
Carcinoma/tratamento farmacológico
Resistência a Medicamentos Antineoplásicos/fisiologia
Estresse do Retículo Endoplasmático/fisiologia
Neoplasias Laríngeas/tratamento farmacológico
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Southwestern Blotting
Western Blotting
Carcinoma/fisiopatologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Cinamatos
Óxidos N-Cíclicos
Primers do DNA/genética
Inativação Gênica
Seres Humanos
Neoplasias Laríngeas/fisiopatologia
Platina/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Marcadores de Spin
Tioureia/análogos & derivados
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cinnamates); 0 (Cyclic N-Oxides); 0 (DNA Primers); 0 (Reactive Oxygen Species); 0 (Spin Labels); 0 (salubrinal); 49DFR088MY (Platinum); BG3F62OND5 (Carboplatin); GYV9AM2QAG (Thiourea); U78ZX2F65X (tempol)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131003
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0076397


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[PMID]:23999007
[Au] Autor:Sanchez-Niño MD; Poveda J; Sanz AB; Mezzano S; Carrasco S; Fernandez-Fernandez B; Burkly LC; Nair V; Kretzler M; Hodgin JB; Ruiz-Ortega M; Selgas R; Egido J; Ortiz A
[Ad] Endereço:Servicio de Nefrologia, IdiPAZ, Madrid 28046, Spain.
[Ti] Título:Fn14 in podocytes and proteinuric kidney disease.
[So] Source:Biochim Biophys Acta;1832(12):2232-43, 2013 Dec.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Non-proliferative proteinuric diseases are the most common primary glomerular disorders causing end-stage renal disease. These disorders may associate low level glomerular inflammation and podocyte expression of inflammatory mediators. However, the factors regulating podocyte expression of inflammatory mediators in vivo in non-immune disorders are poorly understood. We have now explored the regulation and role of TWEAK receptor Fn14 in mediating glomerular inflammation in cultured podocytes and in experimental and human non-immune proteinuria. Transcriptomics disclosed Fn14 and MCP-1 mRNA upregulation in glomeruli from patients with focal segmental glomerulosclerosis, as well as a correlation between the expression of both transcripts. Increased glomerular Fn14 and MCP-1 mRNA was confirmed in a second focal segmental glomerulosclerosis cohort and was also observed in membranous nephropathy. In human non-proliferative proteinuric kidney diseases podocytes displayed Fn14 and MCP-1 expression and NFκB activation. Podocyte Fn14 was increased in murine protein overload-induced proteinuria. In Fn14 knock-out mice with protein overload-induced proteinuria, glomerular and periglomerular macrophage infiltrates were reduced, as were MCP-1 mRNA and podocyte MCP-1 staining and podocyte numbers preserved as compared to wild-type counterparts. Adenovirus-mediated overexpression of TWEAK increased periglomerular macrophage infiltration in mice without prior kidney injury. In cultured podocytes inflammatory cytokines increased Fn14 mRNA and protein levels. TWEAK activated NFκB and increased MCP-1 mRNA and protein, an effect prevented by the NFκB inhibitor parthenolide. In conclusion, Fn14 activation results in NFκB-mediated pro-inflammatory effects on podocytes that may be relevant for the pathogenesis of non-proliferative proteinuric kidney disease of non-immune origin.
[Mh] Termos MeSH primário: Inflamação/metabolismo
Nefropatias/metabolismo
Glomérulos Renais/metabolismo
Podócitos/metabolismo
Proteinúria/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Receptores do Fator de Necrose Tumoral/fisiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Biomarcadores/metabolismo
Southwestern Blotting
Western Blotting
Estudos de Casos e Controles
Células Cultivadas
Quimiocina CCL2/genética
Quimiocina CCL2/metabolismo
Citocina TWEAK
Citocinas/genética
Citocinas/metabolismo
Ensaio de Desvio de Mobilidade Eletroforética
Feminino
Imunofluorescência
Perfilação da Expressão Gênica
Seres Humanos
Técnicas Imunoenzimáticas
Inflamação/genética
Inflamação/patologia
Nefropatias/genética
Nefropatias/patologia
Glomérulos Renais/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Meia-Idade
NF-kappa B/genética
NF-kappa B/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Podócitos/patologia
Proteinúria/genética
Proteinúria/patologia
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Receptores do Fator de Necrose Tumoral/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Receptor de TWEAK
Fatores de Necrose Tumoral/genética
Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Cytokine TWEAK); 0 (Cytokines); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (Receptors, Tumor Necrosis Factor); 0 (TNFRSF12A protein, human); 0 (TNFSF12 protein, human); 0 (TWEAK Receptor); 0 (Tnfrsf12a protein, mouse); 0 (Tnfsf12 protein, mouse); 0 (Tumor Necrosis Factors)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130904
[St] Status:MEDLINE


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[PMID]:22808207
[Au] Autor:Barboro P; Repaci E; D'Arrigo C; Balbi C
[Ad] Endereço:IRCCS Azienda Ospedaliera Universitaria San Martino IST-Istituto Nazionale per la Ricerca sul Cancro, Department of Diagnostic Technologies, Genoa, Italy.
[Ti] Título:The role of nuclear matrix proteins binding to matrix attachment regions (Mars) in prostate cancer cell differentiation.
[So] Source:PLoS One;7(7):e40617, 2012.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In tumor progression definite alterations in nuclear matrix (NM) protein composition as well as in chromatin structure occur. The NM interacts with chromatin via specialized DNA sequences called matrix attachment regions (MARs). In the present study, using a proteomic approach along with a two-dimensional Southwestern assay and confocal laser microscopy, we show that the differentiation of stabilized human prostate carcinoma cells is marked out by modifications both NM protein composition and bond between NM proteins and MARs. Well-differentiated androgen-responsive and slowly growing LNCaP cells are characterized by a less complex pattern and by a major number of proteins binding MAR sequences in comparison to 22Rv1 cells expressing androgen receptor but androgen-independent. Finally, in the poorly differentiated and strongly aggressive androgen-independent PC3 cells the complexity of NM pattern further increases and a minor number of proteins bind the MARs. Furthermore, in this cell line with respect to LNCaP cells, these changes are synchronous with modifications in both the nuclear distribution of the MAR sequences and in the average loop dimensions that significantly increase. Although the expression of many NM proteins changes during dedifferentiation, only a very limited group of MAR-binding proteins seem to play a key role in this process. Variations in the expression of poly (ADP-ribose) polymerase (PARP) and special AT-rich sequence-binding protein-1 (SATB1) along with an increase in the phosphorylation of lamin B represent changes that might trigger passage towards a more aggressive phenotype. These results suggest that elucidating the MAR-binding proteins that are involved in the differentiation of prostate cancer cells could be an important tool to improve our understanding of this carcinogenesis process, and they could also be novel targets for prostate cancer therapy.
[Mh] Termos MeSH primário: Diferenciação Celular
Regiões de Interação com a Matriz
Proteínas Associadas à Matriz Nuclear/metabolismo
Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
[Mh] Termos MeSH secundário: Especificidade de Anticorpos/imunologia
Sequência de Bases
Southwestern Blotting
Western Blotting
Linhagem Celular Tumoral
DNA de Neoplasias/química
Ribonucleoproteínas Nucleares Heterogêneas Grupo U/metabolismo
Seres Humanos
Lamina Tipo B/metabolismo
Masculino
Proteínas de Ligação à Região de Interação com a Matriz/metabolismo
Conformação de Ácido Nucleico
Fosforilação
Poli(ADP-Ribose) Polimerases/metabolismo
Ligação Proteica
Transporte Proteico
Proteínas de Ligação a RNA/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Neoplasm); 0 (Heterogeneous-Nuclear Ribonucleoprotein U); 0 (Lamin Type B); 0 (MATR3 protein, human); 0 (Matrix Attachment Region Binding Proteins); 0 (Nuclear Matrix-Associated Proteins); 0 (RNA-Binding Proteins); 0 (SATB1 protein, human); EC 2.4.2.30 (Poly(ADP-ribose) Polymerases)
[Em] Mês de entrada:1301
[Cu] Atualização por classe:150224
[Lr] Data última revisão:
150224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120719
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0040617


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[PMID]:22706169
[Au] Autor:Li Y; Jiang R; Zhao Y; Xu Y; Ling M; Pang Y; Shen L; Zhou Y; Zhang J; Zhou J; Wang X; Liu Q
[Ad] Endereço:Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 210029, Jiangsu, PR China.
[Ti] Título:Opposed arsenite-mediated regulation of p53-survivin is involved in neoplastic transformation, DNA damage, or apoptosis in human keratinocytes.
[So] Source:Toxicology;300(3):121-31, 2012 Oct 28.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Biphasic dose-response relationship induced by environmental agents is often characterized with the effect of low-dose stimulation and high dose inhibition. Some studies showed that arsenite may induce cell proliferation and apoptosis via biphasic dose-response relationship in human cells; however, mechanisms underlying this phenomenon are not well understood. Our present study shows that, for human keratinocytes (HaCaT) cells, a low concentration of arsenite activates extracellular signal-regulated kinases (ERKs), which leads to up-regulation of nuclear factor κB (NF-κB) binding to DNA and to elevated, NF-κB-dependent expression of mot-2 (a p53 inhibitor) and survivin (an inhibitor of apoptosis). Activation of p53 is blocked, and neoplastic transformation is enhanced. Inhibition of ERKs reduces cell proliferation and neoplastic transformation. In contrast, a high concentration of arsenite activates c-Jun N-terminal kinases (JNKs), positive regulators of p53, by binding to p53 and preventing its murine double minute 2 (mdm2)-mediated degradation. The elevated levels of p53 lead to repair of DNA damage and apoptosis. Inhibition of JNKs increases DNA damage but decreases apoptosis. By identifying a mechanism whereby ERKs and JNKs-mediated regulation of the p53-survivin signal pathway is involved in the biphasic effects of arsenite on human keratinocytes, our data expand understanding of arsenite-induced cell proliferation, neoplastic transformation, DNA damage, and apoptosis.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Arsenitos/toxicidade
Transformação Celular Neoplásica/efeitos dos fármacos
Dano ao DNA
Proteínas Inibidoras de Apoptose/biossíntese
Queratinócitos/efeitos dos fármacos
Compostos de Sódio/toxicidade
Proteína Supressora de Tumor p53/biossíntese
[Mh] Termos MeSH secundário: Animais
Southwestern Blotting
Western Blotting
Técnicas de Cultura de Células
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Transformação Celular Neoplásica/metabolismo
Transformação Celular Neoplásica/patologia
Relação Dose-Resposta a Droga
Proteínas de Choque Térmico HSP70/biossíntese
Seres Humanos
Imunoprecipitação
Queratinócitos/enzimologia
Queratinócitos/metabolismo
Queratinócitos/patologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Camundongos
Camundongos Nus
Proteínas Mitocondriais/biossíntese
Neoplasias/induzido quimicamente
Neoplasias/metabolismo
Neoplasias/patologia
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arsenites); 0 (BIRC5 protein, human); 0 (HSP70 Heat-Shock Proteins); 0 (HSPA9 protein, human); 0 (Inhibitor of Apoptosis Proteins); 0 (Mitochondrial Proteins); 0 (Sodium Compounds); 0 (Tumor Suppressor Protein p53); 48OVY2OC72 (sodium arsenite)
[Em] Mês de entrada:1210
[Cu] Atualização por classe:121115
[Lr] Data última revisão:
121115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120619
[St] Status:MEDLINE
[do] DOI:10.1016/j.tox.2012.06.004



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