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[PMID]:28456966
[Au] Autor:Uh K; Lee K
[Ad] Endereço:Department of Animal and Poultry Sciences, Virginia Tech, Blacksburg, VA, USA.
[Ti] Título:Use of Chemicals to Inhibit DNA Replication, Transcription, and Protein Synthesis to Study Zygotic Genome Activation.
[So] Source:Methods Mol Biol;1605:191-205, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Maternal-to-zygotic transition is an event that developmental control of early embryos is switched from oocyte-derived factors to the zygotic genome. Ability to inhibit DNA replication, transcription, and translation is an important tool in studying events, such as zygotic genome activation, during embyogenesis. Here, we describe approaches to block DNA replication, transcription, and translation using chemical inhibitors. Then we also demonstrate how the transcript level of a maternally inherited gene, ten-eleven translocation methylcytosine dioxygenase 3, responses to the chemical treatments.
[Mh] Termos MeSH primário: Alfa-Amanitina/farmacologia
Cicloeximida/farmacologia
Inibidores da Síntese de Ácido Nucleico/farmacologia
Inibidores da Síntese de Proteínas/farmacologia
Suínos/embriologia
[Mh] Termos MeSH secundário: Animais
Metilação de DNA
Replicação do DNA/efeitos dos fármacos
Dioxigenases/genética
Herança Materna
Biossíntese de Proteínas/efeitos dos fármacos
Suínos/genética
Transcrição Genética/efeitos dos fármacos
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alpha-Amanitin); 0 (Nucleic Acid Synthesis Inhibitors); 0 (Protein Synthesis Inhibitors); 98600C0908 (Cycloheximide); EC 1.13.11.- (Dioxygenases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6988-3_13


  2 / 18683 MEDLINE  
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[PMID]:29185664
[Au] Autor:Staley ZR; Rohr JR; Senkbeil JK; Harwood VJ
[Ti] Título:Agrochemicals indirectly increase survival of E. coli O157:H7 and indicator bacteria by reducing ecosystem services.
[So] Source:Ecol Appl;24(8):1945-53, 2014.
[Is] ISSN:1051-0761
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Storm water and agricultural runoff frequently contain agrochemicals, fecal indicator bacteria (FIB), and zoonotic pathogens. Entry of such contaminants into aquatic ecosystems may affect ecology and human health. This study tested the hypothesis that the herbicide atrazine and the fungicide chlorothalonil indirectly affect the survival of FIB (Escherichia coli and Enterococcus faecalis) and a pathogen (E. coli O157:H7) by altering densities of protozoan predators or by altering competition from autochthonous bacteria. Streptomycin-resistant E. coli, En. faecalis, and E. coli O157:H7 were added to microcosms composed of Florida river water containing natural protozoan and bacterial populations. FIB, pathogen, and protozoan densities were monitored over six days. Known metabolic inhibitors, cycloheximide and streptomycin, were used to inhibit autochthonous protozoa or bacteria, respectively. The inhibitors made it possible to isolate the effects of predation or competition on survival of allochthonous bacteria, and each treatment increased the survival of FIB and pathogens. Chlorothalonil's effect was similar to that of cycloheximide, significantly reducing protozoan densities and elevating densities of FIB and pathogens relative to the control. Atrazine treatment did not affect protozoan densities, but, through an effect on competition, resulted in significantly greater densities of En. faecalis and E. coli O157:H7. Hence, by reducing predaceous protozoa and bacterial competitors that facilitate purifying water bodies of FIBs and human pathogens, chlorothalonil and atrazine indirectly diminished an ecosystem service of fresh water.
[Mh] Termos MeSH primário: Agroquímicos
Ecossistema
Escherichia coli O157/fisiologia
Poluentes Químicos da Água/química
[Mh] Termos MeSH secundário: Antifúngicos/química
Antifúngicos/farmacologia
Atrazina/química
Atrazina/farmacologia
Conservação dos Recursos Naturais
Cicloeximida/química
Cicloeximida/farmacologia
Enterococcus faecalis/fisiologia
Monitoramento Ambiental
Eucariotos/efeitos dos fármacos
Fungicidas Industriais/química
Fungicidas Industriais/farmacologia
Herbicidas/química
Herbicidas/farmacologia
Nitrilos/química
Nitrilos/farmacologia
Microbiologia da Água
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Agrochemicals); 0 (Antifungal Agents); 0 (Fungicides, Industrial); 0 (Herbicides); 0 (Nitriles); 0 (Water Pollutants, Chemical); 98600C0908 (Cycloheximide); J718M71A7A (tetrachloroisophthalonitrile); QJA9M5H4IM (Atrazine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171221
[Lr] Data última revisão:
171221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE


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[PMID]:28803066
[Au] Autor:Do YJ; Sul JW; Jang KH; Kang NS; Kim YH; Kim YG; Kim E
[Ad] Endereço:Department of Biological Sciences, Chungnam National University, Daejeon 34134, Republic of Korea.
[Ti] Título:A novel RIPK1 inhibitor that prevents retinal degeneration in a rat glaucoma model.
[So] Source:Exp Cell Res;359(1):30-38, 2017 Oct 01.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In glaucoma, retinal ganglion cells (RGCs) are exposed to ischemic stress with elevation of the intraocular pressure and are subsequently lost. Necroptosis, a type of regulated necrosis, is known to play a pivotal role in this loss. We observed that receptor-interacting protein kinase 1 (RIPK1), the key player of necroptosis, was activated by diverse ischemic stresses, including TCZ, chemical hypoxia (CH), and oxygen glucose deprivation (OGD). In this study, we introduce a RIPK1-inhibitory compound (RIC) with a novel scaffold. RIC inhibited downstream events following RIPK1 activation, including necrosome formation and mitochondrial dysfunction in RGC5 cells. Moreover, RIC protected RGCs against ischemic injury in the rat glaucoma model, which was induced by acute high intraocular pressure. However, RIC displayed biochemical characteristics that are distinct from those of previous RIPK1 inhibitors (necrostatin-1; Nec-1 and Compound 27; Cpd27). RIC protected RGCs against OGD insult, while Nec-1 and Cpd27 did not. Conversely, Nec-1 and Cpd27 protected RGCs from TNF-stimulated death, while RIC failed to inhibit the death of RGCs. This implies that RIPK1 activates alternative pathways depending on the context of the ischemic insults.
[Mh] Termos MeSH primário: Glaucoma/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
Degeneração Retiniana/tratamento farmacológico
Degeneração Retiniana/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Hipóxia Celular/efeitos dos fármacos
Células Cultivadas
Cicloeximida
Modelos Animais de Doenças
Glaucoma/complicações
Glaucoma/patologia
Glucose/deficiência
Células HT29
Seres Humanos
Injeções Intraperitoneais
Isquemia/complicações
Isquemia/patologia
Masculino
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Necrose
Neuroproteção/efeitos dos fármacos
Oligopeptídeos
Oxigênio
Inibidores de Proteínas Quinases/química
Inibidores de Proteínas Quinases/farmacologia
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas Serina-Treonina Quinases/metabolismo
Ratos Sprague-Dawley
Degeneração Retiniana/complicações
Degeneração Retiniana/patologia
Neurônios Retinianos/efeitos dos fármacos
Neurônios Retinianos/metabolismo
Neurônios Retinianos/patologia
Fator de Necrose Tumoral alfa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oligopeptides); 0 (Protein Kinase Inhibitors); 0 (Tumor Necrosis Factor-alpha); 0 (benzyloxycarbonyl-valyl-alanyl-aspartic acid); 98600C0908 (Cycloheximide); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (RIP1 protein, rat); IY9XDZ35W2 (Glucose); S88TT14065 (Oxygen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170814
[St] Status:MEDLINE


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[PMID]:28781168
[Au] Autor:Wong HH; Lin JQ; Ströhl F; Roque CG; Cioni JM; Cagnetta R; Turner-Bridger B; Laine RF; Harris WA; Kaminski CF; Holt CE
[Ad] Endereço:Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3DY, UK.
[Ti] Título:RNA Docking and Local Translation Regulate Site-Specific Axon Remodeling In Vivo.
[So] Source:Neuron;95(4):852-868.e8, 2017 Aug 16.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nascent proteins can be positioned rapidly at precise subcellular locations by local protein synthesis (LPS) to facilitate localized growth responses. Axon arbor architecture, a major determinant of synaptic connectivity, is shaped by localized growth responses, but it is unknown whether LPS influences these responses in vivo. Using high-resolution live imaging, we examined the spatiotemporal dynamics of RNA and LPS in retinal axons during arborization in vivo. Endogenous RNA tracking reveals that RNA granules dock at sites of branch emergence and invade stabilized branches. Live translation reporter analysis reveals that de novo ß-actin hotspots colocalize with docked RNA granules at the bases and tips of new branches. Inhibition of axonal ß-actin mRNA translation disrupts arbor dynamics primarily by reducing new branch emergence and leads to impoverished terminal arbors. The results demonstrate a requirement for LPS in building arbor complexity and suggest a key role for pre-synaptic LPS in assembling neural circuits.
[Mh] Termos MeSH primário: Axônios/fisiologia
Regulação da Expressão Gênica no Desenvolvimento/genética
RNA/metabolismo
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Animais
Anisomicina/farmacologia
Biotina/metabolismo
Blastômeros
Carbocianinas/metabolismo
Cicloeximida/farmacologia
Nucleotídeos de Desoxiuracil/metabolismo
Embrião não Mamífero
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Técnicas In Vitro
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Mitocôndrias/metabolismo
Morfolinos/farmacologia
Oligonucleotídeos Antissenso/farmacologia
Técnicas de Cultura de Órgãos
Inibidores da Síntese de Proteínas/farmacologia
RNA/genética
Retina/citologia
Xenopus laevis
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3'-deoxy-5-(cyanine dye 5)uridine 5'-trisphosphate); 0 (Actins); 0 (Carbocyanines); 0 (Deoxyuracil Nucleotides); 0 (Luminescent Proteins); 0 (Morpholinos); 0 (Oligonucleotides, Antisense); 0 (Protein Synthesis Inhibitors); 63231-63-0 (RNA); 6C74YM2NGI (Anisomycin); 6SO6U10H04 (Biotin); 98600C0908 (Cycloheximide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE


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[PMID]:28771613
[Au] Autor:Anda S; Zach R; Grallert B
[Ad] Endereço:Department of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
[Ti] Título:Activation of Gcn2 in response to different stresses.
[So] Source:PLoS One;12(8):e0182143, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:All organisms have evolved pathways to respond to different forms of cellular stress. The Gcn2 kinase is best known as a regulator of translation initiation in response to starvation for amino acids. Work in budding yeast has showed that the molecular mechanism of GCN2 activation involves the binding of uncharged tRNAs, which results in a conformational change and GCN2 activation. This pathway requires GCN1, which ensures delivery of the uncharged tRNA onto GCN2. However, Gcn2 is activated by a number of other stresses which do not obviously involve accumulation of uncharged tRNAs, raising the question how Gcn2 is activated under these conditions. Here we investigate the requirement for ongoing translation and tRNA binding for Gcn2 activation after different stresses in fission yeast. We find that mutating the tRNA-binding site on Gcn2 or deleting Gcn1 abolishes Gcn2 activation under all the investigated conditions. These results suggest that tRNA binding to Gcn2 is required for Gcn2 activation not only in response to starvation but also after UV irradiation and oxidative stress.
[Mh] Termos MeSH primário: Proteínas Serina-Treonina Quinases/metabolismo
RNA de Transferência/metabolismo
Proteínas de Schizosaccharomyces pombe/metabolismo
Estresse Fisiológico/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Cicloeximida/farmacologia
Fator de Iniciação 2 em Eucariotos/metabolismo
Peróxido de Hidrogênio/toxicidade
Mutagênese
Estresse Oxidativo/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Fosforilação/efeitos da radiação
Biossíntese de Proteínas/efeitos da radiação
Inibidores da Síntese de Proteínas/farmacologia
Proteínas Serina-Treonina Quinases/química
Proteínas Serina-Treonina Quinases/genética
Schizosaccharomyces/genética
Schizosaccharomyces/metabolismo
Schizosaccharomyces/efeitos da radiação
Proteínas de Schizosaccharomyces pombe/química
Proteínas de Schizosaccharomyces pombe/genética
Alinhamento de Sequência
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Eukaryotic Initiation Factor-2); 0 (Protein Synthesis Inhibitors); 0 (Schizosaccharomyces pombe Proteins); 9014-25-9 (RNA, Transfer); 98600C0908 (Cycloheximide); BBX060AN9V (Hydrogen Peroxide); EC 2.7.11.1 (Gcn2 protein, S pombe); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182143


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[PMID]:28715128
[Au] Autor:Le Cann F; Delehouzé C; Leverrier-Penna S; Filliol A; Comte A; Delalande O; Desban N; Baratte B; Gallais I; Piquet-Pellorce C; Faurez F; Bonnet M; Mettey Y; Goekjian P; Samson M; Vandenabeele P; Bach S; Dimanche-Boitrel MT
[Ad] Endereço:INSERM UMR 1085, l'Environnement et le Travail, Institut de Recherche sur la Santé, Rennes, France.
[Ti] Título:Sibiriline, a new small chemical inhibitor of receptor-interacting protein kinase 1, prevents immune-dependent hepatitis.
[So] Source:FEBS J;284(18):3050-3068, 2017 Sep.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Necroptosis is a regulated form of cell death involved in several disease models including in particular liver diseases. Receptor-interacting protein kinases, RIPK1 and RIPK3, are the main serine/threonine kinases driving this cell death pathway. We screened a noncommercial, kinase-focused chemical library which allowed us to identify Sibiriline as a new inhibitor of necroptosis induced by tumor necrosis factor (TNF) in Fas-associated protein with death domain (FADD)-deficient Jurkat cells. Moreover, Sib inhibits necroptotic cell death induced by various death ligands in human or mouse cells while not protecting from caspase-dependent apoptosis. By using competition binding assay and recombinant kinase assays, we demonstrated that Sib is a rather specific competitive RIPK1 inhibitor. Molecular docking analysis shows that Sib is trapped closed to human RIPK1 adenosine triphosphate-binding site in a relatively hydrophobic pocket locking RIPK1 in an inactive conformation. In agreement with its RIPK1 inhibitory property, Sib inhibits both TNF-induced RIPK1-dependent necroptosis and RIPK1-dependent apoptosis. Finally, Sib protects mice from concanavalin A-induced hepatitis. These results reveal the small-molecule Sib as a new RIPK1 inhibitor potentially of interest for the treatment of immune-dependent hepatitis.
[Mh] Termos MeSH primário: Alcaloides/farmacologia
Hepatite Animal/prevenção & controle
Fatores Imunológicos/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Proteína Serina-Treonina Quinases de Interação com Receptores/genética
Compostos de Espiro/farmacologia
[Mh] Termos MeSH secundário: Alcaloides/química
Animais
Apoptose/efeitos dos fármacos
Apoptose/genética
Caspase 3/genética
Caspase 3/imunologia
Linhagem Celular Transformada
Concanavalina A
Cicloeximida/farmacologia
Fibroblastos/citologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Células HT29
Hepatite Animal/induzido quimicamente
Hepatite Animal/genética
Hepatite Animal/imunologia
Seres Humanos
Imidazóis/farmacologia
Fatores Imunológicos/química
Indóis/farmacologia
Células Jurkat
Masculino
Camundongos
Simulação de Acoplamento Molecular
Necrose/induzido quimicamente
Necrose/genética
Necrose/imunologia
Inibidores de Proteínas Quinases/química
Proteína Serina-Treonina Quinases de Interação com Receptores/antagonistas & inibidores
Proteína Serina-Treonina Quinases de Interação com Receptores/imunologia
Transdução de Sinais
Compostos de Espiro/química
Ligante Indutor de Apoptose Relacionado a TNF/farmacologia
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkaloids); 0 (Imidazoles); 0 (Immunologic Factors); 0 (Indoles); 0 (Protein Kinase Inhibitors); 0 (Spiro Compounds); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF10 protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (necrostatin-1); 0 (sibirine); 11028-71-0 (Concanavalin A); 98600C0908 (Cycloheximide); EC 2.7.11.1 (RIPK1 protein, human); EC 2.7.11.1 (RIPK3 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14176


  7 / 18683 MEDLINE  
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[PMID]:28617824
[Au] Autor:Sakane Y; Kanamoto N; Yamauchi I; Tagami T; Morita Y; Miura M; Sone M; Yasoda A; Kimura T; Nakao K; Inagaki N
[Ad] Endereço:Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine, Kyoto, Japan.
[Ti] Título:Regulation of type 1 iodothyronine deiodinase by LXRα.
[So] Source:PLoS One;12(6):e0179213, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The iodothyronine deiodinases are selenoenzymes that regulate the activity of thyroid hormone via specific inner- or outer-ring deiodination. In humans, type 1 deiodinase (D1) is highly expressed in the liver, but the mechanism by which its gene expression is regulated remains to be elucidated. Liver X receptor α (LXRα), a transcription factor of the nuclear receptor superfamily, is highly expressed in the liver, where it functions as a sensor for excess intracellular oxysterols. LXRα interacts with other nuclear receptors on promoters of genes that contain a binding core sequence for nuclear receptors. In addition, it is reported that the promoter of the gene encoding human D1 (hDIO1) contains the core sequence for one of nuclear receptors, thyroid hormone receptor (TR). We investigated the involvement of LXRα in the regulation of hDIO1, in the liver. We performed hDIO1 promoter-reporter assays using a synthetic LXR agonist, T0901317, and compared promoter activity between a human liver carcinoma cell line, HepG2, and a clone of human embryonic kidney cells, TSA201. We defined the region between nucleotides -131 and -114, especially nucleotides -126 and -125, of the hDIO1 promoter as critical for basal and LXRα-mediated specific transcriptional activation in HepG2 cells. An increase in hDIO1 expression was observed in LXRα-stimulated cells, but absent in cycloheximide-treated cells, indicating that new protein synthesis is required for LXRα-mediated regulation of hDIO1. On the other hand, electrophoretic mobility shift assays revealed that LXRα and RXRα bound to the hDIO1 promoter. We also demonstrated that LXRα and TRß compete with each other on this specific region of the promoter. In conclusion, our results indicated that LXRα plays a specific and important role in activation of TH by regulating D1, and that LXRα binds to and regulates the hDIO1 promoter, competing with TRß on specific sequences within the promoter.
[Mh] Termos MeSH primário: Regulação Enzimológica da Expressão Gênica/fisiologia
Iodeto Peroxidase/biossíntese
Receptores X do Fígado/metabolismo
Fígado/metabolismo
Elementos de Resposta/fisiologia
Ativação Transcricional/fisiologia
[Mh] Termos MeSH secundário: Cicloeximida/farmacologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Células HEK293
Células Hep G2
Seres Humanos
Hidrocarbonetos Fluorados/farmacologia
Iodeto Peroxidase/genética
Receptores X do Fígado/genética
Receptores dos Hormônios Tireóideos/genética
Receptores dos Hormônios Tireóideos/metabolismo
Receptor X Retinoide alfa/genética
Receptor X Retinoide alfa/metabolismo
Sulfonamidas/farmacologia
Ativação Transcricional/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydrocarbons, Fluorinated); 0 (Liver X Receptors); 0 (NR1H3 protein, human); 0 (Receptors, Thyroid Hormone); 0 (Retinoid X Receptor alpha); 0 (Sulfonamides); 0 (TO-901317); 98600C0908 (Cycloheximide); EC 1.11.1.- (iodothyronine deiodinase type I); EC 1.11.1.8 (Iodide Peroxidase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179213


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[PMID]:28476788
[Au] Autor:Mandelkow R; Gümbel D; Ahrend H; Kaul A; Zimmermann U; Burchardt M; Stope MB
[Ad] Endereço:Department of Urology, University of Medicine Greifswald, Greifswald, Germany.
[Ti] Título:Detection and Quantification of Nuclear Morphology Changes in Apoptotic Cells by Fluorescence Microscopy and Subsequent Analysis of Visualized Fluorescent Signals.
[So] Source:Anticancer Res;37(5):2239-2244, 2017 05.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Apoptosis results in specific and stage-dependent morphological alterations of the cell nucleus, including pyknosis and cell shrinking. The experimental investigation of apoptotic processes is still challenging and routinely based on the assessment of molecular events like chromatin fragmentation and caspase enzyme activity. Alternatively, the establishment of a fluorescence microscopy nuclear morphology assay would provide a simple and robust low-cost method for detection and quantification of apoptotic cascades. MATERIALS AND METHODS: Model cell lines LNCaP and MDA-MB-231 were incubated in the presence of the apoptosis-inducer cycloheximide (CHX). After evaluation of apoptotic cascades by terminal deoxynucleotidyl transferase-dUTP nick-end labeling (TUNEL) assay, stained cell nuclei were analyzed regarding area, perimeter, major and minor axis, as well as brightness of nuclear fluorescence signal. RESULTS: When compared to vehicle-treated control cells, administration of CHX led to significantly reduced cell growth and elevated rates of chromatin fragmentation of both cell lines as shown by cell counting and TUNEL assay, respectively. These apoptotic effects were accompanied by apoptosis-specific modulations of the nuclei demonstrated by diminished nuclear morphology parameters, such as area, perimeter, major and minor axis, as well as elevated levels of nuclear staining intensity. CONCLUSION: We present a computerized method for apoptosis detection and quantification using images of fluorescent dye-stained cell nuclei. The advantages of this nuclear morphology assay include the (i) ability to routinely assess apoptosis by a fast, highly reproducible low-cost technique, (ii) applicability of an experimental approach analyzing high numbers of single nuclei and (iii) detection of apoptosis in early, as well as late, stages of the apoptotic cascade.
[Mh] Termos MeSH primário: Apoptose
Núcleo Celular/fisiologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Núcleo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Cicloeximida/farmacologia
Corantes Fluorescentes/farmacologia
Seres Humanos
Marcação In Situ das Extremidades Cortadas
Microscopia de Fluorescência
Inibidores da Síntese de Proteínas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (Protein Synthesis Inhibitors); 98600C0908 (Cycloheximide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE


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[PMID]:28358429
[Au] Autor:Kudou M; Shiozaki A; Kosuga T; Shimizu H; Ichikawa D; Konishi H; Morimura R; Komatsu S; Ikoma H; Fujiwara H; Okamoto K; Marunaka Y; Otsuji E
[Ad] Endereço:Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
[Ti] Título:Heat shock exerts anticancer effects on liver cancer via autophagic degradation of aquaporin 5.
[So] Source:Int J Oncol;50(5):1857-1867, 2017 May.
[Is] ISSN:1791-2423
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Previous studies described that the expression of aquaporin 5 (AQP5) was altered in tumors of various organs. AQP5 is attracting attention as a new cancer therapeutic target. In the present study, heat shock-induced changes in AQP5 expression were evaluated by immunofluorescent staining (IF) and western blotting (WB) of liver cancer cells. AQP5 knockdown experiments or a heat shock treatment were conducted, and their effects on cell volume, proliferation, cell cycle, the activity of apoptosis and migration/invasion were compared. Cycloheximide (CHX) chase experiments and double IF of AQP5 and light chain 3B (LC3B) were performed to investigate the mechanisms underlying changes in AQP5 expression. The results showed that IF and WB revealed decrease in AQP5 expression on cellular membranes and in the cytoplasm of heated cells. AQP5 knockdown and heat shock similarly decreased cell volume, suppressed migration/invasion and proliferation, and induced early apoptosis and partial G0/G1 arrest. CHX chase experiments revealed that heat shock accelerated the degradation of AQP5, which was rescued under CHX and the autophagy inhibitor, bafilomycin A1 (BafA1). Double IF showed the co-localization of AQP5 and LC3B on BafA1-treated heated cells. In conclusion, we demonstrated that heat shock decreased AQP5 on cellular membranes and in the cytoplasm by activating autophagic degradation, and heat shock and AQP5 knockdown exerted similar anticancer effects, suggesting that heat shock exerts anticancer effects via the autophagic degradation of AQP5.
[Mh] Termos MeSH primário: Aquaporina 5/genética
Autofagia/efeitos dos fármacos
Resposta ao Choque Térmico/genética
Neoplasias Hepáticas/tratamento farmacológico
Proteínas Associadas aos Microtúbulos/genética
[Mh] Termos MeSH secundário: Apoptose/genética
Aquaporina 5/biossíntese
Ciclo Celular/genética
Linhagem Celular Tumoral
Proliferação Celular/genética
Cicloeximida/administração & dosagem
Citoplasma/genética
Regulação Neoplásica da Expressão Gênica/genética
Técnicas de Silenciamento de Genes
Seres Humanos
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Macrolídeos/administração & dosagem
Proteínas Associadas aos Microtúbulos/biossíntese
Proteólise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aquaporin 5); 0 (MAP1LC3B protein, human); 0 (Macrolides); 0 (Microtubule-Associated Proteins); 88899-55-2 (bafilomycin A1); 98600C0908 (Cycloheximide)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170720
[Lr] Data última revisão:
170720
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.3892/ijo.2017.3940


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[PMID]:28340282
[Au] Autor:Liu CY; Hsieh FS; Chu PY; Tsai WC; Huang CT; Yu YB; Huang TT; Ko PS; Hung MH; Wang WL; Shiau CW; Chen KF
[Ad] Endereço:Comprehensive Breast Health Centre, Taipei Veterans General Hospital, Taipei, Taiwan.
[Ti] Título:Carfilzomib induces leukaemia cell apoptosis via inhibiting ELK1/KIAA1524 (Elk-1/CIP2A) and activating PP2A not related to proteasome inhibition.
[So] Source:Br J Haematol;177(5):726-740, 2017 Jun.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Enhancing the tumour suppressive activity of protein phosphatase 2A (PP2A) has been suggested to be an anti-leukaemic strategy. KIAA1524 (also termed CIP2A), an oncoprotein inhibiting PP2A, is associated with disease progression in chronic myeloid leukaemia and may be prognostic in cytogenetically normal acute myeloid leukaemia. Here we demonstrated that the selective proteasome inhibitor, carfilzomib, induced apoptosis in sensitive primary leukaemia cells and in sensitive leukaemia cell lines, associated with KIAA1524 protein downregulation, increased PP2A activity and decreased p-Akt, but not with the proteasome inhibition effect of carfilzomib. Ectopic expression of KIAA1524, or pretreatment with the PP2A inhibitor, okadaic acid, suppressed carfilzomib-induced apoptosis and KIAA1524 downregulation in sensitive cells, whereas co-treatment with the PP2A agonist, forskolin, enhanced carfilzomib-induced apoptosis in resistant cells. Mechanistically, carfilzomib affected KIAA1524 transcription through disturbing ELK1 (Elk-1) binding to the KIAA1524 promoter. Moreover, the drug sensitivity and mechanism of carfilzomib in xenograft mouse models correlated well with the effects of carfilzomib on KIAA1524 and p-Akt expression, as well as PP2A activity. Our data disclosed a novel drug mechanism of carfilzomib in leukaemia cells and suggests the potential therapeutic implication of KIAA1524 in leukaemia treatment.
[Mh] Termos MeSH primário: Leucemia/tratamento farmacológico
Oligopeptídeos/farmacologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Animais
Apoptose/efeitos dos fármacos
Autoantígenos/metabolismo
Linhagem Celular Tumoral
Cicloeximida/farmacologia
Regulação para Baixo/efeitos dos fármacos
Feminino
Células HL-60
Seres Humanos
Células K562
Leucemia/fisiopatologia
Masculino
Proteínas de Membrana/metabolismo
Camundongos Nus
Meia-Idade
Transplante de Neoplasias/métodos
Ácido Okadáico/farmacologia
Complexo de Endopeptidases do Proteassoma/metabolismo
Inibidores da Síntese de Proteínas/farmacologia
Células Tumorais Cultivadas
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantigens); 0 (KIAA1524 protein, human); 0 (Membrane Proteins); 0 (Oligopeptides); 0 (Protein Synthesis Inhibitors); 1W21G5Q4N2 (Okadaic Acid); 72X6E3J5AR (carfilzomib); 98600C0908 (Cycloheximide); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14620



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