Base de dados : MEDLINE
Pesquisa : D27.505.519.593 [Categoria DeCS]
Referências encontradas : 31 [refinar]
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  1 / 31 MEDLINE  
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[PMID]:27154027
[Au] Autor:Schwieger J; Esser KH; Lenarz T; Scheper V
[Ad] Endereço:Department of Otolaryngology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany; Department of Zoology, University of Veterinary Medicine Hannover, Bünteweg 17, 30559 Hannover, Germany. Electronic address: schwieger.jana@mh-hannover.de.
[Ti] Título:Establishment of a long-term spiral ganglion neuron culture with reduced glial cell number: Effects of AraC on cell composition and neurons.
[So] Source:J Neurosci Methods;268:106-16, 2016 08 01.
[Is] ISSN:1872-678X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sensorineural deafness is mainly caused by damage to hair cells and degeneration of the spiral ganglion neurons (SGN). Cochlear implants can functionally replace lost hair cells and stimulate the SGN electrically. The benefit from cochlear implantation depends on the number and excitability of these neurons. To identify potential therapies for SGN protection, in vitro tests are carried out on spiral ganglion cells (SGC). NEW METHOD: A glial cell-reduced and neuron-enhanced culture of neonatal rat SGC under mitotic inhibition (cytarabine (AraC)) for up to seven days is presented. Serum containing and neurotrophin-enriched cultures with and without AraC-addition were analyzed after 4 and 7 days. RESULTS: The total number of cells was significantly reduced, while the proportion of neurons was greatly increased by AraC-treatment. Cell type-specific labeling demonstrated that nearly all fibroblasts and most of the glial cells were removed. Neither the neuronal survival, nor the neurite outgrowth or soma diameter were negatively affected. Additionally neurites remain partly free of surrounding non-neuronal cells. COMPARISON WITH EXISTING METHOD: Recent culture conditions allow only for short-term cultivation of neonatal SGC and lack information on the influence of non-neuronal cells on SGN and of direct contact of neurites with test-materials. CONCLUSIONS: AraC-addition reduces the number of non-neuronal cells and increases the ratio of SGN in culture, without negative impact on neuronal viability. This treatment allows longer-term cultivation of SGC and provides deeper insight into SGN-glial cell interaction and the attachment of neurites on test-material surfaces.
[Mh] Termos MeSH primário: Técnicas de Cultura de Células
Neuroglia
Neurônios
Gânglio Espiral da Cóclea
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Contagem de Células
Tamanho Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Citarabina/farmacologia
Feminino
Imuno-Histoquímica
Masculino
Moduladores de Mitose/farmacologia
Neuroglia/citologia
Neuroglia/efeitos dos fármacos
Neuroglia/fisiologia
Crescimento Neuronal/efeitos dos fármacos
Neurônios/citologia
Neurônios/efeitos dos fármacos
Neurônios/fisiologia
Ratos Sprague-Dawley
Gânglio Espiral da Cóclea/citologia
Gânglio Espiral da Cóclea/efeitos dos fármacos
Gânglio Espiral da Cóclea/fisiologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitosis Modulators); 04079A1RDZ (Cytarabine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171127
[Lr] Data última revisão:
171127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160508
[St] Status:MEDLINE


  2 / 31 MEDLINE  
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[PMID]:26707876
[Au] Autor:Gao G; Shen N; Jiang X; Sun H; Xu N; Zhou D; Nong L; Ren K
[Ad] Endereço:Department of Orthopedics, The Affiliated Changzhou No. 2 Hospital of Nanjing Medical University, Changzhou 213003, China.
[Ti] Título:Periodic mechanical stress activates EGFR-dependent Rac1 mitogenic signals in rat nucleus pulpous cells via ERK1/2.
[So] Source:Biochem Biophys Res Commun;469(3):723-30, 2016 Jan 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mitogenic effects of periodic mechanical stress on nucleus pulpous cells have been studied extensively but the mechanisms whereby nucleus pulpous cells sense and respond to mechanical stimulation remain a matter of debate. We explored this question by performing cell culture experiments in our self-developed periodic stress field and perfusion culture system. Under periodic mechanical stress, rat nucleus pulpous cell proliferation was significantly increased (p < 0.05 for each) and was associated with increases in the phosphorylation and activation of EGFR, Rac1, and ERK1/2 (p < 0.05 for each). Pretreatment with the ERK1/2 selective inhibitor PD98059 reduced periodic mechanical stress-induced nucleus pulpous cell proliferation (p < 0.05 for each), while the activation levels of EGFR and Rac1 were not inhibited. Proliferation and phosphorylation of ERK1/2 were inhibited after pretreatment with the Rac1 inhibitor NSC23766 in nucleus pulpous cells in response to periodic mechanical stress (p < 0.05 for each), while the phosphorylation site of EGFR was not affected. Inhibition of EGFR activity with AG1478 abrogated nucleus pulpous cell proliferation (p < 0.05 for each) and attenuated Rac1 and ERK1/2 activation in nucleus pulpous cells subjected to periodic mechanical stress (p < 0.05 for each). These findings suggest that periodic mechanical stress promotes nucleus pulpous cell proliferation in part through the EGFR-Rac1-ERK1/2 signaling pathway, which links these three important signaling molecules into a mitogenic cascade.
[Mh] Termos MeSH primário: Disco Intervertebral/citologia
Disco Intervertebral/fisiologia
Sistema de Sinalização das MAP Quinases/fisiologia
Mecanotransdução Celular/fisiologia
Receptor do Fator de Crescimento Epidérmico/metabolismo
Proteínas rac1 de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/fisiologia
Células Cultivadas
Feminino
Regulação da Expressão Gênica/fisiologia
Masculino
Mitose/fisiologia
Moduladores de Mitose/metabolismo
Fosforilação
Estimulação Física/métodos
Ratos
Ratos Sprague-Dawley
Estresse Mecânico
Estresse Fisiológico/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitosis Modulators); EC 2.7.10.1 (Egfr protein, rat); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.6.1.- (Rac1 protein, rat); EC 3.6.5.2 (rac1 GTP-Binding Protein)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151229
[St] Status:MEDLINE


  3 / 31 MEDLINE  
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[PMID]:25760027
[Au] Autor:Lauand C; Niero EL; Dias VM; Machado-Santelli GM
[Ad] Endereço:Departamento de Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, SP, Brasil.
[Ti] Título:Cell cycle synchronization and BrdU incorporation as a tool to study the possible selective elimination of ErbB1 gene in the micronuclei in A549 cells.
[So] Source:Braz J Med Biol Res;48(5):382-91, 2015 May.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Lung cancer often exhibits molecular changes, such as the overexpression of the ErbB1 gene that encodes epidermal growth factor receptor (EGFR). ErbB1 amplification and mutation are associated with tumor aggressiveness and low response to therapy. The aim of the present study was to design a schedule to synchronize the cell cycle of A549 cell line (a non-small cell lung cancer) and to analyze the possible association between the micronuclei (MNs) and the extrusion of ErbB1 gene extra-copies. After double blocking, by the process of fetal bovine serum deprivation and vincristine treatment, MNs formation was monitored with 5-bromo-2-deoxyuridine (BrdU) incorporation, which is an S-phase marker. Statistical analyses allowed us to infer that MNs may arise both in mitosis as well as in interphase. The MNs were able to replicate their DNA and this process seemed to be non-synchronous with the main cell nuclei. The presence of ErbB1 gene in the MNs was evaluated by fluorescent in situ hybridization (FISH). ErbB1 sequences were detected in the MNs, but a relation between the MNs formation and extrusion of amplified ErbB1 could not be established. The present study sought to elucidate the meaning of MNs formation and its association with the elimination of oncogenes or other amplified sequences from the tumor cells.
[Mh] Termos MeSH primário: Antimetabólitos/metabolismo
Bromodesoxiuridina/metabolismo
Ciclo Celular/genética
Inativação Gênica/fisiologia
Genes erbB-1/genética
Micronúcleos com Defeito Cromossômico
[Mh] Termos MeSH secundário: Animais
Bovinos
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Replicação do DNA
Fase G1
Amplificação de Genes/fisiologia
Seres Humanos
Hibridização in Situ Fluorescente
Micronúcleos com Defeito Cromossômico/induzido quimicamente
Microscopia Confocal
Moduladores de Mitose/farmacologia
Índice Mitótico/estatística & dados numéricos
Fase S
Vincristina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antimetabolites); 0 (Mitosis Modulators); 5J49Q6B70F (Vincristine); G34N38R2N1 (Bromodeoxyuridine)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150312
[St] Status:MEDLINE


  4 / 31 MEDLINE  
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[PMID]:25393660
[Au] Autor:Mustroph ML; Merritt JR; Holloway AL; Pinardo H; Miller DS; Kilby CN; Bucko P; Wyer A; Rhodes JS
[Ad] Endereço:Beckman Institute, University of Illinois at Urbana-Champaign, 405 North Mathews Avenue, Urbana, IL, 61801, USA; Neuroscience Program, Beckman Institute, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
[Ti] Título:Increased adult hippocampal neurogenesis is not necessary for wheel running to abolish conditioned place preference for cocaine in mice.
[So] Source:Eur J Neurosci;41(2):216-26, 2015 Jan.
[Is] ISSN:1460-9568
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Recent evidence suggests that wheel running can abolish conditioned place preference (CPP) for cocaine in mice. Running significantly increases the number of new neurons in the hippocampus, and new neurons have been hypothesised to enhance plasticity and behavioral flexibility. Therefore, we tested the hypothesis that increased neurogenesis was necessary for exercise to abolish cocaine CPP. Male nestin-thymidine kinase transgenic mice were conditioned with cocaine, and then housed with or without running wheels for 32 days. Half of the mice were fed chow containing valganciclovir to induce apoptosis in newly divided neurons, and the other half were fed standard chow. For the first 10 days, mice received daily injections of bromodeoxyuridine (BrdU) to label dividing cells. On the last 4 days, mice were tested for CPP, and then euthanized for measurement of adult hippocampal neurogenesis by counting the number of BrdU-positive neurons in the dentate gyrus. Levels of running were similar in mice fed valganciclovir-containing chow and normal chow. Valganciclovir significantly reduced the numbers of neurons (BrdU-positive/NeuN-positive) in the dentate gyrus of both sedentary mice and runner mice. Valganciclovir-fed runner mice showed similar levels of neurogenesis as sedentary, normal-fed controls. However, valganciclovir-fed runner mice showed the same abolishment of CPP as runner mice with intact neurogenesis. The results demonstrate that elevated adult hippocampal neurogenesis resulting from running is not necessary for running to abolish cocaine CPP in mice.
[Mh] Termos MeSH primário: Cocaína/farmacologia
Giro Denteado/fisiologia
Inibidores da Captação de Dopamina/farmacologia
Comportamento de Procura de Droga/fisiologia
Extinção Psicológica/fisiologia
Corrida/fisiologia
[Mh] Termos MeSH secundário: Ração Animal
Animais
Apoptose/efeitos dos fármacos
Peso Corporal
Bromodesoxiuridina
Condicionamento (Psicologia)/efeitos dos fármacos
Condicionamento (Psicologia)/fisiologia
Giro Denteado/efeitos dos fármacos
Ganciclovir/administração & dosagem
Ganciclovir/análogos & derivados
Imuno-Histoquímica
Masculino
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Moduladores de Mitose/administração & dosagem
Neurogênese/efeitos dos fármacos
Neurogênese/fisiologia
Aprendizagem Espacial/efeitos dos fármacos
Aprendizagem Espacial/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dopamine Uptake Inhibitors); 0 (Mitosis Modulators); G34N38R2N1 (Bromodeoxyuridine); GCU97FKN3R (valganciclovir); I5Y540LHVR (Cocaine); P9G3CKZ4P5 (Ganciclovir)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141114
[St] Status:MEDLINE
[do] DOI:10.1111/ejn.12782


  5 / 31 MEDLINE  
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[PMID]:24909558
[Au] Autor:Alfonso RJ; Gorroño-Etxebarria I; Rabano M; Vivanco Md; Kypta R
[Ad] Endereço:Cell Biology and Stem Cells Unit, CIC bioGUNE, Spain.
[Ti] Título:Dickkopf-3 alters the morphological response to retinoic acid during neuronal differentiation of human embryonal carcinoma cells.
[So] Source:Dev Neurobiol;74(12):1243-54, 2014 Dec.
[Is] ISSN:1932-846X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dickkopf-3 (Dkk-3) and Dkkl-1 (Soggy) are secreted proteins of poorly understood function that are highly expressed in subsets of neurons in the brain. To explore their potential roles during neuronal development, we examined their expression in Ntera-2 (NT2) human embryonal carcinoma cells, which differentiate into neurons upon treatment with retinoic acid (RA). RA treatment increased the mRNA and protein levels of Dkk-3 but not of Dkkl-1. Ectopic expression of both Dkk-3 and Dkkl-1 induced apoptosis in NT2 cells. Gene silencing of Dkk-3 did not affect NT2 cell growth or differentiation but altered their response to RA in suspension cultures. RA treatment of NT2 cells cultured in suspension resulted in morphological changes that led to cell attachment and flattening out of cell aggregates. Although there were no significant differences in the expression levels of cell adhesion molecules in control and Dkk-3-silenced cells, this morphological response was not observed in Dkk-3-silenced cells. These findings suggest that Dkk-3 plays a role in the regulation of cell interactions during RA-induced neuronal differentiation.
[Mh] Termos MeSH primário: Células-Tronco de Carcinoma Embrionário/fisiologia
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Moduladores de Mitose/farmacologia
Neurogênese/fisiologia
Tretinoína/farmacologia
[Mh] Termos MeSH secundário: Apoptose/fisiologia
Western Blotting
Caspase 3/metabolismo
Caspase 7/metabolismo
Adesão Celular/efeitos dos fármacos
Adesão Celular/fisiologia
Linhagem Celular Tumoral
Células-Tronco de Carcinoma Embrionário/citologia
Células-Tronco de Carcinoma Embrionário/efeitos dos fármacos
Inativação Gênica
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/genética
Neurogênese/efeitos dos fármacos
Neurônios/citologia
Neurônios/efeitos dos fármacos
Neurônios/fisiologia
Reação em Cadeia da Polimerase
RNA Mensageiro/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DKK3 protein, human); 0 (DKKL1 protein, human); 0 (Intercellular Signaling Peptides and Proteins); 0 (Mitosis Modulators); 0 (RNA, Messenger); 5688UTC01R (Tretinoin); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (CASP7 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 7)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:141027
[Lr] Data última revisão:
141027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140610
[St] Status:MEDLINE
[do] DOI:10.1002/dneu.22201


  6 / 31 MEDLINE  
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[PMID]:24734530
[Au] Autor:Karabanovas V; Zitkus Z; Kuciauskas D; Rotomskis R; Valius M
[Ti] Título:Surface properties of quantum dots define their cellular endocytic routes, mitogenic stimulation and suppression of cell migration.
[So] Source:J Biomed Nanotechnol;10(5):775-86, 2014 May.
[Is] ISSN:1550-7033
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The practical use of quantum dots (QD) as diagnostic, visualizing and therapeutic nano-agents depends on the understanding of fundamental mechanisms of their entrance and trafficking within cells. Here we show that CdSe/ZnS carboxylic-coated QD (COOH-QD) enter fibroblast cells via lipid raft/caveolin-mediated endocytosis, pass early sorting endosomes and accumulate in the multivesicular bodies, but not in the lysosomes. Later phase of their endocytosis leads to the generation of lipid raft/caveolin-dependent endocytosis inhibition that prevents intracellular uptake of new COOH-QD, but not the QD coupled with platelet-derived growth factor BB (PDGF-QD). PDGF-QD enter fibroblasts by the clathrin-mediated endocytosis and undergo similar intracellular trafficking as COOH-QD, yet they accumulate in lysosomes in contrast to COOH-QD. The PDGF-QD activate PDGF receptor-beta and are mitogenic, however, COOH-QD suppress cell migration and chemotaxis. Data show that surface coating of QD with the biologically active proteins redirects their intracellular traffic routes and changes their biological activity.
[Mh] Termos MeSH primário: Caveolinas/metabolismo
Movimento Celular/fisiologia
Endocitose/fisiologia
Microdomínios da Membrana/fisiologia
Moduladores de Mitose/metabolismo
Mitose/fisiologia
Pontos Quânticos
[Mh] Termos MeSH secundário: Animais
Microdomínios da Membrana/química
Camundongos
Células NIH 3T3
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Caveolins); 0 (Mitosis Modulators)
[Em] Mês de entrada:1405
[Cu] Atualização por classe:140416
[Lr] Data última revisão:
140416
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140417
[St] Status:MEDLINE


  7 / 31 MEDLINE  
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[PMID]:24623308
[Au] Autor:Chen YJ; Lai KC; Kuo HH; Chow LP; Yih LH; Lee TC
[Ad] Endereço:Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.
[Ti] Título:HSP70 colocalizes with PLK1 at the centrosome and disturbs spindle dynamics in cells arrested in mitosis by arsenic trioxide.
[So] Source:Arch Toxicol;88(9):1711-23, 2014 Sep.
[Is] ISSN:1432-0738
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Heat shock protein 70 (HSP70) has been shown to be a substrate of Polo-like kinase 1 (PLK1), and it prevents cells arrested in mitosis by arsenic trioxide (ATO) from dying. Here, we report that HSP70 participates in ATO-induced spindle elongation, which interferes with mitosis progression. Our results demonstrate that HSP70 and PLK1 colocalize at the centrosome in ATO-arrested mitotic cells. HSP70 located at the centrosome was found to be phosphorylated by PLK1 at Ser6³¹ and Ser6³³. Moreover, unlike wild-type HSP70 (HSP70(wt)) and its phosphomimetic mutant (HSP70(SS631,633DD)), a phosphorylation-resistant mutant of HSP70 (HSP70(SS631,633AA)) failed to localize at the centrosome. ATO-induced spindle elongation was abolished in cells overexpressing HSP70(SS631,633AA). Conversely, mitotic spindles in cells ectopically expressing HSP70(SS631,633DD) were more resistant to nocodazole-induced depolymerization than in those expressing HSP70(wt) or HSP70(SS631,633AA). In addition, inhibition of PLK1 significantly reduced HSP70 phosphorylation and induced early onset of apoptosis in ATO-arrested mitotic cells. Taken together, our results indicate that PLK1-mediated phosphorylation and centrosomal localization of HSP70 may interfere with spindle dynamics and prevent apoptosis of ATO-arrested mitotic cells.
[Mh] Termos MeSH primário: Carcinógenos Ambientais/toxicidade
Proteínas de Ciclo Celular/metabolismo
Centrossomo/efeitos dos fármacos
Proteínas de Choque Térmico HSP70/metabolismo
Moduladores de Mitose/toxicidade
Óxidos/toxicidade
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
Fuso Acromático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Apoptose/efeitos dos fármacos
Arsenicais
Proteínas de Ciclo Celular/antagonistas & inibidores
Proteínas de Ciclo Celular/genética
Centrossomo/metabolismo
Inativação Gênica
Células HEK293
Proteínas de Choque Térmico HSP70/antagonistas & inibidores
Proteínas de Choque Térmico HSP70/genética
Células HeLa
Seres Humanos
Mitose/efeitos dos fármacos
Proteínas Mutantes/antagonistas & inibidores
Proteínas Mutantes/metabolismo
Fosforilação/efeitos dos fármacos
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Transporte Proteico/efeitos dos fármacos
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas Serina-Treonina Quinases/genética
Proteínas Proto-Oncogênicas/antagonistas & inibidores
Proteínas Proto-Oncogênicas/genética
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Fuso Acromático/metabolismo
Moduladores de Tubulina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arsenicals); 0 (Carcinogens, Environmental); 0 (Cell Cycle Proteins); 0 (HSP70 Heat-Shock Proteins); 0 (Mitosis Modulators); 0 (Mutant Proteins); 0 (Oxides); 0 (Proto-Oncogene Proteins); 0 (Recombinant Proteins); 0 (Tubulin Modulators); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (polo-like kinase 1); S7V92P67HO (arsenic trioxide)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140314
[St] Status:MEDLINE
[do] DOI:10.1007/s00204-014-1222-x


  8 / 31 MEDLINE  
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[PMID]:24328194
[Au] Autor:Yaku H; Murashima T; Miyoshi D; Sugimoto N
[Ad] Endereço:Advanced Technology Research Laboratories, Panasonic Corporation, 3-4 Hikaridai, Seika-cho, Soraku-gun, Kyoto 619-0237, Japan.
[Ti] Título:In vitro assays predictive of telomerase inhibitory effect of G-quadruplex ligands in cell nuclei.
[So] Source:J Phys Chem B;118(10):2605-14, 2014 Mar 13.
[Is] ISSN:1520-5207
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:G-quadruplex-binding and telomerase-inhibiting capacities of G-quadruplex ligands were examined under a cell nuclei-mimicking condition including excess double-stranded DNA (λ DNA) and molecular crowding cosolute (PEG 200). Under the cell nuclei-mimicking condition, a cationic porphyrin (TMPyP4) did not bind to the G-quadruplex despite the high affinity (Ka = 3.6 × 10(6) M(-1)) under a diluted condition without λ DNA and PEG 200. Correspondingly, TMPyP4 inhibited telomerase activity under the diluted condition (IC50 = 1.6 µM) but not under the cell nuclei-mimicking condition. In contrast, the Ka and IC50 values of an anionic copper phthalocyanine (Cu-APC) under the diluted (2.8 × 10(4) M(-1) and 0.86 µM) and the cell nuclei-mimicking (2.8 × 10(4) M(-1) and 2.1 µM) conditions were similar. In accordance with these results, 10 µM TMPyP4 did not affect the proliferation of HeLa cells, while Cu-APC efficiently inhibited the proliferation (IC50 = 1.4 µM). These results show that the cell nuclei-mimicking condition is effective to predict capacities of G-quadruplex ligands in the cell. In addition, the antiproliferative effect of Cu-APC on normal cells was smaller than that on HeLa cells, indicating that the cell nuclei-mimicking condition is also useful to predict side effects of ligands.
[Mh] Termos MeSH primário: Núcleo Celular/metabolismo
Quadruplex G
Telomerase/metabolismo
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
DNA/metabolismo
Inibidores Enzimáticos/farmacologia
Células HeLa
Seres Humanos
Indóis/farmacologia
Ligantes
Moduladores de Mitose/farmacologia
Modelos Biológicos
Compostos Organometálicos/farmacologia
Polietilenoglicóis/metabolismo
Porfirinas/metabolismo
Eletricidade Estática
Telomerase/antagonistas & inibidores
Telômero/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Indoles); 0 (Ligands); 0 (Mitosis Modulators); 0 (Organometallic Compounds); 0 (Porphyrins); 30IQX730WE (Polyethylene Glycols); 38673-65-3 (tetra(4-N-methylpyridyl)porphine); 3VEX9T7UT5 (copper phthalocyanine); 9007-49-2 (DNA); EC 2.7.7.49 (Telomerase)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131217
[St] Status:MEDLINE
[do] DOI:10.1021/jp410669t


  9 / 31 MEDLINE  
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[PMID]:24152731
[Au] Autor:Shen KF; Osmani SA
[Ad] Endereço:Department of Molecular Genetics and Molecular, Cellular and Developmental Biology Program, Ohio State University, Columbus, OH 43210.
[Ti] Título:Regulation of mitosis by the NIMA kinase involves TINA and its newly discovered partner, An-WDR8, at spindle pole bodies.
[So] Source:Mol Biol Cell;24(24):3842-56, 2013 Dec.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The NIMA kinase is required for mitotic nuclear pore complex disassembly and potentially controls other mitotic-specific events. To investigate this possibility, we imaged NIMA-green fluorescent protein (GFP) using four-dimensional spinning disk confocal microscopy. At mitosis NIMA-GFP locates to spindle pole bodies (SPBs), which contain Cdk1/cyclin B, followed by Aurora, TINA, and the BimC kinesin. NIMA promotes NPC disassembly in a spatially regulated manner starting near SPBs. NIMA is also required for TINA, a NIMA-interacting protein, to locate to SPBs during initiation of mitosis, and TINA is then necessary for locating NIMA back to SPBs during mitotic progression. To help expand the NIMA-TINA pathway, we affinity purified TINA and found it to uniquely copurify with An-WDR8, a WD40-domain protein conserved from humans to plants. Like TINA, An-WDR8 accumulates within nuclei during G2 but disperses from nuclei before locating to mitotic SPBs. Without An-WDR8, TINA levels are greatly reduced, whereas TINA is necessary for mitotic targeting of An-WDR8. Finally, we show that TINA is required to anchor mitotic microtubules to SPBs and, in combination with An-WDR8, for successful mitosis. The findings provide new insights into SPB targeting and indicate that the mitotic microtubule-anchoring system at SPBs involves WDR8 in complex with TINA.
[Mh] Termos MeSH primário: Aspergillus nidulans/genética
Proteínas de Ciclo Celular/genética
Proteínas Fúngicas/genética
Mitose/genética
Proteínas Serina-Treonina Quinases/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Aurora Quinase A
Proteína Quinase CDC2/genética
Proteína Quinase CDC2/metabolismo
Ciclina B/genética
Ciclina B/metabolismo
Proteínas Fúngicas/metabolismo
Fase G2/genética
Proteínas de Fluorescência Verde/genética
Cinesina
Microscopia Confocal
Moduladores de Mitose/metabolismo
Dados de Sequência Molecular
Quinase 1 Relacionada a NIMA
Corpos Polares do Fuso
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (BimC protein, Aspergillus nidulans); 0 (Cell Cycle Proteins); 0 (Cyclin B); 0 (Fungal Proteins); 0 (Mitosis Modulators); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.11.1 (Aurora Kinase A); EC 2.7.11.1 (NEK1 protein, human); EC 2.7.11.1 (NIMA-Related Kinase 1); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.22 (CDC2 Protein Kinase); EC 3.6.4.4 (Kinesin)
[Em] Mês de entrada:1408
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131025
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E13-07-0422


  10 / 31 MEDLINE  
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[PMID]:23918651
[Au] Autor:Lee Y; Bae EJ
[Ad] Endereço:College of Pharmacy, Woosuk University, Jeollabuk-do, Wanju-gun, Korea.
[Ti] Título:Inhibition of mitotic clonal expansion mediates fisetin-exerted prevention of adipocyte differentiation in 3T3-L1 cells.
[So] Source:Arch Pharm Res;36(11):1377-84, 2013 Nov.
[Is] ISSN:0253-6269
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Adipocytes are the key player in adipose tissue inflammation and subsequent systemic insulin resistance and its development involves complex process of proliferation and differentiation of preadipocytes. Fistein, a polyphenol flavonoid, is known to exert anti-inflammatory, anti-carcinogenic and anti-diabetic effects. In this study, we aimed to investigate the effect of fisetin on adipocyte proliferation and differentiation in 3T3-L1 preadipocyte cell line and its mechanism of action. We found that fisetin inhibits adipocyte differentiation in a concentration dependent manner, which were evidenced by Oil Red O staining and the protein expression of mature adipocyte marker genes fatty acid synthase and peroxisome proliferator-activated receptor γ. Moreover, the proliferation of preadipocytes was also markedly suppressed by treatment of fisetin for 24 and 48 h in the differentiation medium. We also found that fisetin inhibition of adipocyte differentiation was largely due to the effect on mitotic clonal expansion. Fisetin suppression of preadipocyte proliferation at early stage of differentiation was accompanied by the changes of expression of a series of cell cycle regulatory proteins. Altogether, our results suggest that the inhibition of adipocyte differentiation by fisetin may be at least in part mediated by cell cycle arrest during adipogenesis.
[Mh] Termos MeSH primário: Adipócitos/citologia
Adipócitos/efeitos dos fármacos
Adipogenia/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Flavonoides/farmacologia
Moduladores de Mitose/farmacologia
Mitose/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/metabolismo
Animais
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Proteínas de Ciclo Celular/metabolismo
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ácido Graxo Sintase Tipo I/metabolismo
Camundongos
PPAR gama/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Flavonoids); 0 (Mitosis Modulators); 0 (PPAR gamma); EC 2.3.1.85 (Fatty Acid Synthase, Type I); OO2ABO9578 (fisetin)
[Em] Mês de entrada:1406
[Cu] Atualização por classe:131107
[Lr] Data última revisão:
131107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130807
[St] Status:MEDLINE
[do] DOI:10.1007/s12272-013-0226-z



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