Base de dados : MEDLINE
Pesquisa : D02.455.849.291.075 [Categoria DeCS]
Referências encontradas : 1568 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 157 ir para página                         

  1 / 1568 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27193098
[Au] Autor:Pathirana R; West P; Hedderley D; Eason J
[Ad] Endereço:The New Zealand Institute for Plant & Food Research Limited, Private Bag 11600, Palmerston North, New Zealand. ranjith.pathirana@plantandfood.co.nz.
[Ti] Título:Cell death patterns in Arabidopsis cells subjected to four physiological stressors indicate multiple signalling pathways and cell cycle phase specificity.
[So] Source:Protoplasma;254(2):635-647, 2017 Mar.
[Is] ISSN:1615-6102
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Corpse morphology, nuclear DNA fragmentation, expression of senescence-associated genes (SAG) and cysteine protease profiles were investigated to understand cell death patterns in a cell cycle-synchronised Arabidopsis thaliana cell suspension culture treated with four physiological stressors in the late G2 phase. Within 4 h of treatment, polyethylene glycol (PEG, 20 %), mannose (100 mM) and hydrogen peroxide (2 mM) caused DNA fragmentation coinciding with cell permeability to Evans Blue (EB) and produced corpse morphology corresponding to apoptosis-like programmed cell death (AL-PCD) with cytoplasmic retraction from the cell wall. Ethylene (8 mL per 250-mL flask) caused permeability of cells to EB without concomitant nuclear DNA fragmentation and cytoplasmic retraction, suggesting necrotic cell death. Mannose inducing glycolysis block and PEG causing dehydration resulted in relatively similar patterns of upregulation of SAG suggesting similar cell death signalling pathways for these two stress factors, whereas hydrogen peroxide caused unique patterns indicating an alternate pathway for cell death induced by oxidative stress. Ethylene did not cause appreciable changes in SAG expression, confirming necrotic cell death. Expression of AtDAD, BoMT1 and AtSAG2 genes, previously shown to be associated with plant senescence, also changed rapidly during AL-PCD in cultured cells. The profiles of nine distinct cysteine protease-active bands ranging in size from ca. 21.5 to 38.5 kDa found in the control cultures were also altered after treatment with the four stressors, with mannose and PEG again producing similar patterns. Results also suggest that cysteine proteases may have a role in necrotic cell death.
[Mh] Termos MeSH primário: Arabidopsis/citologia
Arabidopsis/fisiologia
Ciclo Celular
Transdução de Sinais
Estresse Fisiológico
[Mh] Termos MeSH secundário: Afidicolina/farmacologia
Arabidopsis/efeitos dos fármacos
Arabidopsis/genética
Proteínas de Arabidopsis/genética
Proteínas de Arabidopsis/metabolismo
Ciclo Celular/efeitos dos fármacos
Ciclo Celular/genética
Morte Celular/efeitos dos fármacos
Forma Celular/efeitos dos fármacos
Cisteína Proteases/metabolismo
Diploide
Citometria de Fluxo
Fase G2/efeitos dos fármacos
Fase G2/genética
Regulação da Expressão Gênica de Plantas/efeitos dos fármacos
Genes de Plantas
Histonas/metabolismo
Marcação In Situ das Extremidades Cortadas
Células Vegetais/efeitos dos fármacos
Células Vegetais/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
Estresse Fisiológico/efeitos dos fármacos
Estresse Fisiológico/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arabidopsis Proteins); 0 (Histones); 38966-21-1 (Aphidicolin); EC 3.4.- (Cysteine Proteases)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160520
[St] Status:MEDLINE
[do] DOI:10.1007/s00709-016-0977-8


  2 / 1568 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27594296
[Au] Autor:Inagaki Y; Matsumoto Y; Tang W; Sekimizu K
[Ad] Endereço:Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo.
[Ti] Título:Dividing phase-dependent cytotoxicity profiling of human embryonic lung fibroblast identifies candidate anticancer reagents.
[So] Source:Drug Discov Ther;10(4):195-200, 2016.
[Is] ISSN:1881-7831
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Human Embryonic Lung fibroblasts (HEL cells) are widely used as a normal cell in studies of cell biology and can be easily maintained in the resting phase. Here we aimed to discover compounds that exhibit cytotoxicity against HEL cells in the dividing phase, but not in the resting phase. The cytotoxicity of each compound against HEL cells either in the resting phase or in the dividing phase was determined by MTT assay. Ratios of the IC50 of cells in the resting phase and that of cells in the dividing phase (RRD) for these compounds were compared. We selected 44 compounds that exhibited toxic effects on HEL cells in the dividing phase from a chemical library containing 325 anticancer drugs and enzyme inhibitors. The RRD values of those compounds were widely distributed. Paclitaxel and docetaxel, which are clinically used as anticancer drugs, had RRD values larger than 2000. On the other hand, the RRD value of dimethyl sulfoxide, an organic solvent, was 1. The cytotoxic effect of paclitaxel on HEL cells in the dividing phase was attenuated by aphidicolin, hydroxyurea, and nocodazole, confirming that the cytotoxic effects of paclitaxel are dependent on cells being in the dividing phase. Thapsigargin, whose RRD value was 800, the third highest RRD value in the library, exhibited therapeutic effects in a mouse model of FM3A ascites carcinoma. We suggest that compounds with high RRD values for HEL cells are candidate anticancer chemotherapy seeds.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Divisão Celular/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Fibroblastos/efeitos dos fármacos
Pulmão/citologia
Fase de Repouso do Ciclo Celular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Afidicolina/farmacologia
Carcinoma/tratamento farmacológico
Ciclo Celular/efeitos dos fármacos
Linhagem Celular
Linhagem Celular Tumoral
Dimetil Sulfóxido/farmacologia
Modelos Animais de Doenças
Ensaios de Seleção de Medicamentos Antitumorais
Feminino
Fibroblastos/citologia
Hidroxiureia/farmacologia
Camundongos
Nocodazol/farmacologia
Paclitaxel/farmacologia
Neoplasias Peritoneais/tratamento farmacológico
Solventes/farmacologia
Taxoides/farmacologia
Tapsigargina/farmacologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Enzyme Inhibitors); 0 (Solvents); 0 (Taxoids); 15H5577CQD (docetaxel); 38966-21-1 (Aphidicolin); 67526-95-8 (Thapsigargin); P88XT4IS4D (Paclitaxel); SH1WY3R615 (Nocodazole); X6Q56QN5QC (Hydroxyurea); YOW8V9698H (Dimethyl Sulfoxide)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170221
[Lr] Data última revisão:
170221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160906
[St] Status:MEDLINE
[do] DOI:10.5582/ddt.2016.01049


  3 / 1568 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27265376
[Au] Autor:Speit G; Schütz P; Bausinger J
[Ad] Endereço:Universität Ulm, Institut für Humangenetik, 89069 Ulm, Germany. Electronic address: guenter.speit@uni-ulm.de.
[Ti] Título:Different sensitivities of cultured mammalian cells towards aphidicolin-enhanced DNA effects in the comet assay.
[So] Source:Mutat Res Genet Toxicol Environ Mutagen;803-804:22-6, 2016 Jun.
[Is] ISSN:1879-3592
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The comet assay in combination with the polymerase inhibitor aphidicolin (APC) has been used to measure DNA excision repair activity, DNA repair kinetics and individual DNA repair capacity. Since APC can enhance genotoxic effects of mutagens measured by the comet assay, this approach has been proposed for increasing the sensitivity of the comet assay in human biomonitoring. The APC-modified comet assay has mainly been performed with human blood and it was shown that it not only enhances the detection of DNA damage repaired by nucleotide excision repair (NER) but also damage typically repaired by base excision repair (BER). Recently, we reported that in contrast to blood leukocytes, A549 cells (a human lung adenocarcinoma cell line) seem to be insensitive towards the repair-inhibiting action of APC. To further elucidate the general usefulness of the APC-modified comet assay for studying repair in cultured mammalian cells, we comparatively investigated further cell lines (HeLa, TK6, V79). DNA damage was induced by BPDE (benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide) and MMS (methyl methanesulfonate) in the absence and presence of APC (3 or 15µM). APC was either added for 2h together with the mutagen or cells were pre-incubated for 30min with APC before the mutagen was added. The results indicate that the cell lines tested differ fundamentally with regard to their sensitivity and specificity towards the repair-inhibiting effect of APC. The actual cause for these differences is still unclear but potential molecular explanations are discussed. Irrespective of the underlying mechanism(s), our study revealed practical limitations of the use of the APC-modified comet assay.
[Mh] Termos MeSH primário: Afidicolina/toxicidade
Ensaio Cometa
DNA/efeitos dos fármacos
[Mh] Termos MeSH secundário: Linhagem Celular
Dano ao DNA/efeitos dos fármacos
Dano ao DNA/genética
DNA Polimerase II/metabolismo
DNA Polimerase III/metabolismo
Seres Humanos
Mutagênicos/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mutagens); 38966-21-1 (Aphidicolin); 9007-49-2 (DNA); EC 2.7.7.- (DNA Polymerase II); EC 2.7.7.- (DNA Polymerase III)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170208
[Lr] Data última revisão:
170208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160607
[St] Status:MEDLINE


  4 / 1568 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27179029
[Au] Autor:Barthelemy J; Hanenberg H; Leffak M
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Boonshoft School of Medicine, Wright State University, Dayton, OH 45435, USA.
[Ti] Título:FANCJ is essential to maintain microsatellite structure genome-wide during replication stress.
[So] Source:Nucleic Acids Res;44(14):6803-16, 2016 Aug 19.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Microsatellite DNAs that form non-B structures are implicated in replication fork stalling, DNA double strand breaks (DSBs) and human disease. Fanconi anemia (FA) is an inherited disorder in which mutations in at least nineteen genes are responsible for the phenotypes of genome instability and cancer predisposition. FA pathway proteins are active in the resolution of non-B DNA structures including interstrand crosslinks, G quadruplexes and DNA triplexes. In FANCJ helicase depleted cells, we show that hydroxyurea or aphidicolin treatment leads to loss of microsatellite polymerase chain reaction signals and to chromosome recombination at an ectopic hairpin forming CTG/CAG repeat in the HeLa genome. Moreover, diverse endogenous microsatellite signals were also lost upon replication stress after FANCJ depletion, and in FANCJ null patient cells. The phenotype of microsatellite signal instability is specific for FANCJ apart from the intact FA pathway, and is consistent with DSBs at microsatellites genome-wide in FANCJ depleted cells following replication stress.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Replicação do DNA/genética
Proteínas de Grupos de Complementação da Anemia de Fanconi/metabolismo
Genoma Humano
Repetições de Microssatélites/genética
Estresse Fisiológico/genética
[Mh] Termos MeSH secundário: Afidicolina/farmacologia
Cromossomos Humanos/genética
Replicação do DNA/efeitos dos fármacos
Anemia de Fanconi/genética
Proteína do Grupo de Complementação D2 da Anemia de Fanconi/deficiência
Proteína do Grupo de Complementação D2 da Anemia de Fanconi/metabolismo
Técnicas de Silenciamento de Genes
Células HeLa
Seres Humanos
Reação em Cadeia da Polimerase
Recombinação Genética/genética
Estresse Fisiológico/efeitos dos fármacos
Expansão das Repetições de Trinucleotídeos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BACH1 protein, human); 0 (Basic-Leucine Zipper Transcription Factors); 0 (FANCD2 protein, human); 0 (Fanconi Anemia Complementation Group D2 Protein); 0 (Fanconi Anemia Complementation Group Proteins); 38966-21-1 (Aphidicolin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160515
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkw433


  5 / 1568 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27049344
[Au] Autor:JavanMoghadam S; Weihua Z; Hunt KK; Keyomarsi K
[Ad] Endereço:a Department of Experimental Radiation Oncology , The University of Texas MD Anderson Cancer Center , Houston , TX , USA.
[Ti] Título:Estrogen receptor alpha is cell cycle-regulated and regulates the cell cycle in a ligand-dependent fashion.
[So] Source:Cell Cycle;15(12):1579-90, 2016 Jun 17.
[Is] ISSN:1551-4005
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Estrogen receptor alpha (ERα) has been implicated in several cell cycle regulatory events and is an important predictive marker of disease outcome in breast cancer patients. Here, we aimed to elucidate the mechanism through which ERα influences proliferation in breast cancer cells. Our results show that ERα protein is cell cycle-regulated in human breast cancer cells and that the presence of 17-ß-estradiol (E2) in the culture medium shortened the cell cycle significantly (by 4.5 hours, P < 0.05) compared with unliganded conditions. The alterations in cell cycle duration were observed in the S and G2/M phases, whereas the G1 phase was indistinguishable under liganded and unliganded conditions. In addition, ERα knockdown in MCF-7 cells accelerated mitotic exit, whereas transfection of ERα-negative MDA-MB-231 cells with exogenous ERα significantly shortened the S and G2/M phases (by 9.1 hours, P < 0.05) compared with parental cells. Finally, treatment of MCF-7 cells with antiestrogens revealed that tamoxifen yields a slower cell cycle progression through the S and G2/M phases than fulvestrant does, presumably because of the destabilizing effect of fulvestrant on ERα protein. Together, these results show that ERα modulates breast cancer cell proliferation by regulating events during the S and G2/M phases of the cell cycle in a ligand-dependent fashion. These results provide the rationale for an effective treatment strategy that includes a cell cycle inhibitor in combination with a drug that lowers estrogen levels, such as an aromatase inhibitor, and an antiestrogen that does not result in the degradation of ERα, such as tamoxifen.
[Mh] Termos MeSH primário: Estradiol/farmacologia
Antagonistas de Estrogênios/farmacologia
Receptor alfa de Estrogênio/genética
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica
[Mh] Termos MeSH secundário: Afidicolina/farmacologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Estradiol/análogos & derivados
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor alfa de Estrogênio/metabolismo
Feminino
Fase G1/efeitos dos fármacos
Fase G1/genética
Pontos de Checagem da Fase G2 do Ciclo Celular/genética
Seres Humanos
Ligantes
Lovastatina/farmacologia
Células MCF-7
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Fase S/efeitos dos fármacos
Fase S/genética
Transdução de Sinais
Tamoxifeno/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Antagonists); 0 (Estrogen Receptor alpha); 0 (Ligands); 0 (RNA, Small Interfering); 0 (estrogen receptor alpha, human); 094ZI81Y45 (Tamoxifen); 22X328QOC4 (fulvestrant); 38966-21-1 (Aphidicolin); 4TI98Z838E (Estradiol); 9LHU78OQFD (Lovastatin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170517
[Lr] Data última revisão:
170517
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160407
[St] Status:MEDLINE
[do] DOI:10.1080/15384101.2016.1166327


  6 / 1568 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26871630
[Au] Autor:Wei PC; Chang AN; Kao J; Du Z; Meyers RM; Alt FW; Schwer B
[Ad] Endereço:Program in Cellular and Molecular Medicine, Boston Children's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
[Ti] Título:Long Neural Genes Harbor Recurrent DNA Break Clusters in Neural Stem/Progenitor Cells.
[So] Source:Cell;164(4):644-55, 2016 Feb 11.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Repair of DNA double-strand breaks (DSBs) by non-homologous end joining is critical for neural development, and brain cells frequently contain somatic genomic variations that might involve DSB intermediates. We now use an unbiased, high-throughput approach to identify genomic regions harboring recurrent DSBs in primary neural stem/progenitor cells (NSPCs). We identify 27 recurrent DSB clusters (RDCs), and remarkably, all occur within gene bodies. Most of these NSPC RDCs were detected only upon mild, aphidicolin-induced replication stress, providing a nucleotide-resolution view of replication-associated genomic fragile sites. The vast majority of RDCs occur in long, transcribed, and late-replicating genes. Moreover, almost 90% of identified RDC-containing genes are involved in synapse function and/or neural cell adhesion, with a substantial fraction also implicated in tumor suppression and/or mental disorders. Our characterization of NSPC RDCs reveals a basis of gene fragility and suggests potential impacts of DNA breaks on neurodevelopment and neural functions.
[Mh] Termos MeSH primário: Quebras de DNA
Células-Tronco Neurais/metabolismo
[Mh] Termos MeSH secundário: Animais
Afidicolina/farmacologia
Encéfalo/citologia
Adesão Celular
Moléculas de Adesão Celular Neuronais/metabolismo
Quebras de DNA/efeitos dos fármacos
Reparo do DNA por Junção de Extremidades
Reparo do DNA
Proteínas Ligadas por GPI/metabolismo
Genoma
Seres Humanos
Camundongos
Proteínas do Tecido Nervoso/metabolismo
Sinapses
Fatores de Transcrição/metabolismo
Translocação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Adhesion Molecules, Neuronal); 0 (GPI-Linked Proteins); 0 (NPAS3 protein, human); 0 (Nerve Tissue Proteins); 0 (Transcription Factors); 0 (limbic system-associated membrane protein); 38966-21-1 (Aphidicolin)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160213
[St] Status:MEDLINE


  7 / 1568 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26854228
[Au] Autor:Kafer GR; Li X; Horii T; Suetake I; Tajima S; Hatada I; Carlton PM
[Ad] Endereço:Institute for Integrated Cell-Material Sciences (iCeMS), Kyoto University, Kyoto 606-8501, Japan; CREST, Japan Science and Technology Agency.
[Ti] Título:5-Hydroxymethylcytosine Marks Sites of DNA Damage and Promotes Genome Stability.
[So] Source:Cell Rep;14(6):1283-1292, 2016 Feb 16.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:5-hydroxymethylcytosine (5hmC) is a DNA base created during active DNA demethylation by the recently discovered TET enzymes. 5hmC has essential roles in gene expression and differentiation. Here, we demonstrate that 5hmC also localizes to sites of DNA damage and repair. 5hmC accumulates at damage foci induced by aphidicolin and microirradiation and colocalizes with major DNA damage response proteins 53BP1 and γH2AX, revealing 5hmC as an epigenetic marker of DNA damage. Deficiency for the TET enzymes eliminates damage-induced 5hmC accumulation and elicits chromosome segregation defects in response to replication stress. Our results indicate that the TET enzymes and 5hmC play essential roles in ensuring genome integrity.
[Mh] Termos MeSH primário: Citosina/análogos & derivados
Reparo do DNA
Replicação do DNA
Epigênese Genética
Genoma
Histonas/metabolismo
Proteína 1 de Ligação à Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: 5-Metilcitosina/análogos & derivados
Animais
Afidicolina/farmacologia
Sistemas CRISPR-Cas
Linhagem Celular
Citosina/metabolismo
Dano ao DNA
Metilação de DNA
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Instabilidade Genômica
Células HeLa
Histonas/genética
Células-Tronco Embrionárias Humanas/citologia
Células-Tronco Embrionárias Humanas/efeitos dos fármacos
Células-Tronco Embrionárias Humanas/metabolismo
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/metabolismo
Rad51 Recombinase/genética
Rad51 Recombinase/metabolismo
Proteína 1 de Ligação à Proteína Supressora de Tumor p53/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (H2AFX protein, human); 0 (Histones); 0 (Proto-Oncogene Proteins); 0 (TET2 protein, human); 0 (TP53BP1 protein, human); 0 (Tumor Suppressor p53-Binding Protein 1); 1123-95-1 (5-hydroxymethylcytosine); 38966-21-1 (Aphidicolin); 6R795CQT4H (5-Methylcytosine); 8J337D1HZY (Cytosine); EC 2.7.7.- (RAD51 protein, human); EC 2.7.7.- (Rad51 Recombinase)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160209
[St] Status:MEDLINE


  8 / 1568 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26818565
[Au] Autor:Maya-Mendoza A; Bartek J; Jackson DA; Streuli CH
[Ad] Endereço:a Faculty of Life Sciences and Wellcome Trust Center for Cell-Matrix Research, University of Manchester , Manchester , United Kingdom.
[Ti] Título:Cellular microenvironment controls the nuclear architecture of breast epithelia through ß1-integrin.
[So] Source:Cell Cycle;15(3):345-56, 2016.
[Is] ISSN:1551-4005
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Defects in nuclear architecture occur in a variety of diseases, however the fundamental mechanisms that control the internal structure of nuclei are poorly defined. Here we reveal that the cellular microenvironment has a profound influence on the global internal organization of nuclei in breast epithelia. A 3D microenvironment induces a prolonged but reversible form of cell cycle arrest that features many of the classical markers of cell senescence. This unique form of arrest is dependent on signaling from the external microenvironment through ß1-integrins. It is concomitant with alterations in nuclear architecture that characterize the withdrawal from cell proliferation. Unexpectedly, following prolonged cell cycle arrest in 3D, the senescence-like state and associated reprogramming of nuclear architecture are freely reversible on altering the dimensionality of the cellular microenvironment. Breast epithelia can therefore maintain a proliferative plasticity that correlates with nuclear remodelling. However, the changes in nuclear architecture are cell lineage-specific and do not occur in fibroblasts, and moreover they are overcome in breast cancer cells.
[Mh] Termos MeSH primário: Microambiente Celular
Integrina beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Afidicolina/farmacologia
Técnicas de Cultura de Células
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Senescência Celular
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Feminino
Seres Humanos
Immunoblotting
Células MCF-7
Glândulas Mamárias Animais/citologia
Camundongos
Microscopia Confocal
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Integrin beta1); 38966-21-1 (Aphidicolin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160129
[St] Status:MEDLINE
[do] DOI:10.1080/15384101.2015.1121354


  9 / 1568 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26810263
[Au] Autor:Santos GB; Krogh R; Magalhaes LG; Andricopulo AD; Pupo MT; Emery FS
[Ad] Endereço:Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, 14040-903 Ribeirão Preto, SP, Brazil.
[Ti] Título:Semisynthesis of new aphidicolin derivatives with high activity against Trypanosoma cruzi.
[So] Source:Bioorg Med Chem Lett;26(4):1205-8, 2016 Feb 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chagas disease continues to be a difficult disease to eradicate, largely because of the widespread populations it affects as well as the highly toxic effects of current therapies. Thus, the exploration of innovative scaffolds, ideally with distinct mechanisms of action, is urgently needed. The natural product aphidicolin and its effects on cell cycle division have been widely studied; it is a potent inhibitor of parasitic cells. In the present study, we report for the first time the semisynthesis of a series of aphidicolin derivatives, their unique structural features, and demonstration of their activity against Trypanosoma cruzi cells. Two demonstrated high potency and selectivity against parasitic amastigote cells, and thus show promise as new leads for Chagas disease treatment.
[Mh] Termos MeSH primário: Afidicolina/química
Afidicolina/farmacologia
Tripanossomicidas/síntese química
Trypanosoma cruzi/efeitos dos fármacos
[Mh] Termos MeSH secundário: Afidicolina/uso terapêutico
Doença de Chagas/tratamento farmacológico
Seres Humanos
Testes de Sensibilidade Parasitária
Relação Estrutura-Atividade
Tripanossomicidas/farmacologia
Tripanossomicidas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Trypanocidal Agents); 38966-21-1 (Aphidicolin)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160209
[Lr] Data última revisão:
160209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160127
[St] Status:MEDLINE


  10 / 1568 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26549024
[Au] Autor:Kanu N; Zhang T; Burrell RA; Chakraborty A; Cronshaw J; DaCosta C; Grönroos E; Pemberton HN; Anderton E; Gonzalez L; Sabbioneda S; Ulrich HD; Swanton C; Behrens A
[Ad] Endereço:Mammalian Genetics Laboratory, The Francis Crick Institute, London, UK.
[Ti] Título:RAD18, WRNIP1 and ATMIN promote ATM signalling in response to replication stress.
[So] Source:Oncogene;35(30):4009-19, 2016 Jul 28.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The DNA replication machinery invariably encounters obstacles that slow replication fork progression, and threaten to prevent complete replication and faithful segregation of sister chromatids. The resulting replication stress activates ATR, the major kinase involved in resolving impaired DNA replication. In addition, replication stress also activates the related kinase ATM, which is required to prevent mitotic segregation errors. However, the molecular mechanism of ATM activation by replication stress is not defined. Here, we show that monoubiquitinated Proliferating Cell Nuclear Antigen (PCNA), a marker of stalled replication forks, interacts with the ATM cofactor ATMIN via WRN-interacting protein 1 (WRNIP1). ATMIN, WRNIP1 and RAD18, the E3 ligase responsible for PCNA monoubiquitination, are specifically required for ATM signalling and 53BP1 focus formation induced by replication stress, not ionising radiation. Thus, WRNIP1 connects PCNA monoubiquitination with ATMIN/ATM to activate ATM signalling in response to replication stress and contribute to the maintenance of genomic stability.
[Mh] Termos MeSH primário: Proteínas Mutadas de Ataxia Telangiectasia/fisiologia
Proteínas de Transporte/fisiologia
Replicação do DNA
Proteínas de Ligação a DNA/fisiologia
Transdução de Sinais/fisiologia
Fatores de Transcrição/fisiologia
Ubiquitina-Proteína Ligases/fisiologia
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares
Afidicolina/farmacologia
Dano ao DNA
Instabilidade Genômica
Seres Humanos
Antígeno Nuclear de Célula em Proliferação/metabolismo
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATMIN protein, human); 0 (Carrier Proteins); 0 (DNA-Binding Proteins); 0 (Proliferating Cell Nuclear Antigen); 0 (Transcription Factors); 38966-21-1 (Aphidicolin); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.1 (ATM protein, human); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 3.6.1.3 (WRNIP1 protein, human); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities); EC 6.3.2.19 (RAD18 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151110
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2015.427



página 1 de 157 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde