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[PMID]:28864542
[Au] Autor:Li C; Götz J
[Ad] Endereço:Clem Jones Centre for Ageing Dementia Research (CJCADR), Queensland Brain Institute (QBI), The University of Queensland, Brisbane, Qld, Australia.
[Ti] Título:Somatodendritic accumulation of Tau in Alzheimer's disease is promoted by Fyn-mediated local protein translation.
[So] Source:EMBO J;36(21):3120-3138, 2017 Nov 02.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The cause of protein accumulation in neurodegenerative disease is incompletely understood. In Alzheimer's disease (AD), the axonally enriched protein Tau forms hyperphosphorylated aggregates in the somatodendritic domain. Consequently, a process of subcellular relocalization driven by Tau phosphorylation and detachment from microtubules has been proposed. Here, we reveal an alternative mechanism of protein synthesis of Tau and its hyperphosphorylation in the somatodendritic domain, induced by oligomeric amyloid-ß (Aß) and mediated by the kinase Fyn that activates the ERK/S6 signaling pathway. Activation of this pathway is demonstrated in a range of cellular systems, and in brains from Aß-depositing, Aß-injected, and Fyn-overexpressing mice with Tau accumulation. Both pharmacological inhibition and genetic deletion of Fyn abolish the Aß-induced Tau overexpression via ERK/S6 suppression. Together, these findings present a more cogent mechanism of Tau aggregation in disease. They identify a prominent role for neuronal Fyn in integrating signal transduction pathways that lead to the somatodendritic accumulation of Tau in AD.
[Mh] Termos MeSH primário: Doença de Alzheimer/genética
Precursor de Proteína beta-Amiloide/genética
Neurônios/metabolismo
Biossíntese de Proteínas
Proteínas Proto-Oncogênicas c-fyn/genética
Proteínas tau/genética
[Mh] Termos MeSH secundário: Doença de Alzheimer/metabolismo
Doença de Alzheimer/patologia
Peptídeos beta-Amiloides/administração & dosagem
Precursor de Proteína beta-Amiloide/metabolismo
Animais
Embrião de Mamíferos
Regulação da Expressão Gênica
Células HEK293
Hipocampo/metabolismo
Hipocampo/patologia
Seres Humanos
Injeções Intraventriculares
Sistema de Sinalização das MAP Quinases
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Neurônios/patologia
Neurônios/ultraestrutura
Fragmentos de Peptídeos/administração & dosagem
Proteínas Proto-Oncogênicas c-fyn/metabolismo
Puromicina/farmacologia
Proteínas Quinases S6 Ribossômicas/genética
Proteínas Quinases S6 Ribossômicas/metabolismo
Técnicas Estereotáxicas
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Amyloid beta-Protein Precursor); 0 (Peptide Fragments); 0 (amyloid beta-protein (1-42)); 0 (tau Proteins); 4A6ZS6Q2CL (Puromycin); EC 2.7.10.2 (Fyn protein, mouse); EC 2.7.10.2 (Proto-Oncogene Proteins c-fyn); EC 2.7.11.1 (Ribosomal Protein S6 Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201797724


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[PMID]:28803047
[Au] Autor:Singh R; Williams J; Vince R
[Ad] Endereço:Center for Drug Design, Academic Health Center, University of Minnesota, Minneapolis, MN 55455, USA. Electronic address: singh109@umn.edu.
[Ti] Título:Puromycin based inhibitors of aminopeptidases for the potential treatment of hematologic malignancies.
[So] Source:Eur J Med Chem;139:325-336, 2017 Oct 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Substantial progress has been described in the study of puromycin and its analogs for antibiotic properties. However, the peptidase inhibitory activity of related analogs has not been explored as extensively. Specifically, inhibiting aminopeptidases for achieving antitumor effect has been sparsely investigated. Herein, we address this challenge by reporting the synthesis of a series of analogs based on the structural template of puromycin. We also present exhaustive biochemical and in vitro analyses in support of our thesis. Analyzing the structure-activity relationship revealed a steric requirement for maximum potency. Effective inhibitors of Puromycin-Sensitive Aminopeptidase (PSA) are disclosed here. These potential therapeutic agents display superior in vitro antitumor potency against two leukemic cell lines, as compared to known inhibitors of aminopeptidases.
[Mh] Termos MeSH primário: Aminopeptidases/antagonistas & inibidores
Antineoplásicos/farmacologia
Inibidores Enzimáticos/farmacologia
Neoplasias Hematológicas/tratamento farmacológico
Puromicina/farmacologia
[Mh] Termos MeSH secundário: Aminopeptidases/metabolismo
Animais
Antineoplásicos/síntese química
Antineoplásicos/química
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Células HL-60
Neoplasias Hematológicas/metabolismo
Neoplasias Hematológicas/patologia
Seres Humanos
Estrutura Molecular
Puromicina/síntese química
Puromicina/química
Relação Estrutura-Atividade
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Enzyme Inhibitors); 4A6ZS6Q2CL (Puromycin); EC 3.4.11.- (Aminopeptidases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170814
[St] Status:MEDLINE


  3 / 5217 MEDLINE  
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[PMID]:28779235
[Au] Autor:Zhang QY; Li XD; Liu SQ; Deng CL; Zhang B; Ye HQ
[Ad] Endereço:Key Laboratory of Special Pathogens and Biosafety, Center for Emerging Infectious Diseases, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China.
[Ti] Título:Development of a stable Japanese encephalitis virus replicon cell line for antiviral screening.
[So] Source:Arch Virol;162(11):3417-3423, 2017 Nov.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Japanese encephalitis virus (JEV), an important pathogen in Eastern and Southern Asia and the Pacific, has spread to Australia and other territories in recent years. Although the vaccine for JEV has been used in some countries, development of efficient antiviral drugs is still an urgent requirement. Replicon systems have been widely used in the research of viral replication and antiviral screening for West Nile virus (WNV), yellow fever virus (YFV) and dengue virus (DENV). Here, a novel JEV replicon harboring the Rluc and Pac gene (JEV-Pac-Rluc-Rep) was constructed. Furthermore, we established a BHK-21 cell line harboring JEV-Pac-Rluc-Rep (BHK-21 cell line) through continuous puromycin selection. Characterization of cell line stability showed that the replicon RNA could persistently replicate in this cell line for at least up to 10 rounds of passage. Using a known flavivirus inhibitor, the JEV replicon cell line was validated for antiviral screening. The JEV replicon cell line will be a valuable tool for both compound screening and viral replication studies.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Vírus da Encefalite Japonesa (Espécie)/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Cricetinae
Puromicina
Replicon/genética
Replicon/fisiologia
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 4A6ZS6Q2CL (Puromycin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3508-9


  4 / 5217 MEDLINE  
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[PMID]:28322785
[Au] Autor:Kanungo J
[Ad] Endereço:Division of Neurotoxicology, National Center for Toxicological Research, U.S. Food and Drug Administration, 3900 NCTR Road, Jefferson, AR 72079, USA. Electronic address: jyotshnabala.kanungo@fda.hhs.gov.
[Ti] Título:Puromycin-resistant lentiviral control shRNA vector, pLKO.1 induces unexpected cellular differentiation of P19 embryonic stem cells.
[So] Source:Biochem Biophys Res Commun;486(2):481-485, 2017 Apr 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RNA silencing is used as a common method for investigating loss-of-function effects of genes of interest. In mammalian cells, RNA interference (RNAi) or RNA silencing can be achieved by transient siRNA (small or short interfering RNA) transfection or by stable shRNA (short hairpin RNA) systems. Various vectors are used for efficient delivery of shRNA. Lentiviral vectors offer an efficient delivery system for stable and long-term expression of the shRNA in mammalian cells. The widely used lentiviral pLKO.1 plasmid vector is very popular in RNAi studies. A large RNAi database, a TRC (the RNAi Consortium) library, was established based on the pLKO.1-TRC plasmid vector. This plasmid (also called pLKO.1-puro) has a puromycin-resistant gene for selection in mammalian cells along with designs for generating lentiviral particles as well for RNA silencing. While using the pLKO.1-puro TRC control shRNA plasmid for transfection in murine P19 embryonic stem (ES) cells, it was unexpectedly discovered that this plasmid vector induced robust endodermal differentiation. Since P19 ES cells are pluripotent and respond to external stimuli that have the potential to alter the phenotype and thus its stemness, other cell types used in RNA silencing studies do not display the obvious effect and therefore, may affect experiments in subtle ways that would go undetected. This study for the first time provides evidence that raises concern and warrants extreme caution while using the pLKO.1-puro control shRNA vector because of its unexpected non-specific effects on cellular integrity.
[Mh] Termos MeSH primário: Endoderma/efeitos dos fármacos
Lentivirus/genética
Células-Tronco Embrionárias Murinas/efeitos dos fármacos
Plasmídeos/metabolismo
Puromicina/farmacologia
RNA Interferente Pequeno/genética
[Mh] Termos MeSH secundário: Animais
Artefatos
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Endoderma/citologia
Endoderma/metabolismo
Expressão Gênica/efeitos dos fármacos
Biblioteca Gênica
Inativação Gênica
Lentivirus/metabolismo
Camundongos
Células-Tronco Embrionárias Murinas/citologia
Células-Tronco Embrionárias Murinas/metabolismo
Plasmídeos/química
RNA Interferente Pequeno/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 4A6ZS6Q2CL (Puromycin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170608
[Lr] Data última revisão:
170608
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


  5 / 5217 MEDLINE  
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[PMID]:28314264
[Au] Autor:Bodeau S; Sauzay C; Nyga R; Louandre C; Descamps V; François C; Godin C; Choukroun G; Galmiche A
[Ad] Endereço:Department of Pharmacology and Toxicology, Amiens University Hospital, Amiens, France.
[Ti] Título:Targeting the Unfolded Protein Response as a Potential Therapeutic Strategy in Renal Carcinoma Cells Exposed to Cyclosporine A.
[So] Source:Anticancer Res;37(3):1049-1057, 2017 03.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Organ transplant patients treated with the immunosuppressive drug cyclosporine A often present malignant kidney tumors. Cyclosporine A can promote oncogenesis in a cell-intrinsic manner by increasing the production of vascular endothelial growth factor (VEGF). MATERIALS AND METHODS: We explored the impact of cyclosporine A and the role of the unfolded protein response (UPR) on three human renal cell carcinoma (RCC) cell lines under normoxic and hypoxic (1% O ) conditions. RESULTS: Cyclosporine A regulated the expression of VEGF at the post-transcriptional level. Cyclosporine A induced the inositol requiring enzyme-1α (IRE1α) arm of the UPR and stabilized neosynthesized proteins in RCC cells. Toyocamycin, an inhibitor of IRE1α, abolished the clonogenic growth of RCC cells and reduced induction of VEGF by cyclosporine A under hypoxia. CONCLUSION: Our findings highlight the impact of cyclosporine A on the proteostasis of RCC cells, and suggest the potential therapeutic interest of targeting the UPR against tumors arising in the context of organ transplantation.
[Mh] Termos MeSH primário: Carcinoma de Células Renais/metabolismo
Ciclosporina/química
Regulação Neoplásica da Expressão Gênica
Imunossupressores/química
Neoplasias Renais/metabolismo
Resposta a Proteínas não Dobradas
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral/efeitos dos fármacos
Endorribonucleases/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Hipóxia
Oxigênio/metabolismo
Reação em Cadeia da Polimerase
Proteínas Serina-Treonina Quinases/metabolismo
Puromicina/química
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Toiocamicina/química
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunosuppressive Agents); 0 (RNA, Small Interfering); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 4A6ZS6Q2CL (Puromycin); 83HN0GTJ6D (Cyclosporine); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.1.- (Endoribonucleases); L7995C4D7F (Toyocamycin); S88TT14065 (Oxygen)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170411
[Lr] Data última revisão:
170411
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170319
[St] Status:MEDLINE


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[PMID]:28214366
[Au] Autor:Wu Y; Xu K; Ren C; Li X; Lv H; Han F; Wei Z; Wang X; Zhang Z
[Ad] Endereço:College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, China.
[Ti] Título:Enhanced CRISPR/Cas9-mediated biallelic genome targeting with dual surrogate reporter-integrated donors.
[So] Source:FEBS Lett;591(6):903-913, 2017 Mar.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated protein 9 (Cas9) system has recently emerged as a simple, yet powerful genome engineering tool, which has been widely used for genome modification in various organisms and cell types. However, screening biallelic genome-modified cells is often time-consuming and technically challenging. In this study, we incorporated two different surrogate reporter cassettes into paired donor plasmids, which were used as both the surrogate reporters and the knock-in donors. By applying our dual surrogate reporter-integrated donor system, we demonstrate high frequency of CRISPR/Cas9-mediated biallelic genome integration in both human HEK293T and porcine PK15 cells (34.09% and 18.18%, respectively). Our work provides a powerful genetic tool for assisting the selection and enrichment of cells with targeted biallelic genome modification.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas
Edição de Genes/métodos
Genoma/genética
Modelos Genéticos
[Mh] Termos MeSH secundário: Alelos
Animais
Sequência de Bases
Bleomicina/farmacologia
Linhagem Celular
Resistência a Medicamentos/genética
Citometria de Fluxo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Células HEK293
Seres Humanos
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Microscopia de Fluorescência
Reação em Cadeia da Polimerase
Puromicina/farmacologia
Reprodutibilidade dos Testes
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Luminescent Proteins); 0 (red fluorescent protein); 11056-06-7 (Bleomycin); 147336-22-9 (Green Fluorescent Proteins); 181494-14-4 (Zeocin); 4A6ZS6Q2CL (Puromycin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170219
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12599


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[PMID]:28102767
[Au] Autor:Carter J; Weaver BA; Chiacchio MA; Messersmith AR; Lynch WE; Feske BD; Gumina G
[Ad] Endereço:a Department of Pharmaceutical and Administrative Sciences , Presbyterian College School of Pharmacy , Clinton , SC , USA.
[Ti] Título:Synthesis, stereochemical characterization, and antimicrobial evaluation of a potentially nonnephrotoxic 3'-C-acethydrazide puromycin analog.
[So] Source:Nucleosides Nucleotides Nucleic Acids;36(3):224-241, 2017 Mar 04.
[Is] ISSN:1532-2335
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Puromycin is a peptidyl nucleoside endowed with significant antibiotic and anticancer properties, but also with an unfortunate nephrotoxic character that has hampered its use as a chemotherapeutic agent. Since hydrolysis of puromycin's amide to puromycin aminonucleoside is the first metabolic step leading to nephrotoxicity, we designed a 3'-C-hydrazide analog where the nitrogen and carbon functionality around the amide carbonyl of puromycin are inverted. The title compound, synthesized in 11 steps from D-xylose, cannot be metabolized to the nephrotoxic aminonucleoside. Evaluation of the title compound on Staphylococcus epidermidis and multi-drug resistance Staphylococcus aureus did not show significant antimicrobial activity up to a 400 µM concentration.
[Mh] Termos MeSH primário: Antibacterianos/química
Antibacterianos/farmacologia
Puromicina/química
[Mh] Termos MeSH secundário: Antibacterianos/síntese química
Técnicas de Química Sintética
Cristalografia por Raios X
Farmacorresistência Bacteriana Múltipla/efeitos dos fármacos
Testes de Sensibilidade Microbiana
Puromicina/efeitos adversos
Puromicina/farmacologia
Staphylococcus aureus/efeitos dos fármacos
Staphylococcus epidermidis/efeitos dos fármacos
Estereoisomerismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 4A6ZS6Q2CL (Puromycin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170303
[Lr] Data última revisão:
170303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.1080/15257770.2016.1264590


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[PMID]:27926780
[Au] Autor:Spinnenhirn V; Bitzer A; Aichem A; Groettrup M
[Ad] Endereço:Division of Immunology, Department of Biology, University of Konstanz, Germany.
[Ti] Título:Newly translated proteins are substrates for ubiquitin, ISG15, and FAT10.
[So] Source:FEBS Lett;591(1):186-195, 2017 Jan.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The ubiquitin-like modifier, FAT10, is involved in proteasomal degradation and antigen processing. As ubiquitin and the ubiquitin-like modifier, ISG15, cotranslationally modify proteins, we investigated whether FAT10 could also be conjugated to newly synthesized proteins. Indeed, we found that nascent proteins are modified with FAT10, but not with the same preference for newly synthesized proteins as observed for ISG15. Our data show that puromycin-labeled polypeptides are strongly modified by ISG15 and less intensely by ubiquitin and FAT10. Nevertheless, conjugates of all three modifiers copurify with ribosomes. Taken together, we show that unlike ISG15, ubiquitin and FAT10 are conjugated to a similar degree to newly translated and pre-existing proteins.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Biossíntese de Proteínas
Ubiquitina/metabolismo
Ubiquitinas/metabolismo
[Mh] Termos MeSH secundário: Células HEK293
Seres Humanos
Puromicina/metabolismo
Ribossomos/metabolismo
Especificidade por Substrato
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Cytokines); 0 (UBD protein, human); 0 (Ubiquitin); 0 (Ubiquitins); 4A6ZS6Q2CL (Puromycin); 60267-61-0 (ISG15 protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12512


  9 / 5217 MEDLINE  
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[PMID]:27878264
[Au] Autor:Zhou T; Li Y; Yang L; Liu L; Ju Y; Li C
[Ad] Endereço:Breast Disease Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China.
[Ti] Título:Silencing of ANXA3 expression by RNA interference inhibits the proliferation and invasion of breast cancer cells.
[So] Source:Oncol Rep;37(1):388-398, 2017 Jan.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:The present study aimed to explore the expression of Annexin A3 (ANXA3) in breast cancer cells and the mechanisms involved in the regulatory effects of ANXA3 on proliferation, invasion and migration of breast cancer cells. Fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting were used to measure the expression of ANXA3 mRNA and protein in two breast cancer cell lines (MDA-MB-231 and MCF-7). Three ANXA3 silencing shRNA plasmids (ANXA3-sh1-3) and one negative control plasmid were constructed, and the Lipofectamine transfection method was used for transfecting human breast cancer cell line MDA-MB-231. Flow cytometry was used to measure the transfection efficiency. The expression of ANXA3 protein was measured by western blotting. Cell cycle distribution and apoptosis were assessed by flow cytometry. Migration and invasion of the transfected cells were evaluated using wound healing and Transwell assays, respectively. The expression levels of ANXA3 mRNA and protein were significantly higher in the MDA-MB-231 cells than levels in the MCF-7 cells. Western blotting showed that the ANXA3 protein level was significantly lower in the MDA-MB-231-Sh cells than that in the MDA-MB-231 and MDA-MB-231-NC cells. In addition, the percentage of G0/1 cells and the apoptosis rate were significantly higher, while the cell proliferation rate was significantly lower, in the MDA-MB-231-Sh cells when compared with the MDA-MB-231-NC and MDA-MB-231 cells. The cell migration and invasion abilities were also lower in the MDA-MB-231-Sh cells than these abilities in the MDA-MB-231-NC and MDA-MB-231 cells. The present study investigated the relationships between ANXA3 and proliferation, apoptosis, migration and invasion of breast cancer cells to elucidate the mechanisms involved in the development, progression, invasion and metastasis of breast cancer.
[Mh] Termos MeSH primário: Anexina A3/genética
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
[Mh] Termos MeSH secundário: Anexina A3/metabolismo
Apoptose/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Feminino
Citometria de Fluxo/métodos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Inativação Gênica
Vetores Genéticos
Seres Humanos
Lentivirus/genética
Células MCF-7
Puromicina
Interferência de RNA
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANXA3 protein, human); 4A6ZS6Q2CL (Puromycin); EC 3.1.4.43 (Annexin A3)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170322
[Lr] Data última revisão:
170322
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.3892/or.2016.5251


  10 / 5217 MEDLINE  
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[PMID]:27367189
[Au] Autor:Mirzoev TM; Tyganov SA; Shenkman BS
[Ad] Endereço:Myology Laboratory, Institute of Bio-Medical Problems of the Russian Academy of Sciences, 123007, Moscow, Russian Federation.
[Ti] Título:Akt-dependent and Akt-independent pathways are involved in protein synthesis activation during reloading of disused soleus muscle.
[So] Source:Muscle Nerve;55(3):393-399, 2017 Mar.
[Is] ISSN:1097-4598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The purpose of our study was to assess the contribution of insulin growth factor-1-dependent and phosphatidic acid-dependent signaling pathways to activation of protein synthesis (PS) in rat soleus muscle during early recovery from unloading. METHODS: Wistar rats were divided into: Control, 14HS [14-day hindlimb suspension (HS)], 3R+placebo (3-day reloading + saline administration), 3R+Wort (3-day reloading + wortmannin administration), 3R+But (3-day reloading + 1-butanol administration). SUnSET and Western blot analyses were used in this study. RESULTS: Wortmannin and 1-butanol induced a decrease in protein kinase B (phospho-Akt) and the rate of PS (P < 0.05) versus Control. In 3R+placebo and 3R+Wort, phosphorylation of glycogen synthase kinase 3 beta (phospho-GSK-3ß) was increased versus Control (P < 0.05). Wortmannin administration during reloading did not alter phospho-p70S6K (70 kDa ribosomal protein S6 kinase) versus 3R+placebo. In 3R+But, there was a decline in phospho-GSK-3ß versus 3R+placebo and Control. In 3R+But, there was a decrease in phopho-p70S6K (P < 0.05) versus 3R+placebo. CONCLUSIONS: These results suggest that PS activation during 3-day reloading following 14HS involves both Akt-dependent and Akt-independent pathways. Muscle Nerve 55: 393-399, 2017.
[Mh] Termos MeSH primário: Elevação dos Membros Posteriores
Músculo Esquelético/fisiologia
Proteína Oncogênica v-akt/metabolismo
Biossíntese de Proteínas/fisiologia
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: 1-Butanol/farmacologia
Androstadienos/farmacologia
Animais
Elevação dos Membros Posteriores/fisiologia
Fator de Crescimento Insulin-Like I/metabolismo
Músculo Esquelético/efeitos dos fármacos
Tamanho do Órgão/efeitos dos fármacos
Inibidores de Fosfodiesterase/farmacologia
Biossíntese de Proteínas/efeitos dos fármacos
Inibidores da Síntese de Proteínas/farmacologia
Puromicina/farmacologia
Ratos
Ratos Wistar
Proteínas Quinases S6 Ribossômicas 70-kDa/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androstadienes); 0 (Phosphodiesterase Inhibitors); 0 (Protein Synthesis Inhibitors); 4A6ZS6Q2CL (Puromycin); 67763-96-6 (Insulin-Like Growth Factor I); 8PJ61P6TS3 (1-Butanol); EC 2.7.11.1 (Oncogene Protein v-akt); EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa); XVA4O219QW (wortmannin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170703
[Lr] Data última revisão:
170703
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160702
[St] Status:MEDLINE
[do] DOI:10.1002/mus.25235



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