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[PMID]:29237529
[Au] Autor:Liu TT; Xiao B; Li SY; Li GL; Lu XQ; Liu WP
[Ad] Endereço:Department of Neurology, Xiangya Hospital, Central Southern University, Changsha 410008, China. liuweiping8888@126.com.
[Ti] Título:[Changes in the expression of EphA5/ephrinA5 in the CA3 region of the hippocampus in rats with epilepsy and their role in the pathogenesis of temporal lobe epilepsy].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(12):1272-1277, 2017 Dec.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the changes in the expression of EphA5 and its ligand ephrinA5 in the hippocampus of rats with epilepsy and their role in the pathogenesis of temporal lobe epilepsy (TLE). METHODS: A total of 240 Sprague-Dawley rats were randomly divided into control group and TLE group, with 120 rats in each group. A rat model of lithium-pilocarpine TLE was established, and then the rats were divided into subgroups at 12 and 24 hours and 7, 15, 30, and 60 days after epilepsy was induced. In-situ hybridization was used to measure the mRNA expression of ephrinA5 in the CA3 region and the dentate gyrus of the hippocampus in 9 rats; immunohistochemistry was used to measure the protein expression of EphA5 in the CA3 region and the dentate gyrus of the hippocampus in 9 rats; Neo-Timm silver staining was used to observe mossy fiber sprouting in the CA3 region of the hippocampus in 2 rats. RESULTS: In-situ hybridization showed mRNA expression of ephrinA5 in the CA3 region of the hippocampus, but this was not found in the dentate gyrus. Compared with the control group at the same time point, the TLE group had a significant reduction in the mRNA expression of ephrinA5 in the CA3 region of the hippocampus at 7 and 15 days after epilepsy was induced (P<0.05); at 30 and 60 days after epilepsy was induced, the TLE group had a gradual increase in the mRNA expression of ephrinA5 in the CA3 region of the hippocampus, and there was no significant difference between the TLE and control groups (P>0.05). Immunohistochemistry showed that EphA5 protein was expressed in the CA3 region and the dentate gyrus of the hippocampus and had a similar trend of change as ephrinA5 mRNA. Neo-Timm silver staining showed that the TLE group developed marked mossy fiber sprouting in the CA3 region of the hippocampus at 7 and 15 days after epilepsy was induced. CONCLUSIONS: Downregulation of ephrinA5 and EphA5 in the CA3 region of the hippocampus may participate in the mechanism of mossy fiber sprouting and is closely associated with the development and progression of epilepsy.
[Mh] Termos MeSH primário: Efrina-A5/fisiologia
Epilepsia do Lobo Temporal/etiologia
Hipocampo/química
Receptor EphA5/fisiologia
[Mh] Termos MeSH secundário: Animais
Efrina-A5/análise
Efrina-A5/genética
Epilepsia do Lobo Temporal/metabolismo
Masculino
RNA Mensageiro/análise
Ratos
Ratos Sprague-Dawley
Receptor EphA5/análise
Receptor EphA5/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ephrin-A5); 0 (RNA, Messenger); EC 2.7.10.1 (Epha5 protein, rat); EC 2.7.10.1 (Receptor, EphA5)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE


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[PMID]:28421649
[Au] Autor:Wang X; Xu H; Wu Z; Chen X; Wang J
[Ad] Endereço:Department of Urology, Nantong Tumor Hospital, Nantong, Jiangsu, China.
[Ti] Título:Decreased expression of EphA5 is associated with Fuhrman nuclear grade and pathological tumour stage in ccRCC.
[So] Source:Int J Exp Pathol;98(1):34-39, 2017 Feb.
[Is] ISSN:1365-2613
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The incidence of renal cell carcinoma is increasing all over the world. The molecular mechanisms for tumorigenesis, progression and prognosis are still unknown. The erythropoietin-producing hepatoma amplified sequence (Eph) receptors have been reported to be expressed aberrantly in many types of human cancers and in particular EphA5 may play a role in certain human cancers. In this study, a set of clear cell renal cell carcinoma (ccRCC) tissues were subjected to immunohistochemistry. The relationship between EphA5 protein expression and clinicopathological parameters was statistically analysed. Our data show that EphA5 protein was negatively (0) or weakly (1+) expressed in 48 of 78 (61.5%), moderately (2+) expressed in 15 of 78 (19.2%) and strongly (3+) expressed in 15 of 78 (19.2%) tumour samples of ccRCC. Decreased expression of EphA5 was detected more often in females than in males (P = 0.017, r = -0.267). Expression of EphA5 was related negatively to Fuhrman grade (P = 0.013, r = -0.279) and pathological tumour stage pT (P = 0.003, r = -0.334). No relation between the expression of EphA5 and age of patients was found (P = 0.107, r = 0.184). Fuhrman grade and pT stage are the most important factors used in prognosis of ccRCC. Hence this study may provide a new and useful prognostic marker in the clinical practice of ccRCC.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Carcinoma de Células Renais/metabolismo
Neoplasias Renais/metabolismo
Receptor EphA5/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais/análise
Carcinoma de Células Renais/diagnóstico
Carcinoma de Células Renais/patologia
Feminino
Seres Humanos
Imuno-Histoquímica
Neoplasias Renais/diagnóstico
Neoplasias Renais/patologia
Masculino
Meia-Idade
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 2.7.10.1 (Receptor, EphA5)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1111/iep.12219


  3 / 100 MEDLINE  
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[PMID]:27988259
[Au] Autor:Nguyen TM; Arthur A; Zannettino AC; Gronthos S
[Ad] Endereço:Mesenchymal Stem Cell Laboratory, Adelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia; Cancer Theme, South Australian Health and Medical Research Institute, Adelaide, SA, Australia.
[Ti] Título:EphA5 and EphA7 forward signaling enhances human hematopoietic stem and progenitor cell maintenance, migration, and adhesion via Rac1 activation.
[So] Source:Exp Hematol;48:72-78, 2017 Apr.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The proliferation, differentiation, adhesion, and migration of hematopoietic stem and progenitor cells (HSPCs) are dependent upon bone marrow stromal cells (BMSCs). In this study, we found that human primitive HSPCs (CD34 CD38 ), but not lineage-committed hematopoietic cell populations, express the tyrosine kinase receptors EphA5 and EphA7. Moreover, we found that the ephrinA5 ligand, the high-affinity binding partner of EphA5 and EphA7, is highly expressed by primary human BMSCs. Previous studies have reported that interactions between EphA and ephrinA play important roles in hematopoietic cell trafficking; however, their role in BMSC support of hematopoiesis had not been described previously. Herein, we show that stimulating EphA5 and/or EphA7 forward signaling in HSPCs using soluble ephrinA5-Fc molecules promoted human HSPC-derived colony formation significantly and was associated with increased expression of granulocyte macrophage colony-stimulating factor receptor on HSPCs. Studies using functional blocking peptides to EphA5/7 found that disruption of EphA5/ephrinA5 and/or EphA7/ephrinA5 interactions inhibited HSPC function in BMSC-dependent long-term culture-initiating cell assays. Furthermore, the adhesion and migration of HSPCs was increased significantly in the presence of ephrinA5-Fc molecules compared with human immunoglobulin G-treated controls. Conversely, blocking EphA5 activation led to a reduction of HSPC adhesion, whereas inhibiting EphA5 and/or EphA7 activation hindered HSPC migration. Analysis of HSPC cultured in the presence of ephrinA5-Fc showed that EphA forward signaling stimulated Rac1 gene and protein expression and the Rac1 target molecule WAVE1. Moreover, a significant reduction of ephrinA5-mediated HSPC adhesion and migration was observed in the presence of Rac1 inhibitor. These findings suggest that interactions between EphA and ephrinA5 are important in maintaining the HSPC niche mediated in part by activation of Rac1 signaling.
[Mh] Termos MeSH primário: Movimento Celular
Autorrenovação Celular
Células-Tronco Hematopoéticas/citologia
Células-Tronco Hematopoéticas/fisiologia
Receptor EphA5/metabolismo
Receptor EphA7/metabolismo
Transdução de Sinais
Proteínas rac1 de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Adesão Celular/genética
Comunicação Celular
Diferenciação Celular
Movimento Celular/genética
Autorrenovação Celular/genética
Perfilação da Expressão Gênica
Seres Humanos
Receptor EphA5/genética
Receptor EphA7/genética
Células-Tronco
Células Estromais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.10.1 (Receptor, EphA5); EC 2.7.10.1 (Receptor, EphA7); EC 3.6.5.2 (rac1 GTP-Binding Protein)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161219
[St] Status:MEDLINE


  4 / 100 MEDLINE  
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[PMID]:27651378
[Au] Autor:Gu S; Feng J; Jin Q; Wang W; Zhang S
[Ad] Endereço:Department of Oncology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
[Ti] Título:Reduced expression of EphA5 is associated with lymph node metastasis, advanced TNM stage, and poor prognosis in colorectal carcinoma.
[So] Source:Histol Histopathol;32(5):491-497, 2017 May.
[Is] ISSN:1699-5848
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Colorectal carcinoma (CRC) is the third most common cancer and a major cause of morbidity and mortality throughout the world. The prognosis of patients has improved markedly over the last 15 years because of the introduction of new therapy including molecular target drugs. To comprehensively understand the molecular process of carcinogenesis of colorectal carcinoma is essential for the diagnosis, prognosis and treatment. EphA5 is a member of the Eph family and plays a critical role in carcinogenesis of lung cancer, prostate cancer, and breast cancer. The expression profile and the role of EphA5 in colorectal carcinoma have not been well investigated till now. In this study, a set of colorectal carcinoma specimens was subjected to immunohistochemical assay using an EphA5 specific antibody. The relationship between the expression of EphA5 and clinicopathological parameters was statistically analyzed. EphA5 was positively expressed in all tested normal mucosa specimens (120/120, 100%) and partly in colorectal carcinoma specimens (70/120, 58.3%). The loss of EphA5 protein was associated with depth of wall invasion (P=0.002), poor tumor differentiation (P<0.001), lymph node metastasis (P<0.001), and advanced TNM stage (P<0.001). The survival analysis showed that patients with reduced expression of EphA5 had a poor overall survival (P=0.017). Our data indicate that EphA5 receptor may be a tumor suppressor in colorectal carcinoma and it may be a new therapeutic target for colorectal carcinoma.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Carcinoma/patologia
Neoplasias Colorretais/patologia
Metástase Linfática/patologia
Receptor EphA5/biossíntese
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma/mortalidade
Neoplasias Colorretais/mortalidade
Feminino
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Estadiamento de Neoplasias
Prognóstico
Receptor EphA5/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 2.7.10.1 (EPHA5 protein, human); EC 2.7.10.1 (Receptor, EphA5)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160922
[St] Status:MEDLINE
[do] DOI:10.14670/HH-11-815


  5 / 100 MEDLINE  
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[PMID]:27887627
[Au] Autor:Chen X; Wang X; Wei X; Wang J
[Ad] Endereço:Department of Pathology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, 210002, China.
[Ti] Título:EphA5 protein, a potential marker for distinguishing histological grade and prognosis in ovarian serous carcinoma.
[So] Source:J Ovarian Res;9(1):83, 2016 Nov 25.
[Is] ISSN:1757-2215
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ovarian serous carcinoma (OSC) is the most common ovarian epithelial malignancy. Disregulation of Eph/ephrin signaling has been implicated in oncogenesis and tumor progression. EphA5 receptor is one of large families of Eph tyrosine kinase receptor and is documented in the development of nervous system. Till now, there is no published data about the role of EphA5 in ovarian epithelial neoplasmas. METHODS: This study aims to investigate the expression of EphA5 protein in ovarian serous carcinoma, and its relationship to clinical pathological characteristics. Sixty-one cases of ovarian serous carcinoma, 24 cases of benign ovarian serous tumors, 42 cases of serous borderline tumors and 20 cases of normal fallopian tubes were examined using immunohistochemical staining. The relationship between EphA5 expression and pathological parameters was analyzed. Kaplan-Meier survival function was used to analyze prognosis of patients. RESULTS: Immunostaining analysis demonstrated that the EphA5 protein was highly expressed in 100% (20/20) of normal fallopian tube samples, 100% (24/24) of benign epithelial ovarian tumors, 76% (32/42) of ovarian serous borderline tumors, and 31% (19/61) of ovarian serous carcinomas. Loss of EphA5expression was associated with tumor grade (P < 0.001) and FIGO stage (P = 0.005). The survival analysis showed that patients with negative or weak expression of EphA5 protein had a poor outcome than those with positive expression (P = 0.004). CONCLUSIONS: Our results show that EphA5 may be a potential biomarker for distinguishing high-and low-grade ovarian serous carcinoma and a potential prognostic marker.
[Mh] Termos MeSH primário: Biomarcadores Tumorais
Cistadenocarcinoma Seroso/metabolismo
Cistadenocarcinoma Seroso/patologia
Neoplasias Ovarianas/metabolismo
Neoplasias Ovarianas/patologia
Receptor EphA5/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Cistadenocarcinoma Seroso/mortalidade
Tubas Uterinas/metabolismo
Tubas Uterinas/patologia
Feminino
Expressão Gênica
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Neoplasias Ovarianas/mortalidade
Prognóstico
Receptor EphA5/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 2.7.10.1 (Receptor, EphA5)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161127
[St] Status:MEDLINE


  6 / 100 MEDLINE  
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[PMID]:27402841
[Au] Autor:Wang J; Galvao J; Beach KM; Luo W; Urrutia RA; Goldberg JL; Otteson DC
[Ad] Endereço:From the Departments of Physiological Optics and Vision Science and.
[Ti] Título:Novel Roles and Mechanism for Krüppel-like Factor 16 (KLF16) Regulation of Neurite Outgrowth and Ephrin Receptor A5 (EphA5) Expression in Retinal Ganglion Cells.
[So] Source:J Biol Chem;291(35):18084-95, 2016 08 26.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regenerative medicine holds great promise for the treatment of degenerative retinal disorders. Krüppel-like factors (KLFs) are transcription factors that have recently emerged as key tools in regenerative medicine because some of them can function as epigenetic reprogrammers in stem cell biology. Here, we show that KLF16, one of the least understood members of this family, is a POU4F2 independent transcription factor in retinal ganglion cells (RGCs) as early as embryonic day 15. When overexpressed, KLF16 inhibits RGC neurite outgrowth and enhances RGC growth cone collapse in response to exogenous ephrinA5 ligands. Ephrin/EPH signaling regulates RGC connectivity. The EphA5 promoter contains multiple GC- and GT-rich KLF-binding sites, which, as shown by ChIP-assays, bind KLF16 in vivo In electrophoretic mobility shift assays, KLF16 binds specifically to a single KLF site near the EphA5 transcription start site that is required for KLF16 transactivation. Interestingly, methylation of only six of 98 CpG dinucleotides within the EphA5 promoter blocks its transactivation by KLF16 but enables transactivation by KLF2 and KLF15. These data demonstrate a role for KLF16 in regulation of RGC neurite outgrowth and as a methylation-sensitive transcriptional regulator of EphA5 expression. Together, these data identify differential low level methylation as a novel mechanism for regulating KLF16-mediated EphA5 expression across the retina. Because of the critical role of ephrin/EPH signaling in patterning RGC connectivity, understanding the role of KLFs in regulating neurite outgrowth and Eph receptor expression will be vital for successful restoration of functional vision through optic nerve regenerative therapies.
[Mh] Termos MeSH primário: Fatores de Transcrição Kruppel-Like/metabolismo
Neuritos/metabolismo
Receptor EphA5/biossíntese
Elementos de Resposta/fisiologia
Células Ganglionares da Retina/metabolismo
Transdução de Sinais/fisiologia
Ativação Transcricional/fisiologia
[Mh] Termos MeSH secundário: Animais
Metilação de DNA
Fatores de Transcrição Kruppel-Like/genética
Camundongos
Camundongos Knockout
Receptor EphA5/genética
Células Ganglionares da Retina/citologia
Transcrição Genética/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Klf16 protein, mouse); 0 (Kruppel-Like Transcription Factors); EC 2.7.10.1 (Receptor, EphA5)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160713
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.732339


  7 / 100 MEDLINE  
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[PMID]:27241944
[Au] Autor:McCreary JK; Truica LS; Friesen B; Yao Y; Olson DM; Kovalchuk I; Cross AR; Metz GA
[Ad] Endereço:Canadian Centre for Behavioural Neuroscience, Department of Neuroscience, University of Lethbridge, Lethbridge, AB T1K3M4, Canada.
[Ti] Título:Altered brain morphology and functional connectivity reflect a vulnerable affective state after cumulative multigenerational stress in rats.
[So] Source:Neuroscience;330:79-89, 2016 Aug 25.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prenatal stress is a risk factor for abnormal neuroanatomical, cognitive, behavioral and mental health outcomes with potentially transgenerational consequences. Females in general seem more resilient to the effects of prenatal stress than males. Here, we examined if repeated stress across generations may diminish stress resiliency and cumulatively enhance the susceptibility for adverse health outcomes in females. Pregnant female rats of three successive generations were exposed to stress from gestational days 12-18 to generate multigenerational prenatal stress (MPS) in the maternal lineage. Stress response was measured by plasma corticosterone levels and open-field exploration in each generation. Neuromorphological consequences of MPS were investigated in the F3 generation using in vivo manganese-enhanced magnetic resonance imaging (MEMRI), T2-relaxometry, and cytoarchitectonics in relation to candidate gene expression involved in brain plasticity and mental health. Each additional generation of prenatal stress incrementally elevated hypothalamic-pituitary-adrenal axis activation, anxiety-like and aversive behaviors in adult female offspring. Elevated stress responses in the MPS F3 generation were accompanied by reduced neural density in prefrontal cortex, hippocampus and whole brain along with altered brain activation patterns in in vivo MEMRI. MPS increased ephrin receptor A5 (Epha5), neuronal growth regulator (Negr1) and synaptosomal-associated protein 25 (Snap25) gene expression and reduced fibroblast growth factor 12 (Fgf12) in prefrontal cortex. These genes regulate neuronal maturation, arborization and synaptic plasticity and may explain altered brain cytoarchitectonics and connectivity. These findings emphasize that recurrent stress across generations may cumulatively increase stress vulnerability and the risk of adverse health outcomes through perinatal programing in females.
[Mh] Termos MeSH primário: Encéfalo/patologia
Encéfalo/fisiopatologia
Emoções/fisiologia
Efeitos Tardios da Exposição Pré-Natal
Estresse Psicológico
[Mh] Termos MeSH secundário: Animais
Encéfalo/diagnóstico por imagem
Encéfalo/crescimento & desenvolvimento
Contagem de Células
Meios de Contraste
Corticosterona/sangue
Modelos Animais de Doenças
Comportamento Exploratório/fisiologia
Feminino
Fatores de Crescimento de Fibroblastos/metabolismo
Regulação da Expressão Gênica/fisiologia
Imagem por Ressonância Magnética
Manganês
Vias Neurais/diagnóstico por imagem
Vias Neurais/crescimento & desenvolvimento
Vias Neurais/patologia
Vias Neurais/fisiopatologia
Neurônios/patologia
Neurônios/fisiologia
Gravidez
Ratos Long-Evans
Receptor EphA5/metabolismo
Resiliência Psicológica
Estresse Psicológico/fisiopatologia
Proteína 25 Associada a Sinaptossoma/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Contrast Media); 0 (Snap25 protein, rat); 0 (Synaptosomal-Associated Protein 25); 0 (fibroblast growth factor 12, rat); 42Z2K6ZL8P (Manganese); 62031-54-3 (Fibroblast Growth Factors); EC 2.7.10.1 (Epha5 protein, rat); EC 2.7.10.1 (Receptor, EphA5); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160601
[St] Status:MEDLINE


  8 / 100 MEDLINE  
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[PMID]:26986674
[Au] Autor:Ghosh Moulick R; Afanasenkau D; Choi SE; Albers J; Lange W; Maybeck V; Utesch T; Offenhäusser A
[Ad] Endereço:Institute for Bioelectronics (ICS-8), Forschungszentrum Jülich , Wilhelm-Johnen Straße, 52425 Jülich, Germany.
[Ti] Título:Reconstitution of Fusion Proteins in Supported Lipid Bilayers for the Study of Cell Surface Receptor-Ligand Interactions in Cell-Cell Contact.
[So] Source:Langmuir;32(14):3462-9, 2016 Apr 12.
[Is] ISSN:1520-5827
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bioactive molecules such as adhesion ligands, growth factors, or enzymes play an important role in modulating cell behavior such as cell adhesion, spreading, and differentiation. Deciphering the mechanism of ligand-mediated cell adhesion and associated signaling is of great interest not only for fundamental biophysical investigations but also for applications in medicine and biotechnology. In the presented work, we developed a new biomimetic platform that enables culturing primary neurons and testing cell surface-receptor ligand interactions in cell-cell contacts as, e.g., in neuronal synapses. This platform consists of a supported lipid bilayer modified with incorporated neuronal adhesion proteins conjugated with the Fc-domain of IgG (ephrin A5 Fc-chimera). We extensively characterized properties of these protein containing bilayers using fluorescence recovery after photobleaching (FRAP), quartz crystal microbalance with dissipation (QCM-D), and immunostaining. We conclude that the Fc-domain is the part responsible for the incorporation of the protein into the bilayer. The biomimetic platform prepared by this new approach was able to promote neuronal cell adhesion and maintain growth as well as facilitate neuronal maturation as shown by electrophysiological measurements. We believe that our approach can be extended to insert other proteins to create a general culture platform for neurons and other cell types.
[Mh] Termos MeSH primário: Efrina-A5/metabolismo
Fragmentos Fc das Imunoglobulinas/metabolismo
Receptor EphA5/metabolismo
Proteínas Recombinantes de Fusão/metabolismo
[Mh] Termos MeSH secundário: Animais
Materiais Biomiméticos
Adesão Celular
Células Cultivadas
Córtex Cerebral/citologia
Córtex Cerebral/metabolismo
Efrina-A5/química
Efrina-A5/genética
Feminino
Seres Humanos
Fragmentos Fc das Imunoglobulinas/química
Fragmentos Fc das Imunoglobulinas/genética
Bicamadas Lipídicas
Camundongos
Neurônios/citologia
Neurônios/fisiologia
Técnicas de Patch-Clamp
Fosfatidilcolinas/química
Ratos Wistar
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ephrin-A5); 0 (Immunoglobulin Fc Fragments); 0 (Lipid Bilayers); 0 (Phosphatidylcholines); 0 (Recombinant Fusion Proteins); EC 2.7.10.1 (Receptor, EphA5); TE895536Y5 (1-palmitoyl-2-oleoylphosphatidylcholine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160318
[St] Status:MEDLINE
[do] DOI:10.1021/acs.langmuir.5b04644


  9 / 100 MEDLINE  
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[PMID]:26784321
[Au] Autor:Gupta G; Song J
[Ad] Endereço:Department of Biological Sciences, Faculty of Science, National University of Singapore, Singapore, Singapore.
[Ti] Título:C-Terminal Auto-Regulatory Motif of Hepatitis C Virus NS5B Interacts with Human VAPB-MSP to Form a Dynamic Replication Complex.
[So] Source:PLoS One;11(1):e0147278, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatitis C virus (HCV) is a pathogen of global importance and nearly 200 million people are chronically infected with HCV. HCV is an enveloped single-stranded RNA virus, which is characteristic of the formation of the host membrane associated replication complex. Previous functional studies have already established that the human ER-anchored VAPB protein acts as a host factor to form a complex with HCV NS5A and NS5B, which may be established as a drug target. However, there is lacking of biophysical characterization of the structures and interfaces of the complex, partly due to the dynamic nature of the complex formation and dissociation, which is extensively involved in intrinsically-disordered domains. Here by an integrated use of domain dissection and NMR spectroscopy, for the first time we have successfully deciphered that the HCV NS5B utilizes its auto-regulatory C-linker to bind the VAPB-MSP domain to form a dynamic complex. This finding implies that the NS5B C-linker is capable of playing dual roles by a switch between the folded and disordered states. Interestingly, our previous and present studies together reveal that both HCV NS5A and NS5B bind to the MSP domains of the dimeric VAP with significantly overlapped interfaces and similar affinities. The identification that EphA2 and EphA5 bind to the MSP domain with higher affinity than EphA4 provides a biophysical basis for further exploring whether other than inducing ALS-like syndrome, the HCV infection might also trigger pathogenesis associated with signalling pathways mediated by EphA2 and EphA5.
[Mh] Termos MeSH primário: Hepacivirus/metabolismo
Proteínas de Transporte Vesicular/química
Proteínas de Transporte Vesicular/metabolismo
Proteínas não Estruturais Virais/química
Proteínas não Estruturais Virais/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Hepacivirus/química
Seres Humanos
Modelos Moleculares
Ressonância Magnética Nuclear Biomolecular
Ligação Proteica
Estrutura Terciária de Proteína
Receptor EphA2/metabolismo
Receptor EphA5/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (NS-5 protein, hepatitis C virus); 0 (VAPB protein, human); 0 (Vesicular Transport Proteins); 0 (Viral Nonstructural Proteins); EC 2.7.10.1 (EPHA5 protein, human); EC 2.7.10.1 (Receptor, EphA2); EC 2.7.10.1 (Receptor, EphA5)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0147278


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[PMID]:26637791
[Au] Autor:Farley JE; Freeman MR
[Ad] Endereço:Department of Neurobiology/HHMI, University of Massachusetts Medical School, Worcester, MA 01605, USA.
[Ti] Título:Letting Go of JuNK by Disassembly of Adhesive Complexes.
[So] Source:Neuron;88(5):848-850, 2015 Dec 02.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immature neural circuits form excessive synaptic connections that are later refined through pruning of exuberant branches. In this issue, Bornstein et al. identify a role for JNK signaling in selective axon elimination through disassembly of cell adhesion complexes.
[Mh] Termos MeSH primário: Adesão Celular/genética
Sistema de Sinalização das MAP Quinases/genética
Corpos Pedunculados/citologia
Corpos Pedunculados/crescimento & desenvolvimento
Plasticidade Neuronal/genética
Receptor EphA5/genética
[Mh] Termos MeSH secundário: Animais
[Pt] Tipo de publicação:COMMENT; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.10.1 (Receptor, EphA5)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151206
[St] Status:MEDLINE



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