Base de dados : MEDLINE
Pesquisa : G02.111.820 [Categoria DeCS]
Referências encontradas : 345469 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 34547 ir para página                         

  1 / 345469 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29444082
[Au] Autor:Khan MI; Su YK; Zou J; Yang LW; Chou RH; Yu C
[Ad] Endereço:National Tsing Hua University, Chemistry Department, Hsinchu, Taiwan.
[Ti] Título:S100B as an antagonist to block the interaction between S100A1 and the RAGE V domain.
[So] Source:PLoS One;13(2):e0190545, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ca2+-binding human S100A1 protein is a type of S100 protein. S100A1 is a significant mediator during inflammation when Ca2+ binds to its EF-hand motifs. Receptors for advanced glycation end products (RAGE) correspond to 5 domains: the cytoplasmic, transmembrane, C2, C1, and V domains. The V domain of RAGE is one of the most important target proteins for S100A1. It binds to the hydrophobic surface and triggers signaling transduction cascades that induce cell growth, cell proliferation, and tumorigenesis. We used nuclear magnetic resonance (NMR) spectroscopy to characterize the interaction between S100A1 and the RAGE V domain. We found that S100B could interact with S100A1 via NMR 1H-15N HSQC titrations. We used the HADDOCK program to generate the following two binary complexes based on the NMR titration results: S100A1-RAGE V domain and S100A1-S100B. After overlapping these two complex structures, we found that S100B plays a crucial role in blocking the interaction site between RAGE V domain and S100A1. A cell proliferation assay WST-1 also supported our results. This report could potentially be useful for new protein development for cancer treatment.
[Mh] Termos MeSH primário: Antígenos de Neoplasias/metabolismo
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Subunidade beta da Proteína Ligante de Cálcio S100/fisiologia
Proteínas S100/metabolismo
[Mh] Termos MeSH secundário: Cálcio/metabolismo
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Ressonância Magnética Nuclear Biomolecular
Ligação Proteica
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (S100 Calcium Binding Protein beta Subunit); 0 (S100 Proteins); 0 (S100A1 protein); 0 (S100B protein, human); EC 2.7.11.22 (MOK protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190545


  2 / 345469 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29408396
[Au] Autor:Wang W; Zhang H; Wei X; Yang L; Yang B; Zhang L; Li J; Jiang YQ
[Ad] Endereço:State Key Laboratory of Crop Stress Biology for Arid Areas, College of Life Sciences, Northwest A & F University, Yangling, Shaanxi 712100, China.
[Ti] Título:Functional characterization of calcium-dependent protein kinase (CPK) 2 gene from oilseed rape (Brassica napus L.) in regulating reactive oxygen species signaling and cell death control.
[So] Source:Gene;651:49-56, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Calcium-dependent protein kinases (CPKs), being Ser/Thr protein kinases found only in plants and some protozoans are calcium sensors that regulate diverse biological processes. However, the function and mode of CPKs in oilseed rape (Brassica napus) remain elusive. In this study, we identified CPK2 from oilseed rape as a novel regulator of reactive oxygen species (ROS) and cell death. BnaCPK2 was identified to be located at the endoplasmic reticulum membrane. Expression of BnaCPK2 was induced during Bax-induced cell death. Overexpression of the constitutively active form of BnaCPK2 led to significantly more accumulation of ROS and cell death than the full-length CPK2, which is supported by various measurements of physiological data. In addition, a quantitative RT-PCR survey revealed that the expression levels of a few marker genes are significantly changed as a result of CPK2 expression. Mating-based split ubiquitin system (mbSUS) and bimolecular fluorescence complementation (BiFC) were used to screen and confirm the BnaCPK2 interacting proteins. We identified and confirmed that CPK2 interacted with NADPH oxidase-like respiratory burst oxidase homolog D (RbohD), but not with RbohF. Based on its function and interacting partners, we propose that BnaCPK2 plays an important role in ROS and cell death control through interacting with RbohD.
[Mh] Termos MeSH primário: Brassica napus/genética
Morte Celular/genética
Proteínas de Plantas/genética
Proteínas Quinases/genética
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Brassica napus/enzimologia
Clonagem Molecular
DNA de Plantas
Proteínas de Plantas/metabolismo
Proteínas Quinases/metabolismo
Análise de Sequência de DNA
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Plant); 0 (Plant Proteins); 0 (Reactive Oxygen Species); EC 2.7.- (Protein Kinases); EC 2.7.1.- (calcium-dependent protein kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  3 / 345469 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29382572
[Au] Autor:Lv C; Mo C; Liu H; Wu C; Li Z; Li J; Wang Y
[Ad] Endereço:Key Laboratory of Bio-resources and Eco-environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610065, PR China.
[Ti] Título:Dopamine D2-like receptors (DRD2 and DRD4) in chickens: Tissue distribution, functional analysis, and their involvement in dopamine inhibition of pituitary prolactin expression.
[So] Source:Gene;651:33-43, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dopamine (DA) D2-like (and D1-like) receptors are suggested to mediate the dopamine actions in the anterior pituitary and/or CNS of birds. However, the information regarding the structure, functionality, and expression of avian D2-like receptors have not been fully characterized. In this study, we cloned two D2-like receptors (cDRD2, cDRD4) from chicken brain using RACE PCR. The cloned cDRD4 is a 378-amino acid receptor, which shows 57% amino acid (a.a.) identity with mouse DRD4. As in mammals, two cDRD2 isoforms, cDRD2L (long isoform, 437 a.a.) and cDRD2S (short isoform, 408 a.a.), which differ in their third intracellular loop, were identified in chickens. Using cell-based luciferase reporter assays or Western blot, we demonstrated that cDRD4, cDRD2L and cDRD2S could be activated by dopamine and quinpirole (a D2-like receptor agonist) dose-dependently, and their activation inhibits cAMP signaling pathway and stimulates MAPK/ERK signaling cascade, indicating that they are functional receptors capable of mediating dopamine actions. Quantitative real-time PCR revealed that cDRD2 and cDRD4 are widely expressed in chicken tissues with abundant expression noted in anterior pituitary, and their expressions are likely controlled by their promoters near exon 1, as demonstrated by dual-luciferase reporter assays in DF-1 cells. In accordance with cDRD2/cDRD4 expression in the pituitary, DA or quinpirole could partially inhibit vasoactive intestinal peptide-induced prolactin expression in cultured chick pituitary cells. Together, our data proves the functionality of DRD2 and DRD4 in birds and aids to uncover the conserved roles of DA/D2-like receptor system in vertebrates, such as its action on the pituitary.
[Mh] Termos MeSH primário: Galinhas/metabolismo
Dopamina/metabolismo
Hipófise/metabolismo
Prolactina/biossíntese
Receptores de Dopamina D2/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Galinhas/genética
Clonagem Molecular
DNA Complementar
Feminino
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Masculino
Prolactina/antagonistas & inibidores
Regiões Promotoras Genéticas
Receptores de Dopamina D2/genética
Receptores de Dopamina D2/fisiologia
Transdução de Sinais
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Receptors, Dopamine D2); 9002-62-4 (Prolactin); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE


  4 / 345469 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29373584
[Au] Autor:Zhao X; Li R; Jin H; Jin H; Wang Y; Zhang W; Wang H; Chen W
[Ad] Endereço:Tianjin Institute of Health and Environmental Medicine, Tianjin, China.
[Ti] Título:Epigallocatechin-3-gallate confers protection against corticosterone-induced neuron injuries via restoring extracellular signal-regulated kinase 1/2 and phosphatidylinositol-3 kinase/protein kinase B signaling pathways.
[So] Source:PLoS One;13(1):e0192083, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Extensive studies suggested epigallocatechin-3-gallate (EGCG) has significant neuroprotection against multiple central neural injuries, but the underlying mechanisms still remain poorly elucidated. Here we provide evidence to support the possible involvement of extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol-3 kinase/ protein kinase B (PI3K/AKT) pathways in EGCG-mediated protection against corticosterone-induced neuron injuries. As an essential stress hormone, corticosterone could induce obvious neurotoxicity in primary hippocampal neurons. Pre-treatment with EGCG ameliorated the corticosterone-induced neuronal injuries; however, it was blocked by pharmacological inhibitors for ERK1/2 (U0126) and PI3K/AKT (LY294002). Furthermore, the results confirmed that EGCG restored the corticosterone-induced decrease of ERK1/2 and PI3K/AKT phosphorylation, and attenuated the corticosterone-induced reduction of peroxisome proliferators-activated receptor-γ coactivator-1α (PGC-1α) expression and ATP production. Taken together, these findings indicated that EGCG has significant neuroprotection against corticosterone-induced neuron injuries partly via restoring the ERK1/2 and PI3K/AKT signaling pathways as well as the PGC-1α-mediated ATP production.
[Mh] Termos MeSH primário: Catequina/análogos & derivados
Corticosterona/efeitos adversos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/biossíntese
Animais
Catequina/farmacologia
Células Cultivadas
Hipocampo/citologia
Hipocampo/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Fosforilação
Ratos
Ratos Wistar
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuroprotective Agents); 8L70Q75FXE (Adenosine Triphosphate); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192083


  5 / 345469 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29353044
[Au] Autor:Yamamoto H; Kurachi M; Naruse M; Shibasaki K; Ishizaki Y
[Ad] Endereço:Department of Molecular and Cellular Neurobiology, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
[Ti] Título:BMP4 signaling in NPCs upregulates Bcl-xL to promote their survival in the presence of FGF-2.
[So] Source:Biochem Biophys Res Commun;496(2):588-593, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that BMP4 does not promote proliferation or differentiation of CD44-positive astrocyte precursor cells (APCs) but greatly promotes their survival in the presence of fibroblast growth factor-2 (FGF-2). In this study, we examined if BMP4 acts as a survival factor also for neural stem/progenitor cells (NPCs) isolated from ganglionic eminence of neonatal mouse brain. We found BMP4 promotes survival but not proliferation or differentiation of these cells, just as in the case for CD44-positive APCs. Microarray analysis revealed some candidate molecules in the signaling pathway downstream of BMP4. Among them, we focused on Id1 (inhibitor of DNA-binding 1) and Bcl-xL in this study. Expression of both genes was promoted in the presence of BMP4, and this promotion was reduced by dorsomorphin, an inhibitor of BMP4 signaling. Furthermore, cytochrome c release from mitochondria was significantly reduced in the presence of BMP4, suggesting up-regulation of Bcl-xL activity by BMP4. Id1 siRNA reduced the expression of Bcl-xL, and negated survival promoting effect of BMP4. These data suggest that BMP4 promotes survival of NPCs by enhancing the anti-apoptotic function of Bcl-xL via BMP4-Smad1/5/8-Id1 signaling.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 4/metabolismo
Fator 2 de Crescimento de Fibroblastos/metabolismo
Células-Tronco Neurais/metabolismo
Transdução de Sinais
Proteína bcl-X/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Diferenciação Celular
Proliferação Celular
Sobrevivência Celular
Células Cultivadas
Camundongos Endogâmicos C57BL
Células-Tronco Neurais/citologia
Regulação para Cima
Proteína bcl-X/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bcl2l1 protein, mouse); 0 (Bone Morphogenetic Protein 4); 0 (bcl-X Protein); 103107-01-3 (Fibroblast Growth Factor 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE


  6 / 345469 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29351887
[Au] Autor:Jin R; Chen Q; Yao S; Bai E; Fu W; Wang L; Wang J; Du X; Wei T; Xu H; Jiang C; Qiu P; Wu J; Li W; Liang G
[Ad] Endereço:Department of Digestive Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China; Chemical Biology Research Center, College of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
[Ti] Título:Synthesis and anti-tumor activity of EF24 analogues as IKKß inhibitors.
[So] Source:Eur J Med Chem;144:218-228, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:EF24 is an IKKß inhibitor (IC : 72 µM) containing various anti-tumor activities. In this study, a series of EF24 analogs targeting IKKß were designed and synthesized. Several IKKß inhibitors with better activities than EF24 were screened out and B3 showed best IKKß inhibitory (IC : 6.6 µM). Molecular docking and dynamic simulation experiments further confirmed this inhibitory effect. B3 obviously suppressed the viability of Hela229, A549, SGC-7901 and MGC-803 cells. Then, in SGC-7901 and MGC-803 cells, B3 blocked the NF-κB signal pathway by inhibiting IKKß phosphorylation, and followed arrested the cell cycle at G2/M phase by suppressing the Cyclin B1 and Cdc2 p34 expression, induced the cell apoptosis by down-regulating Bcl-2 protein and up-regulating cleaved-caspase3. Moreover, B3 significantly reduced tumor growth and suppressed the IKKß-NF-κB signal pathway in SGC-7901 xenograft model. In total, this study present a potential IKKß inhibitor as anti-tumor precursor.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Compostos de Benzilideno/química
Compostos de Benzilideno/farmacologia
Quinase I-kappa B/antagonistas & inibidores
Piperidonas/química
Piperidonas/farmacologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/síntese química
Antineoplásicos/uso terapêutico
Apoptose/efeitos dos fármacos
Compostos de Benzilideno/síntese química
Compostos de Benzilideno/uso terapêutico
Linhagem Celular Tumoral
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Seres Humanos
Quinase I-kappa B/metabolismo
Camundongos Nus
Simulação de Acoplamento Molecular
NF-kappa B/metabolismo
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Neoplasias/patologia
Fosforilação/efeitos dos fármacos
Piperidonas/síntese química
Piperidonas/uso terapêutico
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3,5-bis(2-fluorobenzylidene)piperidin-4-one); 0 (Antineoplastic Agents); 0 (Benzylidene Compounds); 0 (NF-kappa B); 0 (Piperidones); EC 2.7.11.10 (I-kappa B Kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE


  7 / 345469 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29346425
[Au] Autor:Hooper A; Fuller PM; Maguire J
[Ad] Endereço:Tufts University School of Medicine, Department of Neuroscience, Boston, Massachusetts.
[Ti] Título:Hippocampal corticotropin-releasing hormone neurons support recognition memory and modulate hippocampal excitability.
[So] Source:PLoS One;13(1):e0191363, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Corticotropin-releasing hormone (CRH) signaling in the hippocampus has been established to be important for mediating the effects of stress on learning and memory. Given our laboratory's recent characterization of a subset of hippocampal CRH neurons as a novel class of GABAergic interneurons, we hypothesized that these local GABAergic hippocampal CRH neurons may influence hippocampal function. Here we applied an array of molecular tools to selectively label and manipulate hippocampal CRH neurons in mice, in order to assess this interneuron population's impact on hippocampus-dependent behaviors and hippocampal network excitability. Genetically-targeted ablation of hippocampal CRH neurons in vivo impaired object recognition memory and substantially enhanced the severity of kainic acid-induced seizures. Conversely, selective activation of CRH neurons in vitro suppressed the excitability of the mossy fiber-CA3 pathway. Additional experiments are needed to reconcile the functions of GABA and CRH signaling of hippocampal CRH neurons on hippocampal function. However, our results indicate that this interneuron population plays an important role in maintaining adaptive network excitability, and provide a specific circuit-level mechanism for this role.
[Mh] Termos MeSH primário: Região CA3 Hipocampal/metabolismo
Hormônio Liberador da Corticotropina/metabolismo
Neurônios GABAérgicos/metabolismo
Memória
[Mh] Termos MeSH secundário: Animais
Região CA3 Hipocampal/citologia
Eletroencefalografia
Locomoção
Camundongos
Camundongos Transgênicos
Técnicas de Patch-Clamp
Transdução de Sinais
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; VALIDATION STUDIES
[Nm] Nome de substância:
56-12-2 (gamma-Aminobutyric Acid); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191363


  8 / 345469 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29337391
[Au] Autor:Ishii T; Niikura Y; Kurata K; Muroi M; Tanamoto K; Nagase T; Sakaguchi M; Yamashita N
[Ad] Endereço:Department of Pharmacotherapy, Research Institute of Pharmaceutical Sciences, Musashino University, Tokyo, Japan.
[Ti] Título:Time-dependent distinct roles of Toll-like receptor 4 in a house dust mite-induced asthma mouse model.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:House dust mites (HDMs) are a common source of allergens that trigger both allergen-specific and innate immune responses in humans. Here, we examined the effect of allergen concentration and the involvement of Toll-like receptor 4 (TLR4) in the process of sensitization to house dust mite allergens in an HDM extract-induced asthma mouse model. Intranasal administration of HDM extract induced an immunoglobulin E response and eosinophilic inflammation in a dose-dependent manner from 2.5 to 30 µg/dose. In TLR4-knockout mice, the infiltration of eosinophils and neutrophils into the lung was decreased compared with that in wild-type mice in the early phase of inflammation (total of three doses). However, in the late phase of inflammation (total of seven doses), eosinophil infiltration was significantly greater in TLR4-knockout mice than in wild-type mice. This suggests that the roles of TLR4 signaling are different between the early phase and the later phase of HDM allergen-induced inflammation. Thus, innate immune response through TLR4 regulated the response to HDM allergens, and the regulation was altered during the phase of inflammation.
[Mh] Termos MeSH primário: Alérgenos/imunologia
Antígenos de Dermatophagoides/imunologia
Asma/imunologia
Imunidade Inata/imunologia
Pyroglyphidae/imunologia
Receptor 4 Toll-Like/imunologia
[Mh] Termos MeSH secundário: Resistência das Vias Respiratórias/imunologia
Animais
Líquido da Lavagem Broncoalveolar/citologia
Modelos Animais de Doenças
Eosinófilos/patologia
Feminino
Imunização
Imunoglobulina E/imunologia
Inflamação/imunologia
Pulmão/citologia
Pulmão/imunologia
Pulmão/patologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Infiltração de Neutrófilos/imunologia
Neutrófilos/patologia
Transdução de Sinais/imunologia
Receptor 4 Toll-Like/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Antigens, Dermatophagoides); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12641


  9 / 345469 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29337059
[Au] Autor:Lin L; Li M; Lin L; Xu X; Jiang G; Wu L
[Ad] Endereço:Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China; Tongji University School of Medicine, Shanghai 200092, China.
[Ti] Título:FPPS mediates TGF-ß1-induced non-small cell lung cancer cell invasion and the EMT process via the RhoA/Rock1 pathway.
[So] Source:Biochem Biophys Res Commun;496(2):536-541, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway, was recently shown to play a role in cancer progression. However, its role in non-small cell lung cancer (NSCLC) metastasis and the underlying mechanism remain unclear. In this study, FPPS expression was significantly correlated with TNM stage, and metastasis. Inhibition or knockdown of FPPS blocked TGF-ß1-induced cell invasion and epithelial-to-mesenchymal transition (EMT) process. FPPS expression of FPPS was induced by TGF-ß1 and FPPS promoted cell invasion and EMT via the RhoA/Rock1 pathway. In conclusion, FPPS mediates TGF-ß1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. These findings suggest new treatment strategies to reduce mortality associated with metastasis in patients with NSCLC.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Transição Epitelial-Mesenquimal
Geraniltranstransferase/metabolismo
Neoplasias Pulmonares/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Idoso
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Linhagem Celular Tumoral
Feminino
Regulação Neoplásica da Expressão Gênica
Geraniltranstransferase/análise
Geraniltranstransferase/genética
Seres Humanos
Pulmão/metabolismo
Pulmão/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
Meia-Idade
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Transforming Growth Factor beta1); EC 2.5.1.10 (Geranyltranstransferase); EC 2.7.11.1 (ROCK1 protein, human); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


  10 / 345469 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28457941
[Au] Autor:Menazza S; Sun J; Appachi S; Chambliss KL; Kim SH; Aponte A; Khan S; Katzenellenbogen JA; Katzenellenbogen BS; Shaul PW; Murphy E
[Ad] Endereço:Systems Biology Center, National Heart Lung and Blood Institute, NIH, Bethesda, MD, United States.
[Ti] Título:Non-nuclear estrogen receptor alpha activation in endothelium reduces cardiac ischemia-reperfusion injury in mice.
[So] Source:J Mol Cell Cardiol;107:41-51, 2017 Jun.
[Is] ISSN:1095-8584
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Steroid hormone receptors including estrogen receptors (ER) classically function as ligand-regulated transcription factors. However, estrogens also elicit cellular effects through binding to extra-nuclear ER (ERα, ERß, and G protein-coupled ER or GPER) that are coupled to kinases. How extra-nuclear ER actions impact cardiac ischemia-reperfusion (I/R) injury is unknown. We treated ovariectomized wild-type female mice with estradiol or an estrogen-dendrimer conjugate (EDC), which selectively activates extra-nuclear ER, or vehicle interventions for two weeks. I/R injury was then evaluated in isolated Langendorff perfused hearts. Two weeks of treatment with estradiol significantly decreased infarct size and improved post-ischemic contractile function. Similarly, EDC treatment significantly decreased infarct size and increased post-ischemic functional recovery compared to vehicle-treated hearts. EDC also caused an increase in myocardial protein S-nitrosylation, consistent with previous studies showing a role for this post-translational modification in cardioprotection. In further support of a role for S-nitrosylation, inhibition of nitric oxide synthase, but not soluble guanylyl cyclase blocked the EDC mediated protection. The administration of ICI182,780, which is an agonist of G-protein coupled estrogen receptor (GPER) and an antagonist of ERα and ERß, did not result in protection; however, ICI182,780 significantly blocked EDC-mediated cardioprotection, indicating participation of ERα and/or ERß. In studies determining the specific ER subtype and cellular target involved, EDC decreased infarct size and improved functional recovery in mice lacking ERα in cardiomyocytes. In contrast, protection was lost in mice deficient in endothelial cell ERα. Thus, extra-nuclear ERα activation in endothelium reduces cardiac I/R injury in mice, and this likely entails increased protein S-nitrosylation. Since EDC does not stimulate uterine growth, in the clinical setting EDC-like compounds may provide myocardial protection without undesired uterotrophic and cancer-promoting effects.
[Mh] Termos MeSH primário: Receptor alfa de Estrogênio/genética
Receptor beta de Estrogênio/genética
Isquemia/genética
Traumatismo por Reperfusão/genética
[Mh] Termos MeSH secundário: Animais
Endotélio/metabolismo
Endotélio/patologia
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor beta de Estrogênio/antagonistas & inibidores
Estrogênios/genética
Estrogênios/metabolismo
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Isquemia/metabolismo
Isquemia/patologia
Camundongos
Ovariectomia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Receptores Estrogênicos/antagonistas & inibidores
Receptores Acoplados a Proteínas-G/antagonistas & inibidores
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Estrogens); 0 (GPR30 protein, mouse); 0 (Receptors, Estrogen); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE



página 1 de 34547 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