Base de dados : MEDLINE
Pesquisa : D12.776.157.530.450.074.750.750.875 [Categoria DeCS]
Referências encontradas : 245 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 25 ir para página                         

  1 / 245 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29216956
[Au] Autor:Yu SL; Xu LF; Wu JX; Yao CJ; Hu QY; Zhang CX; Zhao XY; Wei HY; Wang XK; Chen G
[Ad] Endereço:Department of Environmental Health, School of Public Health, Nantong University, Nantong 226019, Jiangsu, China.
[Ti] Título:Increased PIT1 and PIT2 Expression in Streptozotocin (STZ)-induced Diabetic Mice Contributes to Uptake of iAs(V).
[So] Source:Biomed Environ Sci;30(11):792-801, 2017 Nov.
[Is] ISSN:0895-3988
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study aimed to investigate the susceptibility of mice with streptozotocin(STZ)-induced diabetes mellitus (TIDM) to the uptake of pentavalent inorganic arsenic (iAsV) and the possible molecular mechanism. METHODS: TIDM was induced in mice by STZ. TIDM and normal mice were treated with 15.0 mg/kg Na2HAsO4·12H2O by intragastric administration. Then, the concentrations of arsenic in various tissues were measured by atomic fluorescence spectrometry. The gene expression levels of Pit1 and Pit2 were quantified by real-time RT-PCR, and their protein levels were detected by Western blotting in mouse heart, kidney, and liver tissues. RESULTS: The concentrations of arsenic in STZ-induced TIDM mouse tissues were higher at 2 h after intragastric administration of Na2HAsO4·12H2O. Compared with the levels in normal mice, PIT1 and PIT2, which play a role in the uptake of iAsV, were upregulated in the livers and hearts of TIDM mice. PIT1 but not PIT2 was higher in TIDM mouse kidneys. The upregulation of Pit1 and Pit2 expression could be reversed by insulin treatment. CONCLUSION: The increased uptake of iAsV in TIDM mouse tissues may be associated with increased PIT1 and/or PIT2 expression.
[Mh] Termos MeSH primário: Arsênico/farmacocinética
Diabetes Mellitus Experimental/metabolismo
Poluentes Ambientais/farmacocinética
Regulação da Expressão Gênica/fisiologia
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/metabolismo
Fator de Transcrição Pit-1/metabolismo
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
Camundongos Endogâmicos ICR
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/genética
Fator de Transcrição Pit-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Pit1 protein, mouse); 0 (Sodium-Phosphate Cotransporter Proteins, Type III); 0 (Transcription Factor Pit-1); N712M78A8G (Arsenic)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.3967/bes2017.107


  2 / 245 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28097511
[Au] Autor:Kostic VS; Petrovic IN
[Ad] Endereço:Clinic of Neurology, Clinical Centre of Serbia, Faculty of Medicine, University of Belgrade, Dr Subotica 6, Belgrade, 11000, Serbia. vladimir.s.kostic@gmail.com.
[Ti] Título:Brain Calcification and Movement Disorders.
[So] Source:Curr Neurol Neurosci Rep;17(1):2, 2017 Jan.
[Is] ISSN:1534-6293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brain calcifications may be an incidental finding on neuroimaging in normal, particularly older individuals, but can also indicate numerous hereditary and nonhereditary syndromes, and metabolic, environmental, infectious, autoimmune, mitochondrial, traumatic, or toxic disorders. Bilateral calcifications most commonly affecting the basal ganglia may often be found in idiopathic cases, and a new term, primary familial brain calcification (PFBC), has been proposed that recognizes the genetic causes of the disorder and that calcifications occurred well beyond the basal ganglia. PFBC, usually inherited in an autosomal dominant fashion, is both an intrafamilial and an interfamilial heterogeneous disorder, clinically characterized by an insidious and progressive development of movement disorders, cognitive decline, and psychiatric symptoms, but also cerebellar ataxia, pyramidal signs, and sometimes isolated seizures and headaches/migraines. Heterozygous mutations in four genes (SLC20A2, PDGFRB, PDGFB, XPR1) have recently proved to be the causes of the autosomal dominant forms of PFBC, also suggesting disrupted phosphate homeostasis as "an underlying and converging" pathophysiological mechanism. However, to date, it is not possible to anticipate with acceptable certainty any of known genetic causes of PFBC on the basis of the type, severity, pattern of distribution, or combination of movement disorders (mainly parkinsonism, with or without tremor, but also dystonia, chorea, paroxysmal kinesigenic dyskinesia, orofacial dyskinesia, and gait and speech disorders).
[Mh] Termos MeSH primário: Encefalopatias/fisiopatologia
Calcinose/genética
Transtornos dos Movimentos/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Transtornos dos Movimentos/etiologia
Mutação
Proteínas Proto-Oncogênicas c-sis/genética
Receptores Acoplados a Proteínas-G/genética
Receptores Virais/genética
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-sis); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Virus); 0 (SLC20A2 protein, human); 0 (Sodium-Phosphate Cotransporter Proteins, Type III); 0 (xenotropic and polytropic retrovirus receptor); 1B56C968OA (becaplermin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1007/s11910-017-0710-9


  3 / 245 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28017251
[Au] Autor:Gagliardi M; Morelli M; Iannello G; Colica C; Annesi G; Quattrone A
[Ad] Endereço:Institute of Molecular Bioimaging and Physiology, National Research Council, Section of Germaneto, Catanzaro, Italy. Electronic address: monicg_2002@yahoo.it.
[Ti] Título:A SLC20A2 mutation identified in an asymptomatic patient with brain calcification.
[So] Source:J Neurol Sci;372:70-72, 2017 Jan 15.
[Is] ISSN:1878-5883
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Encefalopatias/genética
Calcinose/genética
Mutação/genética
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/genética
[Mh] Termos MeSH secundário: Encéfalo/diagnóstico por imagem
Encefalopatias/complicações
Encefalopatias/diagnóstico por imagem
Calcinose/complicações
Calcinose/diagnóstico por imagem
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Meia-Idade
Tomógrafos Computadorizados
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (SLC20A2 protein, human); 0 (Sodium-Phosphate Cotransporter Proteins, Type III)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161227
[St] Status:MEDLINE


  4 / 245 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27943094
[Au] Autor:Larsen FT; Jensen N; Autzen JK; Kongsfelt IB; Pedersen L
[Ad] Endereço:Department of Molecular Biology and Genetics, Aarhus University, C. F. Møllers Allé 3, Building 1130, 8000, Aarhus, Denmark.
[Ti] Título:Primary Brain Calcification Causal PiT2 Transport-Knockout Variants can Exert Dominant Negative Effects on Wild-Type PiT2 Transport Function in Mammalian Cells.
[So] Source:J Mol Neurosci;61(2):215-220, 2017 Feb.
[Is] ISSN:1559-1166
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary brain calcification (PBC) is a neurodegenerative disorder characterized by calcium-phosphate deposits in the basal ganglia and often also other areas of the brain. The prevalent clinical manifestations are cognitive impairment, neuropsychiatric symptoms, and movement disorders. In recent years, monoallelic variants in SLC20A2, which encodes the type III sodium-dependent inorganic phosphate (P ) transporter 2 (PiT2), have been linked to the familial form of PBC in 40-50% of the families reported worldwide as well as to sporadic cases of PBC. Further insight into the disease mechanism is, however, needed. Based on co-expression studies of wild-type and variant PiT2 in Xenopus laevis oocytes, the molecular disease mechanism associated with SLC20A2 missense variants has formerly been suggested to be haploinsufficiency. We have here used mammalian cells isolated from a Slc20a2 mouse and co-expression of human wild-type and variant PiT2. Two of the variants studied have both been reported twice in unrelated PBC cases: PiT2D28N in two sporadic cases and PiT2E575K in a familial and a sporadic case. We find that in mammalian cells, the analyzed SLC20A2 missense variants can exert their effect in a dominant negative manner resulting in decreased wild-type PiT2 P transport. Thus, compared to monoallelic lack of functional PiT2 protein expression, which reasonably points towards haploinsufficiency, certain SLC20A2 missense variants may be more detrimental for cellular P uptake and potentially contribute to an earlier disease onset and/or a more severe phenotype as observed for Slc20a2 mice compared to Slc20a2 mice.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Calcinose/genética
Mutação de Sentido Incorreto
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/genética
[Mh] Termos MeSH secundário: Animais
Encéfalo/patologia
Calcinose/metabolismo
Células Cultivadas
Fibroblastos/metabolismo
Seres Humanos
Transporte de Íons
Camundongos
Camundongos Endogâmicos C57BL
Fenótipo
Fosfatos/metabolismo
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphates); 0 (SLC20A2 protein, human); 0 (Sodium-Phosphate Cotransporter Proteins, Type III)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE
[do] DOI:10.1007/s12031-016-0868-7


  5 / 245 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27842912
[Au] Autor:Chai YJ; Yi JW; Oh SW; Kim YA; Yi KH; Kim JH; Lee KE
[Ad] Endereço:Department of Surgery, Seoul National University Boramae Medical Center, Seoul, Korea; Cancer Research Institute, Seoul National University Hospital and College of Medicine, Seoul, Korea.
[Ti] Título:Upregulation of SLC2 (GLUT) family genes is related to poor survival outcomes in papillary thyroid carcinoma: Analysis of data from The Cancer Genome Atlas.
[So] Source:Surgery;161(1):188-194, 2017 Jan.
[Is] ISSN:1532-7361
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The Warburg effect describes increased glucose uptake in cancer cells, and glucose transporter proteins are overexpressed in many tumors. In this study, we evaluated the expression of 14 SLC2A genes encoding glucose transporter proteins in papillary thyroid carcinoma patients. METHODS: Clinical information and gene expression data from 499 papillary thyroid carcinoma patients were downloaded from The Cancer Genome Atlas database. Correlations between SLC2 gene family (SLC2A1-14) mRNA expression levels and clinicopathologic factors were analyzed. RESULTS: There were 14 mortalities during follow-up (median, 21.6 months). Patient overall mortality was associated with age ≥45 years, extrathyroidal extension, higher TNM stage, and increased expression of SLC2A1, SLC2A3, and SLC2A14 mRNA. Greater SLC2A1, SLC2A3, and SLC2A14 expression was associated with increased mortality (odds ratio: 11.692, 95% confidence interval: 3.362-36.938; odds ratio: 12.725, 95% confidence interval: 4.247-40.187; and odds ratio: 13.768, 95% confidence interval: 4.208-61.710, respectively). Kaplan-Meier survival analysis indicated that overall survival was shorter in patients with high rather than low SCL2 expression (SLC2A1, P = .003; SLC2A3, P < .001; and SLC2A14, P < .001). CONCLUSION: Upregulation of the SLC2A1, SLC2A3, and SLC2A14 genes was associated with increased mortality in papillary thyroid carcinoma patients, and SLC2 gene expression levels are potentially useful prognostic indicators.
[Mh] Termos MeSH primário: Carcinoma/genética
Predisposição Genética para Doença/epidemiologia
Transportador de Glucose Tipo 3/genética
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/genética
Neoplasias da Glândula Tireoide/genética
[Mh] Termos MeSH secundário: Adulto
Carcinoma/mortalidade
Carcinoma/cirurgia
Carcinoma Papilar
Bases de Dados Factuais
Intervalo Livre de Doença
Feminino
Projeto Genoma Humano
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
RNA Mensageiro/análise
Curva ROC
Estudos Retrospectivos
Análise de Sobrevida
Neoplasias da Glândula Tireoide/mortalidade
Neoplasias da Glândula Tireoide/cirurgia
Tireoidectomia/métodos
Tireoidectomia/mortalidade
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transporter Type 3); 0 (RNA, Messenger); 0 (SLC20A1 protein, human); 0 (SLC2A3 protein, human); 0 (Sodium-Phosphate Cotransporter Proteins, Type III)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE


  6 / 245 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27565711
[Au] Autor:Nguyen TT; Quan X; Xu S; Das R; Cha SK; Kong ID; Shong M; Wollheim CB; Park KS
[Ad] Endereço:Department of Physiology, Wonju College of Medicine, Yonsei University, Wonju, Korea.
[Ti] Título:Intracellular alkalinization by phosphate uptake via type III sodium-phosphate cotransporter participates in high-phosphate-induced mitochondrial oxidative stress and defective insulin secretion.
[So] Source:FASEB J;30(12):3979-3988, 2016 Dec.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Elevated plasma levels of inorganic phosphate (P ) are harmful, causing, among other complications, vascular calcification and defective insulin secretion. The underlying molecular mechanisms of these complications remain poorly understood. We demonstrated the role of P transport across the plasmalemma on P toxicity in INS-1E rat clonal ß cells and rat pancreatic islet cells. Type III sodium-phosphate cotransporters (NaP s) are the predominant P transporters expressed in insulin-secreting cells. Transcript and protein levels of sodium-dependent phosphate transporter 1 and 2 (PiT-1 and -2), isotypes of type III NaP , were up-regulated by high-P incubation. In patch-clamp experiments, extracellular P elicited a Na -dependent, inwardly rectifying current, which was markedly reduced under acidic extracellular conditions. Cellular uptake of P elicited cytosolic alkalinization; intriguingly, this pH change facilitated P transport into the mitochondrial matrix. Increased mitochondrial P uptake accelerated superoxide generation, mitochondrial permeability transition (mPT), and endoplasmic reticulum stress-mediated translational attenuation, leading to reduced insulin content and impaired glucose-stimulated insulin secretion. Silencing of PiT-1/2 prevented P -induced superoxide generation and mPT, and restored insulin secretion. We propose that P transport across the plasma membrane and consequent cytosolic alkalinization could be a therapeutic target for protection from P toxicity in insulin-secreting cells, as well as in other cell types.-Nguyen, T. T., Quan, X., Xu, S., Das, R., Cha, S.-K., Kong, I. D., Shong, M., Wollheim, C. B., Park, K.-S. Intracellular alkalinization by phosphate uptake via type III sodium-phosphate cotransporter participates in high-phosphate-induced mitochondrial oxidative stress and defective insulin secretion.
[Mh] Termos MeSH primário: Transporte Biológico/efeitos dos fármacos
Transporte de Íons/genética
Mitocôndrias/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Fosfatos/farmacologia
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/metabolismo
[Mh] Termos MeSH secundário: Animais
Membrana Celular/metabolismo
Células Cultivadas
Homeostase/efeitos dos fármacos
Insulina/secreção
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/metabolismo
Células Secretoras de Insulina/secreção
Mitocôndrias/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (Phosphates); 0 (Sodium-Phosphate Cotransporter Proteins, Type III)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160828
[St] Status:MEDLINE


  7 / 245 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27491899
[Au] Autor:Fernandes CS; Barbosa I; Castro R; Pina AS; Coroadinha AS; Barbas A; Roque AC
[Ad] Endereço:UCIBIO, REQUIMTE, Departamento de Química, Faculdade de Ciências e Tecnológia, Universidade Nova de Lisboa, Caparica, Portugal.
[Ti] Título:Retroviral particles are effectively purified on an affinity matrix containing peptides selected by phage-display.
[So] Source:Biotechnol J;11(12):1513-1524, 2016 Dec.
[Is] ISSN:1860-7314
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Retroviral particles are expensive to manufacture, mostly due to the downstream processing steps which result in low recoveries (≈30%) and concentration factors. In this work, a dodecapeptide phage-display library was panned against retrovirus like particles expressing the envelope protein Ampho4070A (VLPs-AMPHO) and VLPs without the target protein, used as a negative control (VLPs). A depletion/selection panning protocol was successfully used to deal with the structural complexity of the target, and a total of three distinct peptide sequences displaying preferential binding towards VLPs-AMPHO were found. Peptide 3 (CAAALAKPHTENHLLT), which appeared as one lead candidate, was synthesized and immobilized onto two purification matrices, cross-linked agarose and magnetic particles. The matrices selectively bound VLPs-AMPHO and in both cases recovery yields higher than 90% were obtained when employing mild elution conditions, while maintaining viral particle morphology and size.
[Mh] Termos MeSH primário: Biblioteca de Peptídeos
Peptídeos/metabolismo
Retroviridae
Vírion/isolamento & purificação
Vírion/metabolismo
[Mh] Termos MeSH secundário: Cromatografia de Afinidade/métodos
Peptídeos/química
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/química
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/metabolismo
Vírion/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptide Library); 0 (Peptides); 0 (Sodium-Phosphate Cotransporter Proteins, Type III)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170131
[Lr] Data última revisão:
170131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160806
[St] Status:MEDLINE
[do] DOI:10.1002/biot.201600025


  8 / 245 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27380911
[Au] Autor:Bezerra DP; Oliveira JR
[Ad] Endereço:Keizo Asami Laboratory-Federal University of Pernambuco (UFPE), Recife, PE, Brazil.
[Ti] Título:New Studies on Knockout Mouse for the SLC20A2 Gene Show Much More Than Brain Calcifications.
[So] Source:J Mol Neurosci;59(4):565-6, 2016 08.
[Is] ISSN:1559-1166
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Encefalopatias/genética
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/genética
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Calcinose/genética
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Sodium-Phosphate Cotransporter Proteins, Type III)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160707
[St] Status:MEDLINE
[do] DOI:10.1007/s12031-016-0778-8


  9 / 245 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27245298
[Au] Autor:David S; Ferreira J; Quenez O; Rovelet-Lecrux A; Richard AC; Vérin M; Jurici S; Le Ber I; Boland A; Deleuze JF; Frebourg T; Mendes de Oliveira JR; Hannequin D; Campion D; Nicolas G
[Ad] Endereço:Inserm U1079, Rouen University, IRIB, Normandy University, Rouen, France.
[Ti] Título:Identification of partial SLC20A2 deletions in primary brain calcification using whole-exome sequencing.
[So] Source:Eur J Hum Genet;24(11):1630-1634, 2016 Nov.
[Is] ISSN:1476-5438
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Primary brain calcification (PBC) is a dominantly inherited calcifying disorder of the brain. SLC20A2 loss-of-function variants account for the majority of families. Only one genomic deletion encompassing SLC20A2 and six other genes has been reported. We performed whole-exome sequencing (WES) in 24 unrelated French patients with PBC, negatively screened for sequence variant in the known genes SLC20A2, PDGFB, PDGFRB and XPR1. We used the CANOES tool to detect copy number variations (CNVs). We detected two deletions of exon 2 of SLC20A2 in two unrelated patients, which segregated with PBC in one family. We then reanalyzed the same series using a QMPSF assay including one amplicon in each exon of SLC20A2 and detected two supplemental partial deletions in two patients: one deletion of exon 4 and one deletion of exons 4 and 5. These deletions were missed by the first screening step of CANOES but could finally be detected after readjustment of bioinformatic parameters and use of a genotyping step of CANOES. This study reports the first partial deletions of SLC20A2 and strengthens its position as the major PBC-causative gene. It is possible to detect short CNVs from WES data, although the sensitivity of such tools should be evaluated in comparison with other methods.
[Mh] Termos MeSH primário: Encefalopatias/genética
Calcinose/genética
Exoma
Deleção de Genes
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/genética
[Mh] Termos MeSH secundário: Idoso
Algoritmos
Encefalopatias/diagnóstico
Calcinose/diagnóstico
Feminino
Seres Humanos
Masculino
Meia-Idade
Análise de Sequência de DNA/métodos
Síndrome
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (SLC20A2 protein, human); 0 (Sodium-Phosphate Cotransporter Proteins, Type III)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160602
[St] Status:MEDLINE
[do] DOI:10.1038/ejhg.2016.50


  10 / 245 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27165707
[Au] Autor:Seya K; Furukawa K; Chiyoya M; Yu Z; Kikuchi H; Daitoku K; Motomura S; Murakami M; Oshima Y; Fukuda I
[Ad] Endereço:Department of Pharmacology, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki 036-8562, Japan.
[Ti] Título:1-Methyl-2-undecyl-4(1H)-quinolone, a derivative of quinolone alkaloid evocarpine, attenuates high phosphate-induced calcification of human aortic valve interstitial cells by inhibiting phosphate cotransporter PiT-1.
[So] Source:J Pharmacol Sci;131(1):51-7, 2016 May.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:An abnormally high serum phosphate level induces calcific aortic stenosis (CAS), which is characterized by ectopic valve calcification and stenosis of the orifice area. Inhibition of ectopic calcification is a critical function of any internal medical therapy for CAS disease. The aim of the present study was to investigate the inhibitory effects of several derivatives of evocarpine, methanolic extracts from the fruits of Evodia rutaecarpa Bentham (Japanese name: Go-Shu-Yu) on the high phosphate-induced calcification of human aortic valve interstitial cells (HAVICs) obtained from patients with CAS. High phosphate (3.2 mM) concentrations significantly increased the calcification of HAVICs after 7 days of culture. This calcification was completely inhibited in the presence of sodium phosphonoformate (PFA), a selective inhibitor of the type III sodium-dependent phosphate cotransporter (PiT-1). PiT-1 contributes to phosphate uptake, resulting in calcification. 1-Methyl-2-undecyl-4(1H)-quinolone (MUQ; 30-300 nM), but not evocarpine or its derivatives dihydroevocarpine and 1-methyl-2-nonyl-4(1H)-quinolone, inhibited the high phosphate-induced HAVICs calcification in a concentration-dependent manner. Although all of the evocarpine derivatives attenuated alkaline phosphatase activity, only MUQ also decreased PiT-1 gene expression with cellular PiT-1 protein diminution. These results suggest that MUQ mitigated high phosphate-induced HAVICs calcification by inhibiting PiT-1 gene expression.
[Mh] Termos MeSH primário: Estenose da Valva Aórtica/metabolismo
Valva Aórtica/patologia
Calcinose/metabolismo
Quinolonas/farmacologia
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/antagonistas & inibidores
[Mh] Termos MeSH secundário: Idoso
Fosfatase Alcalina/genética
Fosfatase Alcalina/metabolismo
Valva Aórtica/citologia
Valva Aórtica/metabolismo
Células Cultivadas
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Meia-Idade
Fosfatos
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/genética
Proteínas Cotransportadoras de Sódio-Fosfato Tipo III/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1-methyl-2-undecyl-4(1H)-quinolone); 0 (Phosphates); 0 (Quinolones); 0 (Sodium-Phosphate Cotransporter Proteins, Type III); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160512
[St] Status:MEDLINE



página 1 de 25 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