Base de dados : MEDLINE
Pesquisa : D04.210.500.247.222.474.250 [Categoria DeCS]
Referências encontradas : 478 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 48 ir para página                         

  1 / 478 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28728841
[Au] Autor:Chaudhary MK; Singh S; Rizvi SI
[Ad] Endereço:Department of Biochemistry, University of Allahabad, Allahabad 211002, India. Electronic address: mkcbiochem@gmail.com.
[Ti] Título:Redox imbalance in a model of rat mimicking Hutchinson-Gilford progeria syndrome.
[So] Source:Biochem Biophys Res Commun;491(2):361-367, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although several etiological factors contribute to the complexity of the aging process, the ultimate component of macromolecular damage and consequent cell death involves the altered redox balance inclined towards increased ROS production and/or decreased antioxidant protection. Given that, the chronic dihydrotachysterol (DHT) intoxication in rats induce Hutchinson Gilford progeria like syndrome, the present study provides the evidence for altered redox balance as evidenced by alteration in parameters of oxidative stress in blood plasma and erythrocytes including MDA, GSH, FRAP AOPP PMRS, AGEs, AChE and osmotic fragility which substantiate the suitability of the model for aging studies.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Antioxidantes/metabolismo
Eritrócitos/efeitos dos fármacos
Oxirredução/efeitos dos fármacos
Progéria/sangue
Espécies Reativas de Oxigênio/sangue
[Mh] Termos MeSH secundário: Acetilcolinesterase/sangue
Produtos da Oxidação Avançada de Proteínas/sangue
Envelhecimento/efeitos dos fármacos
Envelhecimento/patologia
Animais
Di-Hidrotaquisterol
Modelos Animais de Doenças
Eritrócitos/metabolismo
Feminino
Proteínas Ligadas por GPI/sangue
Glutationa/sangue
Seres Humanos
Malondialdeído/sangue
Estresse Oxidativo
Progéria/induzido quimicamente
Progéria/patologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Advanced Oxidation Protein Products); 0 (Antioxidants); 0 (GPI-Linked Proteins); 0 (Reactive Oxygen Species); 4Y8F71G49Q (Malondialdehyde); EC 3.1.1.7 (ACHE protein, human); EC 3.1.1.7 (Acetylcholinesterase); GAN16C9B8O (Glutathione); R5LM3H112R (Dihydrotachysterol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE


  2 / 478 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28139295
[Au] Autor:Khositseth S; Charngkaew K; Boonkrai C; Somparn P; Uawithya P; Chomanee N; Payne DM; Fenton RA; Pisitkun T
[Ad] Endereço:Department of Pediatrics, Faculty of Medicine, Thammasat University, Pathumthani, Thailand. Electronic address: Sookkasem@yahoo.com.
[Ti] Título:Hypercalcemia induces targeted autophagic degradation of aquaporin-2 at the onset of nephrogenic diabetes insipidus.
[So] Source:Kidney Int;91(5):1070-1087, 2017 May.
[Is] ISSN:1523-1755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypercalcemia can cause renal dysfunction such as nephrogenic diabetes insipidus (NDI), but the mechanisms underlying hypercalcemia-induced NDI are not well understood. To elucidate the early molecular changes responsible for this disorder, we employed mass spectrometry-based proteomic analysis of inner medullary collecting ducts (IMCD) isolated from parathyroid hormone-treated rats at onset of hypercalcemia-induced NDI. Forty-one proteins, including the water channel aquaporin-2, exhibited significant changes in abundance, most of which were decreased. Bioinformatic analysis revealed that many of the downregulated proteins were associated with cytoskeletal protein binding, regulation of actin filament polymerization, and cell-cell junctions. Targeted LC-MS/MS and immunoblot studies confirmed the downregulation of 16 proteins identified in the initial proteomic analysis and in additional experiments using a vitamin D treatment model of hypercalcemia-induced NDI. Evaluation of transcript levels and estimated half-life of the downregulated proteins suggested enhanced protein degradation as the possible regulatory mechanism. Electron microscopy showed defective intercellular junctions and autophagy in the IMCD cells from both vitamin D- and parathyroid hormone-treated rats. A significant increase in the number of autophagosomes was confirmed by immunofluorescence labeling of LC3. Colocalization of LC3 and Lamp1 with aquaporin-2 and other downregulated proteins was found in both models. Immunogold electron microscopy revealed aquaporin-2 in autophagosomes in IMCD cells from both hypercalcemia models. Finally, parathyroid hormone withdrawal reversed the NDI phenotype, accompanied by termination of aquaporin-2 autophagic degradation and normalization of both nonphoshorylated and S256-phosphorylated aquaporin-2 levels. Thus, enhanced autophagic degradation of proteins plays an important role in the initial mechanism of hypercalcemic-induced NDI.
[Mh] Termos MeSH primário: Aquaporina 2/metabolismo
Autofagia
Diabetes Insípido Nefrogênico/fisiopatologia
Hipercalcemia/complicações
Túbulos Renais Coletores/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Cromatografia Líquida
Diabetes Insípido Nefrogênico/etiologia
Diabetes Insípido Nefrogênico/metabolismo
Di-Hidrotaquisterol/toxicidade
Modelos Animais de Doenças
Regulação para Baixo
Imunofluorescência
Meia-Vida
Seres Humanos
Hipercalcemia/induzido quimicamente
Junções Intercelulares/metabolismo
Junções Intercelulares/ultraestrutura
Túbulos Renais Coletores/metabolismo
Glicoproteínas de Membrana Associadas ao Lisossomo/metabolismo
Masculino
Microscopia Imunoeletrônica
Proteínas Associadas aos Microtúbulos/metabolismo
Hormônio Paratireóideo/farmacologia
Fosforilação
Proteólise
Proteômica/métodos
Ratos
Ratos Sprague-Dawley
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aqp2 protein, rat); 0 (Aquaporin 2); 0 (LC3 protein, rat); 0 (Lamp1 protein, rat); 0 (Lysosome-Associated Membrane Glycoproteins); 0 (Microtubule-Associated Proteins); 0 (Parathyroid Hormone); R5LM3H112R (Dihydrotachysterol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE


  3 / 478 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25075826
[Au] Autor:de Matos RE; Connolly MJ; Starkey SR; Morrisey JK
[Ad] Endereço:Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.
[Ti] Título:Suspected primary hypoparathyroidism in a domestic ferret (Mustela putorius furo).
[So] Source:J Am Vet Med Assoc;245(4):419-24, 2014 Aug 15.
[Is] ISSN:1943-569X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CASE DESCRIPTION: A 4-year-old castrated male domestic ferret (Mustela putorius furo) was examined because of a 3-week history of intermittent seizures, signs of depression, hypocalcemia, and hyperphosphatemia. CLINICAL FINDINGS: Plasma biochemical analysis confirmed hyperphosphatemia (17.7 mg/dL) and low concentrations of total (4.3 mg/dL) and ionized (0.49 mmol/L) calcium. Serum parathyroid hormone concentration (2.30 pmol/L) was low or in the low part of the reference interval. TREATMENT AND OUTCOME: Calcium gluconate was administered (2.0 mg/kg/h [0.9 mg/lb/h], IV), followed by a transition to administration of calcium carbonate (53 mg/kg [24.1 mg/lb], PO, q 12 h) and dihydrotachysterol (0.02 mg/kg/d [0.009 mg/lb/d], PO). Attitude of the ferret improved and seizures ceased as blood calcium concentrations increased. The ferret was reexamined because of seizures approximately 1 year after oral maintenance administration of dihydrotachysterol and calcium was initiated. The ferret responded well to emergency and long-term treatment but then was lost to follow-up monitoring. The ferret died approximately 2 years after the initial evaluation and treatment. Hypertrophic cardiomyopathy was diagnosed during necropsy, but the parathyroid glands could not be identified. CLINICAL RELEVANCE: To the authors' knowledge, primary hypoparathyroidism has not previously been reported in a ferret. The condition should be considered for ferrets with hypocalcemia and hyperphosphatemia without azotemia. Treatment with dihydrotachysterol and oral supplementation of calcium appeared to be a viable option for long-term management.
[Mh] Termos MeSH primário: Carbonato de Cálcio/uso terapêutico
Gluconato de Cálcio/uso terapêutico
Di-Hidrotaquisterol/uso terapêutico
Furões
Hipoparatireoidismo/veterinária
Vitaminas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Carbonato de Cálcio/administração & dosagem
Gluconato de Cálcio/administração & dosagem
Di-Hidrotaquisterol/administração & dosagem
Hipocalcemia/veterinária
Hipoparatireoidismo/sangue
Hipoparatireoidismo/tratamento farmacológico
Masculino
Vitaminas/administração & dosagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vitamins); H0G9379FGK (Calcium Carbonate); R5LM3H112R (Dihydrotachysterol); SQE6VB453K (Calcium Gluconate)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:140731
[Lr] Data última revisão:
140731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140731
[St] Status:MEDLINE
[do] DOI:10.2460/javma.245.4.419


  4 / 478 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:24766747
[Au] Autor:Pletz MW; Terkamp C; Schumacher U; Rohde G; Schütte H; Welte T; Bals R; CAPNETZ-Study Group
[Ad] Endereço:Center for Infectious Diseases and Infection Control, Jena University Hospital, Erlanger Allee 101, 07740 Jena, Germany. mathias.pletz@med.uni-jena.de.
[Ti] Título:Vitamin D deficiency in community-acquired pneumonia: low levels of 1,25(OH)2 D are associated with disease severity.
[So] Source:Respir Res;15:53, 2014 Apr 27.
[Is] ISSN:1465-993X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: We aimed to explore the association between vitamin D levels and the severity, mortality and microbiological etiology of community-acquired pneumonia. METHODS: Vitamin D levels (both, the reservoir form 25-OH and the activated form 1,25-OH2) of 300 randomly selected patients with community-acquired pneumonia due to pre-specified pathogens included in the German competence network (CAPNETZ) study were measured. Prior to statistical analysis, values of 25-OH and 1,25-OH2 were power-transformed to achieve parametric distribution. All further analyses were performed with seasonally and age adjusted values. RESULTS: There was only a modest (Spearman Coefficient 0.38) positive correlation between 25-OH and 1,25-OH2. For 1,25-OH2 but not 25-OH, the general linear model revealed a significant inverse correlation between serum concentration and CURB score (p = 0.011). Liver and respiratory co-morbidity were associated with significantly lower 25-OH values and renal co-morbidity with significantly lower 1,25-OH2 values. No significant differences of 1,25-OH2 or 25-OH between different pathogens (influenza virus, Legionella spp., Streptococcus pneumoniae) were detected. CONCLUSION: For 1,25-OH2, we found a significant and independent (controlled for age, season and pathogen) negative correlation to pneumonia severity. Therefore, supplementation of non-activated vitamin D to protect from pneumonia may be non-sufficient in patients that have a decreased capacity to hydroxylate 25-OH to 1,25-OH2.
[Mh] Termos MeSH primário: Di-Hidrotaquisterol/análogos & derivados
Pneumonia/sangue
Estações do Ano
Índice de Gravidade de Doença
Deficiência de Vitamina D/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores/sangue
Estudos de Coortes
Infecções Comunitárias Adquiridas/sangue
Infecções Comunitárias Adquiridas/diagnóstico
Infecções Comunitárias Adquiridas/epidemiologia
Estudos Transversais
Di-Hidrotaquisterol/sangue
Feminino
Seres Humanos
Masculino
Meia-Idade
Pneumonia/diagnóstico
Pneumonia/epidemiologia
Estudos Prospectivos
Vitamina D/sangue
Deficiência de Vitamina D/diagnóstico
Deficiência de Vitamina D/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (1,25-dihydroxydihydrotachysterol(2)); 0 (Biomarkers); 1406-16-2 (Vitamin D); R5LM3H112R (Dihydrotachysterol)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140429
[St] Status:MEDLINE
[do] DOI:10.1186/1465-9921-15-53


  5 / 478 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:24127509
[Au] Autor:Boumans D; de Vries PA; Rikken NE; Laverman GD
[Ad] Endereço:Department of Rheumatology, Medisch Spectrum Twente, Enschede, the Netherlands.
[Ti] Título:Prolonged hypocalcaemia after pamidronate infusion in Riedel's thyroiditis associated hypoparathyroidism.
[So] Source:Neth J Med;71(8):442-3, 2013 Oct.
[Is] ISSN:1872-9061
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Conservadores da Densidade Óssea/efeitos adversos
Difosfonatos/efeitos adversos
Hipercalcemia/tratamento farmacológico
Hipocalcemia/induzido quimicamente
Hipoparatireoidismo/complicações
Tireoidite/complicações
[Mh] Termos MeSH secundário: Conservadores da Densidade Óssea/uso terapêutico
Carbonato de Cálcio/uso terapêutico
Di-Hidrotaquisterol/uso terapêutico
Feminino
Gastroenterite/complicações
Seres Humanos
Hipercalcemia/etiologia
Hipoparatireoidismo/tratamento farmacológico
Meia-Idade
Insuficiência Renal/complicações
Tireoidite/tratamento farmacológico
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Bone Density Conservation Agents); 0 (Diphosphonates); H0G9379FGK (Calcium Carbonate); OYY3447OMC (pamidronate); R5LM3H112R (Dihydrotachysterol)
[Em] Mês de entrada:1406
[Cu] Atualização por classe:131015
[Lr] Data última revisão:
131015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131016
[St] Status:MEDLINE


  6 / 478 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:22800939
[Au] Autor:Battula S; Hao S; Pedraza PL; Stier CT; Ferreri NR
[Ad] Endereço:Department of Pharmacology, New York Medical College, Valhalla, NY 10595, United States.
[Ti] Título:Tumor necrosis factor-alpha induces renal cyclooxygenase-2 expression in response to hypercalcemia.
[So] Source:Prostaglandins Other Lipid Mediat;99(1-2):45-50, 2012 Oct.
[Is] ISSN:1098-8823
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The effect of tumor necrosis factor-alpha (TNF) on cyclooxygenase-2 (COX-2) expression in the renal outer medulla (OM) was determined in a model of dihydrotachysterol (DHT)-induced hypercalcemia. Increases in serum calcium and water intake were observed during ingestion of a DHT-containing diet in both wild type (WT) and TNF deficient mice (TNF(-/-)). Polyuria and a decrease in body weight were observed in response to DHT treatment in WT and TNF(-/-) mice. A transient elevation in urinary TNF was observed in WT mice treated with DHT. Moreover, increased urinary levels of prostaglandin E(2) (PGE(2)) and a corresponding increase in COX-2 expression in the OM were observed in WT mice fed DHT. Increased COX-2 expression was not observed in TNF(-/-) mice fed DHT, and the characteristics of PGE(2) synthesis were distinct from those in WT mice. This study demonstrates that COX-2 expression in the OM, secondary to hypercalemia, is TNF-dependent.
[Mh] Termos MeSH primário: Ciclo-Oxigenase 2/biossíntese
Hipercalcemia/metabolismo
Medula Renal/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Animais
Di-Hidrotaquisterol
Hipercalcemia/induzido quimicamente
Masculino
Camundongos
Poliúria/induzido quimicamente
Fator de Necrose Tumoral alfa/deficiência
Fator de Necrose Tumoral alfa/urina
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Tumor Necrosis Factor-alpha); EC 1.14.99.1 (Cyclooxygenase 2); R5LM3H112R (Dihydrotachysterol)
[Em] Mês de entrada:1301
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120718
[St] Status:MEDLINE
[do] DOI:10.1016/j.prostaglandins.2012.07.001


  7 / 478 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:21796548
[Au] Autor:Erdogan A; Yilmaz U
[Ad] Endereço:Baskent University, Faculty of Medicine, Department of astroenterology, Alanya, Antalya, Turkey. erdoganaskin@hotmail.com
[Ti] Título:Is there a relationship between Helicobacter pylori and gastric autoimmunity?
[So] Source:Turk J Gastroenterol;22(2):134-8, 2011.
[Is] ISSN:2148-5607
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Helicobacter pylori-associated corpus atrophy and autoimmune gastric atrophy share similar histopathologic and clinical aspects. In our study, the relation between Helicobacter pylori and autoimmune gastritis was investigated. METHODS: Eighty-two consecutive histologically and serologically Helicobacter pylori-positive and 96 Helicobacter pylori-negative patients were enrolled in the study. All patients underwent diagnostic upper esophagogastroduodenal endoscopy. Three biopsy specimens from the antrum and corpus greater curvature were obtained for histologic evaluation. Serum samples were collected for detection of anti-parietal cell antibody, anti-Helicobacter pylori IgG and vitamin B12. Statistical analyses were determined with Student t-test and chi-square test. Statistical significance was determined with a p-value <0.05. RESULTS: Of 82 Helicobacter pylori-positive patients, 45 were female and 36 were male, with a mean age 45.1 ± 15.1. There was no significant difference in age, gender and corpus atrophy between the Helicobacter pylori-positive and -negative groups. Eleven Helicobacter pylori-positive patients (13.4%) and 14 (14.6%) Helicobacter pylori-negative patients were positive for anti-parietal cell antibody; the difference between the two groups was not statistically significant (p>0.05). Differences in esophagogastroduodenal endoscopy findings, antrum and corpus inflammation, antrum and corpus atrophy, and vitamin B12 levels were found to be insignificant between parietal cell antibody-positive and -negative groups (p>0.05). CONCLUSIONS: We did not find any relation between Helicobacter pylori infection and anti-parietal cell antibody, a marker of autoimmune gastritis. Long-term follow-up of Helicobacter pylori-infected patients and also determination of the relation between eradication of Helicobacter pylori and autoimmune atrophic gastritis are needed.
[Mh] Termos MeSH primário: Doenças Autoimunes/epidemiologia
Gastrite/epidemiologia
Infecções por Helicobacter/epidemiologia
Helicobacter pylori/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Anticorpos Antibacterianos/sangue
Autoanticorpos/sangue
Doenças Autoimunes/imunologia
Doenças Autoimunes/microbiologia
Estudos de Casos e Controles
Di-Hidrotaquisterol
Feminino
Mucosa Gástrica/imunologia
Mucosa Gástrica/microbiologia
Mucosa Gástrica/patologia
Gastrite/imunologia
Gastrite/patologia
Infecções por Helicobacter/imunologia
Infecções por Helicobacter/patologia
Seres Humanos
Imunoglobulina G/sangue
Masculino
Meia-Idade
Células Parietais Gástricas/imunologia
Células Parietais Gástricas/microbiologia
Prevalência
Fatores de Risco
Estudos Soroepidemiológicos
Vitamina B 12/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Bacterial); 0 (Autoantibodies); 0 (Immunoglobulin G); P6YC3EG204 (Vitamin B 12); R5LM3H112R (Dihydrotachysterol)
[Em] Mês de entrada:1112
[Cu] Atualização por classe:150518
[Lr] Data última revisão:
150518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110729
[St] Status:MEDLINE


  8 / 478 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:19486662
[Au] Autor:Kjelstrup S; Barragán D; Bedeaux D
[Ad] Endereço:Centre for Advanced Study, at The Norwegian Academy of Science and Letters, Oslo, Norway. signe.kjelstrup@chem.ntnu.no
[Ti] Título:Coefficients for active transport and thermogenesis of Ca2+-ATPase isoforms.
[So] Source:Biophys J;96(11):4376-86, 2009 Jun 03.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Coefficients for active transport of ions and heat in vesicles with Ca(2+)-ATPase from sarcoplasmic reticulum are defined in terms of a newly proposed thermodynamic theory and calculated using experiments reported in the literature. The coefficients characterize in a quantitative manner different performances of the enzyme isoforms. Four enzyme isoforms are examined, namely from white and red muscle tissue, from blood platelets, and from brown adipose mitochondria. The results indicate that the isoforms have a somewhat specialized function. White muscle tissue and brown adipose tissue have the same active transport coefficient ratio, but the activity level of the enzyme in white muscle is higher than in brown adipose tissue. The thermogenesis ratio is high in both white muscle and brown adipose tissue, in agreement with a specific role in nonshivering thermogenesis. Other isoforms do not have this ability to generate heat. A calcium-dependence of the coefficients is found, which can be understood as being in accordance with the role of this ion as a messenger in muscle contraction as well as in thermogenesis. The investigation points to new experiments related to structure as well as to function of the isoforms.
[Mh] Termos MeSH primário: Transporte Biológico Ativo
Isoenzimas/química
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/química
Termogênese
[Mh] Termos MeSH secundário: Tecido Adiposo Marrom/química
Tecido Adiposo Marrom/enzimologia
Algoritmos
Animais
Plaquetas/química
Plaquetas/enzimologia
Cálcio/química
Membrana Celular/química
Membrana Celular/enzimologia
Di-Hidrotaquisterol/química
Temperatura Alta
Seres Humanos
Mitocôndrias/química
Mitocôndrias/enzimologia
Fibras Musculares de Contração Rápida/química
Fibras Musculares de Contração Rápida/enzimologia
Fibras Musculares de Contração Lenta/química
Fibras Musculares de Contração Lenta/enzimologia
Coelhos
Ratos
Termodinâmica
Vesículas Transportadoras/química
Vesículas Transportadoras/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Isoenzymes); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases); R5LM3H112R (Dihydrotachysterol); SY7Q814VUP (Calcium)
[Em] Mês de entrada:0908
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090603
[St] Status:MEDLINE
[do] DOI:10.1016/j.bpj.2009.02.070


  9 / 478 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:18280666
[Au] Autor:Lin YF; Chai Y
[Ad] Endereço:Department of Anesthesiology, University of California, Davis, CA 95616, USA. yflin@ucdavis.edu
[Ti] Título:Functional modulation of the ATP-sensitive potassium channel by extracellular signal-regulated kinase-mediated phosphorylation.
[So] Source:Neuroscience;152(2):371-80, 2008 Mar 18.
[Is] ISSN:0306-4522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ATP-sensitive potassium (K(ATP)) channels play an important role in controlling insulin secretion and vascular tone as well as protecting neurons under metabolic stress. We have previously demonstrated that stimulation of the K(ATP) channel by nitric oxide (NO) requires activation of Ras- and extracellular signal-regulated kinase (ERK) of the mitogen-activated protein kinase (MAPK) family. However, the mechanistic link between ERK and the K(atp) channel remained unknown. To investigate how ERK modulates the function of K(ATP) channels, we performed single-channel recordings in combination with site-directed mutagenesis. The Kir6.2/SUR1 channel, a neuronal K(ATP) channel isoform, was expressed in human embryonic kidney (HEK) 293 cells by transient transfection. Direct application of the activated ERK2 to the cytoplasmic surface of excised, inside-out patches markedly enhanced the single-channel activity of Kir6.2/SUR1 channels. The normalized open probability (NPo) and opening frequency were significantly increased, whereas the mean closed duration was reduced. The single-channel conductance level was not affected. The ERK2-induced stimulation of Kir6.2/SUR1 channels was prevented by heat-inactivation of the enzyme. Furthermore, alanine substitutions of T341 and S385 to disrupt the potential ERK phosphorylation sites present in the Kir6.2 subunit significantly abrogated the stimulatory effects of ERK2, while aspartate substitutions of T341 and S385 to mimic the (negative) charge effect of phosphorylation rendered a small yet significant reduction in the ATP sensitivity of the channel. Taken together, here we report for the first time that ERK2/MAPK activates neuronal-type K(ATP) channels, and this stimulation requires ERK phosphorylation of the Kir6.2 subunit at T341 and S385 residues. The ERK2-induced K(ATP) channel stimulation can be accounted for by changes in channel gating that destabilize the closed states and by reduction in the ATP sensitivity. As Kir6.2 is the pore-forming subunit of K(ATP) channels, ERK2-mediated phosphorylation may represent a common mechanism for K(ATP) channel regulation in different tissues.
[Mh] Termos MeSH primário: MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Ativação do Canal Iônico/fisiologia
Canais de Potássio Corretores do Fluxo de Internalização/fisiologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/farmacologia
Análise de Variância
Ácido Aspártico/metabolismo
Linhagem Celular Transformada
Di-Hidrotaquisterol/farmacologia
Relação Dose-Resposta a Droga
Ativação Enzimática/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
MAP Quinases Reguladas por Sinal Extracelular/genética
MAP Quinases Reguladas por Sinal Extracelular/farmacologia
Proteínas de Fluorescência Verde/biossíntese
Temperatura Alta
Seres Humanos
Ativação do Canal Iônico/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
Potenciais da Membrana/fisiologia
Potenciais da Membrana/efeitos da radiação
Mutagênese Sítio-Dirigida/métodos
Técnicas de Patch-Clamp/métodos
Fosforilação
Transfecção/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Kir6.2 channel); 0 (Potassium Channels, Inwardly Rectifying); 147336-22-9 (Green Fluorescent Proteins); 30KYC7MIAI (Aspartic Acid); 8L70Q75FXE (Adenosine Triphosphate); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); R5LM3H112R (Dihydrotachysterol)
[Em] Mês de entrada:0807
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080219
[St] Status:MEDLINE
[do] DOI:10.1016/j.neuroscience.2008.01.003


  10 / 478 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
[PMID]:17401435
[Au] Autor:Chung J; Koyama T; Ohsawa M; Shibamiya A; Hoshi A; Hirosawa S
[Ad] Endereço:Laboratory Molecular Genetics of Hematology, Graduate School of Health Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
[Ti] Título:1,25(OH)(2)D(3) blocks TNF-induced monocytic tissue factor expression by inhibition of transcription factors AP-1 and NF-kappaB.
[So] Source:Lab Invest;87(6):540-7, 2007 Jun.
[Is] ISSN:0023-6837
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An essential coagulation factor, tissue factor (TF), is rapidly expressed by human monocytes when exposed to a variety of agonists, such as lipopolysaccharide or tumor necrosis factor (TNF). We previously found that 1alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) and its potent synthetic analogs downregulate TF and upregulate thrombomodulin expression on monocytic cells, counteracting the effects of TNF at the level of transcription. The human TF gene has characteristic binding sequences for activator protein-1 (AP-1) (c-Jun/c-Fos), nuclear factor-kappaB (NF-kappaB), Sp-1, and early growth response factor-1 (Egr-1). In this study, we investigated the regulatory mechanisms by which 1,25(OH)(2)D(3) inhibits TNF-induced TF expression in human monocytic cells. 1,25(OH)(2)D(3) reduced basal and TNF-induced TF activities. Gel-shift assay and luciferase assay with the respective reporter vectors showed that 1,25(OH)(2)D(3) reduced basal and TNF-induced activities of the nuclear proteins AP-1 and NF-kappaB, but not Egr-1. 1,25(OH)(2)D(3) inhibited TNF-induced phosphorylation of c-Jun without affecting phosphorylation of the other pathways. On the other hand, 1,25(OH)(2)D(3) directly inhibited nuclear binding and activities of NF-kappaB in the nucleus without affecting phosphorylation of the NF-kappaB activation pathway. These results indicate that 1,25(OH)(2)D(3) suppresses basal and TNF-induced TF expression in monocytic cells by inhibition of AP-1 and NF-kappaB activation pathways, but not of Egr-1. Our results may help to elucidate the regulatory mechanisms of 1,25(OH)(2)D(3) in TF induction, and may have physiological significance in the clinical challenge to use potential 1,25(OH)(2)D(3) analogs in antithrombotic therapy as well as immunomodulation and antineoplastic therapy of leukemia.
[Mh] Termos MeSH primário: Di-Hidrotaquisterol/análogos & derivados
Monócitos/metabolismo
NF-kappa B/antagonistas & inibidores
Tromboplastina/antagonistas & inibidores
Fator de Transcrição AP-1/antagonistas & inibidores
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Células Cultivadas
Di-Hidrotaquisterol/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Monócitos/efeitos dos fármacos
Tromboplastina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Transcription Factor AP-1); 0 (Tumor Necrosis Factor-alpha); 65878-49-1 (1,25-dihydroxydihydrotachysterol(3)); 9035-58-9 (Thromboplastin); R5LM3H112R (Dihydrotachysterol)
[Em] Mês de entrada:0707
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070403
[St] Status:MEDLINE



página 1 de 48 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