Base de dados : MEDLINE
Pesquisa : D03.633.100.759.646.138.124 [Categoria DeCS]
Referências encontradas : 22549 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 2255 ir para página                         

  1 / 22549 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29416045
[Au] Autor:Basco D; Zhang Q; Salehi A; Tarasov A; Dolci W; Herrera P; Spiliotis I; Berney X; Tarussio D; Rorsman P; Thorens B
[Ad] Endereço:Center for Integrative Genomics, University of Lausanne, 1015, Lausanne, Switzerland.
[Ti] Título:α-cell glucokinase suppresses glucose-regulated glucagon secretion.
[So] Source:Nat Commun;9(1):546, 2018 02 07.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glucagon secretion by pancreatic α-cells is triggered by hypoglycemia and suppressed by high glucose levels; impaired suppression of glucagon secretion is a hallmark of both type 1 and type 2 diabetes. Here, we show that α-cell glucokinase (Gck) plays a role in the control of glucagon secretion. Using mice with α-cell-specific inactivation of Gck (αGckKO mice), we find that glucokinase is required for the glucose-dependent increase in intracellular ATP/ADP ratio and the closure of K channels in α-cells and the suppression of glucagon secretion at euglycemic and hyperglycemic levels. αGckKO mice display hyperglucagonemia in the fed state, which is associated with increased hepatic gluconeogenic gene expression and hepatic glucose output capacity. In adult mice, fed hyperglucagonemia is further increased and glucose intolerance develops. Thus, glucokinase governs an α-cell metabolic pathway that suppresses secretion at or above normoglycemic levels; abnormal suppression of glucagon secretion deregulates hepatic glucose metabolism and, over time, induces a pre-diabetic phenotype.
[Mh] Termos MeSH primário: Células Secretoras de Glucagon/metabolismo
Glucagon/secreção
Glucoquinase/genética
Intolerância à Glucose/metabolismo
Glucose/metabolismo
Hipoglicemia/metabolismo
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Transporte Biológico
Feminino
Expressão Gênica
Células Secretoras de Glucagon/patologia
Glucoquinase/deficiência
Intolerância à Glucose/genética
Intolerância à Glucose/patologia
Hipoglicemia/genética
Hipoglicemia/patologia
Insulina/metabolismo
Canais KATP/genética
Canais KATP/metabolismo
Fígado/metabolismo
Masculino
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Insulin); 0 (KATP Channels); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate); 9007-92-5 (Glucagon); EC 2.7.1.2 (Glucokinase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-03034-0


  2 / 22549 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28467684
[Au] Autor:Wang L; Kazmierczak K; Yuan CC; Yadav S; Kawai M; Szczesna-Cordary D
[Ad] Endereço:Departments of Anatomy and Cell Biology and Internal Medicine, University of Iowa, IA, USA.
[Ti] Título:Cardiac contractility, motor function, and cross-bridge kinetics in N47K-RLC mutant mice.
[So] Source:FEBS J;284(12):1897-1913, 2017 06.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We have investigated the physiology and mechanical profiles of skinned papillary muscle fibers from transgenic mice expressing the N47K mutation in the myosin regulatory light chain (RLC), shown to cause hypertrophic cardiomyopathy in humans. The results were compared with wild-type (WT) mice, both expressing the human ventricular RLC. Rate constants of a cross-bridge (XB) cycle were deduced from tension transients induced by sinusoidal length changes during maximal Ca activation, and were studied as a function of MgATP, MgADP, and Pi concentrations. N47K mutant showed slower XB cycles but higher actin-activated ATPase activity compared with WT. Consequently, N47K exhibited larger tension than WT. K (ADP association constant) and K (equilibrium constant of force generation) were larger in N47K, and K (ATP association constant) was slightly larger in N47K vs. WT, demonstrating stronger nucleotide binding and force generation abilities of the mutant, but no changes in rigor acto-myosin binding were observed. Tension per XB was similar among groups, but N47K exhibited more XB distribution in the attached state. Larger values of tension and higher ATPase in N47K suggested that more cross-bridges participated in tension production in the mutant myocardium compared with WT. In vivo analysis of heart function, performed in ~ 12.5-month-old mice by echocardiography and invasive hemodynamics, demonstrated a significant decrease in dP/dt -end-diastolic volume relationship, indicating a depression of ventricular contractility in N47K mice. Our findings suggest that the N47K mutation exerts its action through direct alterations of myosin motor function that ultimately result in pathological hypertrophic remodeling in N47K hearts.
[Mh] Termos MeSH primário: Atividade Motora/fisiologia
Mutação
Contração Miocárdica/fisiologia
Cadeias Leves de Miosina/genética
Músculos Papilares/fisiopatologia
[Mh] Termos MeSH secundário: Actinas/metabolismo
Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Cálcio/metabolismo
Seres Humanos
Cinética
Camundongos
Camundongos Transgênicos
Cadeias Leves de Miosina/metabolismo
Miosinas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (Myosin Light Chains); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.4.1 (Myosins); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14096


  3 / 22549 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29374687
[Au] Autor:Hietanen T; Kapanen M; Kellokumpu-Lehtinen PL
[Ad] Endereço:Department of Oncology, Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland tenho@hietanen.net.
[Ti] Título:Natural Killer Cell Viability After Hyperthermia Alone or Combined with Radiotherapy with or without Cytokines.
[So] Source:Anticancer Res;38(2):655-663, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The effects of hyperthermia and irradiation, alone and in combination, on natural killer (NK) cell viability were investigated in vitro. The roles of interleukin-2 (IL-2) and interferon (IFN) α, ß and γ in rescuing NK cells from hyperthermia and irradiation were studied. MATERIALS AND METHODS: Non-selected NK cells were used as effector cells and K-562 cells as target cells. NK and K-562 cells were treated at 37 to 45°C for 0 to 180 min. The cells were irradiated at room temperature using single doses from 0 to 60 Gy. Recombinant IL-2 at 100 to 450 U/ml and recombinant IFNα, ß and γ at 1,000 U/ml were used for different periods of time. NK cell viability was measured by intracellular adenosine tri-, and diphosphate (ATP, ADP) levels via luminometer, trypan blue exclusion and propidium iodide (PI) staining. Binding capacity of NK effector cells to target K-562 cells was also microscopically assessed. RESULTS: Thermal treatments between 37 and 41°C did not significantly affect the ATP levels of NK cells. Between 41°C and 42°C, ATP levels significantly decreased, whilst there was an insignificant reduction up to 45°C. At 42°C or higher, no recovery was detectable. At 42°C, the ATP level of NK cells rescued by IL-2 were significantly higher than those of controls at 37°C. IFNα, ß and γ had no significant effects. A combination of heating at 42°C and irradiation at 20 Gy significantly reduced the ATP levels (p<0.001) more than heating and irradiation alone. At 42°C, IL-2 abolished the reduction of ATP levels by heating and irradiation. This effect was dependent on heating time and irradiation dose. The ATP/ADP ratio did not significantly change when NK cells were heated for different times at 42°C. Thermal treatment of target K-562 cells at temperatures from 37 to 45°C reduced the number of NK cells binding K-652 cells. CONCLUSION: In vitro, NK cell viability was strongly reduced between 41°C and 42°C. At 42°C, the combination of irradiation and thermal treatment reduced the ATP levels in NK cells. However, IL-2 restored cell viability depending on thermal and radiation doses.
[Mh] Termos MeSH primário: Citocinas/farmacologia
Hipertermia Induzida/métodos
Células Matadoras Naturais/efeitos da radiação
Radioterapia/métodos
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Sobrevivência Celular
Células Cultivadas
Seres Humanos
Interleucina-2/farmacologia
Células K562
Células Matadoras Naturais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-2); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


  4 / 22549 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28450391
[Au] Autor:Korge P; Calmettes G; John SA; Weiss JN
[Ad] Endereço:From the UCLA Cardiovascular Research Laboratory and the Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095.
[Ti] Título:Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex III.
[So] Source:J Biol Chem;292(24):9882-9895, 2017 06 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent evidence has implicated succinate-driven reverse electron transport (RET) through complex I as a major source of damaging reactive oxygen species (ROS) underlying reperfusion injury after prolonged cardiac ischemia. However, this explanation may be incomplete, because RET on reperfusion is self-limiting and therefore transient. RET can only generate ROS when mitochondria are well polarized, and it ceases when permeability transition pores (PTP) open during reperfusion. Because prolonged ischemia/reperfusion also damages electron transport complexes, we investigated whether such damage could lead to ROS production after PTP opening has occurred. Using isolated cardiac mitochondria, we demonstrate a novel mechanism by which antimycin-inhibited complex III generates significant amounts of ROS in the presence of Mg and NAD and the absence of exogenous substrates upon inner membrane pore formation by alamethicin or Ca -induced PTP opening. We show that H O production under these conditions is related to Mg -dependent NADH generation by malic enzyme. H O production is blocked by stigmatellin, indicating its origin from complex III, and by piericidin, demonstrating the importance of NADH-related ubiquinone reduction for ROS production under these conditions. For maximal ROS production, the rate of NADH generation has to be equal or below that of NADH oxidation, as further increases in [NADH] elevate ubiquinol-related complex III reduction beyond the optimal range for ROS generation. These results suggest that if complex III is damaged during ischemia, PTP opening may result in succinate/malate-fueled ROS production from complex III due to activation of malic enzyme by increases in matrix [Mg ], [NAD ], and [ADP].
[Mh] Termos MeSH primário: Complexo III da Cadeia de Transporte de Elétrons/metabolismo
Malato Desidrogenase/metabolismo
Mitocôndrias Cardíacas/metabolismo
Espécies Reativas de Oxigênio/agonistas
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Alameticina/farmacologia
Animais
Antimicina A/análogos & derivados
Antimicina A/farmacologia
Biocatálise/efeitos dos fármacos
Sinalização do Cálcio/efeitos dos fármacos
Complexo III da Cadeia de Transporte de Elétrons/antagonistas & inibidores
Ativação Enzimática/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Peróxido de Hidrogênio/metabolismo
Ionóforos/farmacologia
Magnésio/metabolismo
Malato Desidrogenase/química
Mitocôndrias Cardíacas/química
Mitocôndrias Cardíacas/efeitos dos fármacos
NAD/metabolismo
Oxirredução
Polienos/farmacologia
Porosidade/efeitos dos fármacos
Piridinas/farmacologia
Coelhos
Espécies Reativas de Oxigênio/metabolismo
Ubiquinona/metabolismo
[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 (Ionophores); 0 (Polyenes); 0 (Pyridines); 0 (Reactive Oxygen Species); 0U46U6E8UK (NAD); 11118-72-2 (antimycin); 1339-63-5 (Ubiquinone); 27061-78-5 (Alamethicin); 61D2G4IYVH (Adenosine Diphosphate); 642-15-9 (Antimycin A); 8VT513UJ9R (piericidin A); 91682-96-1 (stigmatellin); BBX060AN9V (Hydrogen Peroxide); EC 1.1.1.37 (Malate Dehydrogenase); EC 1.10.2.2 (Electron Transport Complex III); I38ZP9992A (Magnesium)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171228
[Lr] Data última revisão:
171228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.768317


  5 / 22549 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28458520
[Au] Autor:Moschos MM; Moustafa GA; Papakonstantinou VD; Tsatsos M; Laios K; Antonopoulou S
[Ad] Endereço:1st Department of Ophthalmology, Medical School, University of Athens, Athens, Greece.
[Ti] Título:Anti-platelet effects of anti-glaucomatous eye drops: an in vitro study on human platelets.
[So] Source:Drug Des Devel Ther;11:1267-1272, 2017.
[Is] ISSN:1177-8881
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Altered platelet aggregability has been implicated in the pathogenesis of glaucoma. This study aims to investigate the anti-platelet potential of intraocular pressure lowering drops, with the possibility of establishing it as an additional mechanism of anti-glaucomatous action. MATERIALS AND METHODS: The anti-aggregating effects of a series of anti-glaucomatous eye drops were determined on human platelets in the platelet aggregation model, using four known aggregating factors (platelet activating factor [PAF], adenosine diphosphate [ADP], thrombin receptor-activating peptide [TRAP], and arachidonic acid [AA]). RESULTS: Almost all of the tested samples inhibited platelet aggregation induced by PAF, ADP, TRAP, and AA, except for Alphagan, which did not demonstrate inhibition of ADP- and TRAP-induced aggregation at a wide range of concentrations. Trusopt, Betoptic, and Azarga eye drops were the most potent inhibitors of all four aggregating factors, while Alphagan was the least potent ( <0.05). CONCLUSION: This study shows that anti-glaucomatous eye drops possess anti-platelet effects, and this was shown for the first time by experimenting on human platelets.
[Mh] Termos MeSH primário: Difosfato de Adenosina/farmacologia
Ácido Araquidônico/farmacologia
Glaucoma/tratamento farmacológico
Complexo Mediador/farmacologia
Soluções Oftálmicas/farmacologia
Fator de Ativação de Plaquetas/farmacologia
[Mh] Termos MeSH secundário: Difosfato de Adenosina/administração & dosagem
Ácido Araquidônico/administração & dosagem
Plaquetas/efeitos dos fármacos
Seres Humanos
Complexo Mediador/administração & dosagem
Soluções Oftálmicas/administração & dosagem
Fator de Ativação de Plaquetas/administração & dosagem
Agregação Plaquetária/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mediator Complex); 0 (Ophthalmic Solutions); 0 (Platelet Activating Factor); 27YG812J1I (Arachidonic Acid); 61D2G4IYVH (Adenosine Diphosphate)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171222
[Lr] Data última revisão:
171222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.2147/DDDT.S131582


  6 / 22549 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29215839
[Au] Autor:Barinov EF; Mamedaliyeva SA; Tverdokhleb TA; , Balykina AO
[Ti] Título:[Interaction of epinephrine and ADP in regulation of platelet function in chronic cerebral ischemia ].
[So] Source:Patol Fiziol Eksp Ter;61(2):51-5, 2017 Apr-Jun.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The purpose is devoted to test of hypothesis that patients with chronic cerebral ischemia (CCI) have decreased secretion of platelet ADP as the reason of platelet aggregation restriction in response to stimulation of adrenaline. Methods. We used platelet-rich plasma which was separated by centrifugation from peripheral blood of 55 patients with a diagnosis of CCI of stage 1-2. Platelets aggregation was studied on aggregometer Chrono - Log (USA). ADP and Epinephrine were used for platelet stimulation at effective concentration (EC50). Modulatory role of ADP subthreshold doses (0.5 mM) in platelet activation was analyzed with its addition to a suspension of platelets stimulated by agonists (EC50). Results. In 35 patients (group 1) with platelet hyperreactivity to ADP (EC50) response of platelets to Epinephrine was heterogeneous: in 17 cases (48.6%) there was high response (50%) and in 18 cases (51.4%) there was low platelet response to Epinephrine. 20 patients (group 2) had hyporesponsiveness of platelets upon stimulation by both agonists. It was established that the low initial response of platelets to Epinephrinе in vitro might be due to reduced secretion of ADP, i.e. limited adaptive response since administration of ADP subthreshold doses enhances adrenoreactivity of platelets. If pathochemical violations underlying the formation of platelet disadaptation are reversible, it is possible to recover the reaction of platelets to Epinephrine. Conclusion. In reducing the functional response of platelets to Epinephrinе key issue is establishing the reversibility of violations of platelets adaptive response of platelets.
[Mh] Termos MeSH primário: Difosfato de Adenosina/farmacologia
Plaquetas/metabolismo
Isquemia Encefálica/sangue
Epinefrina/farmacologia
Ativação Plaquetária/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Idoso
Plaquetas/patologia
Isquemia Encefálica/patologia
Doença Crônica
Feminino
Seres Humanos
Masculino
Meia-Idade
Testes de Função Plaquetária
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
61D2G4IYVH (Adenosine Diphosphate); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171221
[Lr] Data última revisão:
171221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE


  7 / 22549 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29045413
[Au] Autor:Korzeniewski B
[Ad] Endereço:Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, Poland.
[Ti] Título:Contribution of proton leak to oxygen consumption in skeletal muscle during intense exercise is very low despite large contribution at rest.
[So] Source:PLoS One;12(10):e0185991, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A computer model was used to simulate the dependence of protonmotive force (Δp), proton leak and phenomenological (involving proton leak) ATP/O2 ratio on work intensity in skeletal muscle. Δp, NADH and proton leak decreased with work intensity. The contribution of proton leak to oxygen consumption ([Formula: see text]) decreased from about 60% at rest to about 3 and 1% at moderate and heavy/severe exercise, respectively, while the ATP/O2 ratio increased from 2.1 to 5.5 and 5.7. A two-fold increase in proton leak activity or its decrease to zero decreased/increased the ATP/O2 ratio by only about 3 and 1% during moderate and heavy/severe exercise, respectively. The low contribution of proton leak to [Formula: see text] in intensively working skeletal muscle was mostly caused by a huge increase in ATP usage intensity during rest-to-work transition, while OXPHOS, and thus oxidative ATP supply and [Formula: see text] related to it, was mostly stimulated by high each-step activation (ESA) of OXPHOS complexes. The contribution of proton leak to [Formula: see text] and ATP/O2 ratio in isolated mitochondria should not be directly extrapolated to working muscle, as mitochondria lack ESA, at least in the absence of Ca2+, and therefore [Formula: see text] cannot be elevated as much as in intact muscle.
[Mh] Termos MeSH primário: Exercício/fisiologia
Músculo Esquelético/fisiologia
Consumo de Oxigênio/fisiologia
Prótons
Descanso/fisiologia
[Mh] Termos MeSH secundário: Difosfato de Adenosina/farmacologia
Trifosfato de Adenosina/biossíntese
Seres Humanos
Força Próton-Motriz
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protons); 61D2G4IYVH (Adenosine Diphosphate); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185991


  8 / 22549 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28945220
[Au] Autor:Schwarz Y; Zhao N; Kirchhoff F; Bruns D
[Ad] Endereço:Molecular Neurophysiology, Center for Integrative Physiology and Molecular Medicine, Saarland University, Homburg, Germany.
[Ti] Título:Astrocytes control synaptic strength by two distinct v-SNARE-dependent release pathways.
[So] Source:Nat Neurosci;20(11):1529-1539, 2017 Nov.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Communication between glia cells and neurons is crucial for brain functions, but the molecular mechanisms and functional consequences of gliotransmission remain enigmatic. Here we report that astrocytes express synaptobrevin II and cellubrevin as functionally non-overlapping vesicular SNARE proteins on glutamatergic vesicles and neuropeptide Y-containing large dense-core vesicles, respectively. Using individual null-mutants for Vamp2 (synaptobrevin II) and Vamp3 (cellubrevin), as well as the corresponding compound null-mutant for genes encoding both v-SNARE proteins, we delineate previously unrecognized individual v-SNARE dependencies of astrocytic release processes and their functional impact on neuronal signaling. Specifically, we show that astroglial cellubrevin-dependent neuropeptide Y secretion diminishes synaptic signaling, while synaptobrevin II-dependent glutamate release from astrocytes enhances synaptic signaling. Our experiments thereby uncover the molecular mechanisms of two distinct v-SNARE-dependent astrocytic release pathways that oppositely control synaptic strength at presynaptic sites, elucidating new avenues of communication between astrocytes and neurons.
[Mh] Termos MeSH primário: Astrócitos/secreção
Proteínas SNARE/secreção
Transdução de Sinais/fisiologia
Sinapses/secreção
[Mh] Termos MeSH secundário: Difosfato de Adenosina/farmacologia
Animais
Astrócitos/efeitos dos fármacos
Astrócitos/fisiologia
Células Cultivadas
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Potenciais Pós-Sinápticos Excitadores/fisiologia
Feminino
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Técnicas de Cultura de Órgãos
Transdução de Sinais/efeitos dos fármacos
Sinapses/efeitos dos fármacos
Sinapses/fisiologia
Xantinas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (SNARE Proteins); 0 (Xanthines); 61D2G4IYVH (Adenosine Diphosphate); 9PTP4FOI9E (1,3-dipropyl-8-cyclopentylxanthine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4647


  9 / 22549 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28919057
[Au] Autor:Zamora RA; Gonzalez-Órdenes F; Castro-Fernández V; Guixé V
[Ad] Endereço:Departamento de Biología, Facultad de Ciencias, Universidad de Chile, Las Palmeras 3425, Ñuñoa, Santiago, Chile.
[Ti] Título:ADP-dependent phosphofructokinases from the archaeal order Methanosarcinales display redundant glucokinase activity.
[So] Source:Arch Biochem Biophys;633:85-92, 2017 Nov 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The genome of Methanosarcinales organisms presents both ADP-dependent glucokinase and phosphofructokinase genes. However, Methanococcoides burtonii has a truncate glucokinase gene with a large deletion at the C-terminal, where the catalytic GXGD motif is located. Characterization of its phosphofructokinase annotated protein shows that is a bifunctional enzyme able to supply the absence of the glucokinase activity. Moreover, kinetic analyses of the phosphofructokinase annotated enzyme from, Methanohalobium evestigatum demonstrated that this enzyme is also bifunctional. The high conservation of the active site residues of all the enzymes from the order Methanosarcinales suggest that they should be bifunctional, as was previously reported for the ADP-dependent kinases from Methanococcales, highlighting the redundancy of the glucokinase activity in this archaeal group. The presence of active glycolytic enzymes would be important when glycogen storage of these organisms needs to be degraded to be used as energy source. Kinetic and structural information allows us to establish a substrate specificity signature that identifies specific GK or PFK, and bifunctional enzymes in this family.
[Mh] Termos MeSH primário: Difosfato de Adenosina/química
Proteínas Arqueais/química
Glucoquinase/química
Methanosarcinales/enzimologia
Fosfotransferases (Aceptor do Grupo Álcool)/química
[Mh] Termos MeSH secundário: Difosfato de Adenosina/metabolismo
Sequência de Aminoácidos
Proteínas Arqueais/genética
Proteínas Arqueais/metabolismo
Sítios de Ligação
Clonagem Molecular
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Glucoquinase/genética
Glucoquinase/metabolismo
Cinética
Methanosarcinales/classificação
Methanosarcinales/genética
Modelos Moleculares
Fosforilação
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Filogenia
Ligação Proteica
Conformação Proteica em alfa-Hélice
Conformação Proteica em Folha beta
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Especificidade por Substrato
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Archaeal Proteins); 0 (Recombinant Proteins); 61D2G4IYVH (Adenosine Diphosphate); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.146 (ADP D-fructose-6-phosphate 1-phosphotransferase); EC 2.7.1.2 (Glucokinase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


  10 / 22549 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28918750
[Au] Autor:Song Z; Pan J; Xie L; Gong G; Han S; Zhang W; Hu Y
[Ad] Endereço:China State Institute of Pharmaceutical Industry, Zhangjiang Institute, Shanghai, 201203, China. bebydou@hotmail.com.
[Ti] Título:Expression, Purification, and Activity of ActhiS, a Thiazole Biosynthesis Enzyme from Acremonium chrysogenum.
[So] Source:Biochemistry (Mosc);82(7):852-860, 2017 Jul.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thiamine pyrophosphate is an essential coenzyme in all organisms. Its biosynthesis involves independent syntheses of the precursors, pyrimidine and thiazole, which are then coupled. In our previous study with overexpressed and silent mutants of ActhiS (thiazole biosynthesis enzyme from Acremonium chrysogenum), we found that the enzyme level correlated with intracellular thiamine content in A. chrysogenum. However, the exact structure and function of ActhiS remain unclear. In this study, the enzyme-bound ligand was characterized as the ADP adduct of 5-(2-hydroxyethyl)-4-methylthiazole-2-carboxylic acid (ADT) using HPLC and H NMR. The ligand-free ActhiS expressed in M9 minimal medium catalyzed conversion of NAD+ and glycine to ADT in the presence of iron. Furthermore, the C217 residue was identified as the sulfur donor for the thiazole moiety. These observations confirm that ActhiS is a thiazole biosynthesis enzyme in A. chrysogenum, and it serves as a sulfur source for the thiazole moiety.
[Mh] Termos MeSH primário: Acremonium/enzimologia
Proteínas Fúngicas/genética
Proteínas Fúngicas/metabolismo
Tiazóis/metabolismo
[Mh] Termos MeSH secundário: Difosfato de Adenosina/química
Difosfato de Adenosina/metabolismo
Sequência de Aminoácidos
Cromatografia Líquida de Alta Pressão
Proteínas Fúngicas/química
Proteínas Fúngicas/isolamento & purificação
Glicina/metabolismo
Ligantes
Espectroscopia de Ressonância Magnética
Espectrometria de Massas
Mutagênese Sítio-Dirigida
NAD/metabolismo
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/química
Proteínas Recombinantes/isolamento & purificação
Alinhamento de Sequência
Tiamina Pirofosfato/metabolismo
Tiazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungal Proteins); 0 (Ligands); 0 (Recombinant Proteins); 0 (Thiazoles); 0U46U6E8UK (NAD); 61D2G4IYVH (Adenosine Diphosphate); Q57971654Y (Thiamine Pyrophosphate); TE7660XO1C (Glycine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297917070112



página 1 de 2255 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