Base de dados : MEDLINE
Pesquisa : D02.455.326.271.122.260 [Categoria DeCS]
Referências encontradas : 108 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 11 ir para página                         

  1 / 108 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25845493
[Au] Autor:Leclercq K; Afrikanova T; Langlois M; De Prins A; Buenafe OE; Rospo CC; Van Eeckhaut A; de Witte PA; Crawford AD; Smolders I; Esguerra CV; Kaminski RM
[Ad] Endereço:Neuroscience TA, UCB Biopharma, Braine-l'Alleud, Belgium.
[Ti] Título:Cross-species pharmacological characterization of the allylglycine seizure model in mice and larval zebrafish.
[So] Source:Epilepsy Behav;45:53-63, 2015 Apr.
[Is] ISSN:1525-5069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treatment-resistant seizures affect about a third of patients suffering from epilepsy. To fulfill the need for new medications targeting treatment-resistant seizures, a number of rodent models offer the opportunity to assess a variety of potential treatment approaches. The use of such models, however, has proven to be time-consuming and labor-intensive. In this study, we performed pharmacological characterization of the allylglycine (AG) seizure model, a simple in vivo model for which we demonstrated a high level of treatment resistance. (d,l)-Allylglycine inhibits glutamic acid decarboxylase (GAD) - the key enzyme in γ-aminobutyric acid (GABA) biosynthesis - leading to GABA depletion, seizures, and neuronal damage. We performed a side-by-side comparison of mouse and zebrafish acute AG treatments including biochemical, electrographic, and behavioral assessments. Interestingly, seizure progression rate and GABA depletion kinetics were comparable in both species. Five mechanistically diverse antiepileptic drugs (AEDs) were used. Three out of the five AEDs (levetiracetam, phenytoin, and topiramate) showed only a limited protective effect (mainly mortality delay) at doses close to the TD50 (dose inducing motor impairment in 50% of animals) in mice. The two remaining AEDs (diazepam and sodium valproate) displayed protective activity against AG-induced seizures. Experiments performed in zebrafish larvae revealed behavioral AED activity profiles highly analogous to those obtained in mice. Having demonstrated cross-species similarities and limited efficacy of tested AEDs, we propose the use of AG in zebrafish as a convenient and high-throughput model of treatment-resistant seizures.
[Mh] Termos MeSH primário: Alilglicina
Anticonvulsivantes/uso terapêutico
Modelos Animais de Doenças
Convulsões/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Diazepam/uso terapêutico
Frutose/análogos & derivados
Frutose/uso terapêutico
Masculino
Camundongos
Fenitoína/uso terapêutico
Piracetam/análogos & derivados
Piracetam/uso terapêutico
Convulsões/induzido quimicamente
Resultado do Tratamento
Ácido Valproico/uso terapêutico
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anticonvulsants); 0H73WJJ391 (topiramate); 1069-48-3 (Allylglycine); 230447L0GL (etiracetam); 30237-26-4 (Fructose); 614OI1Z5WI (Valproic Acid); 6158TKW0C5 (Phenytoin); Q3JTX2Q7TU (Diazepam); ZH516LNZ10 (Piracetam)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:150507
[Lr] Data última revisão:
150507
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150408
[St] Status:MEDLINE


  2 / 108 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:24491152
[Au] Autor:Krannig KS; Sun J; Schlaad H
[Ad] Endereço:Max Planck Institute of Colloids and Interfaces , Department of Colloid Chemistry, Research Campus Golm, 14424 Potsdam, Germany.
[Ti] Título:Stimuli-responsivity of secondary structures of glycopolypeptides derived from poly(L-glutamate-co-allylglycine).
[So] Source:Biomacromolecules;15(3):978-84, 2014 Mar 10.
[Is] ISSN:1526-4602
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Copolypeptides containing L-glutamate and various amounts of either D-/DL-/L-allylglycine or D-/DL-/L-(3-(ß-D-glucopyranosyl)thio)propylglycine defect units were studied by circular dichroism (CD) and infrared (FT-IR) spectroscopy according to their secondary structures in dependence of pH and temperature. All samples adopt random coil conformation at high pH and α-helix at low pH without evidence for ß-sheet formation. Folding into the α-helix structure is strongly affected by the number and configuration of allylglycine defects (which intrinsically stabilize ß-sheets). Helix folding is facilitated upon the attachment of D-glucopyranose to the L- (but not the D-) allylglycine units, which is attributed to a different secondary structure preference of the L-(3-(ß-D-glucopyranosyl)thio)propylglycine (L: random coil; D: ß-sheet) and a majority rule effect.
[Mh] Termos MeSH primário: Alilglicina/química
Ácido Glutâmico/química
Glicopeptídeos/química
[Mh] Termos MeSH secundário: Dicroísmo Circular
Concentração de Íons de Hidrogênio
Conformação Molecular
Estrutura Secundária de Proteína
Espectroscopia de Infravermelho com Transformada de Fourier
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Glycopeptides); 1069-48-3 (Allylglycine); 3KX376GY7L (Glutamic Acid)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:140310
[Lr] Data última revisão:
140310
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140205
[St] Status:MEDLINE
[do] DOI:10.1021/bm401883p


  3 / 108 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:23636466
[Au] Autor:Andolina D; Maran D; Valzania A; Conversi D; Puglisi-Allegra S
[Ad] Endereço:Santa Lucia Foundation, Rome, Italy. diego.andolina@gmail.com
[Ti] Título:Prefrontal/amygdalar system determines stress coping behavior through 5-HT/GABA connection.
[So] Source:Neuropsychopharmacology;38(10):2057-67, 2013 Sep.
[Is] ISSN:1740-634X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Coping is defined as the behavioral and physiological effort made to master stressful situations. The ability to cope with stress leads either to healthy or to pathogenic outcomes. The medial prefrontal cortex (mpFC) and amygdala are acknowledged as having a major role in stress-related behaviors, and mpFC has a critical role in the regulation of amygdala-mediated arousal in response to emotionally salient stimuli. Prefrontal cortical serotonin (5-hydroxytryptamine (5-HT)) is involved in corticolimbic circuitry, and GABA has a major role in amygdala functioning. Here, using mice, it was assessed whether amygdalar GABA regulation by prefrontal 5-HT is involved in processing stressful experiences and in determining coping outcomes. First (experiment 1), bilateral selective 5-HT depletion in mpFC of mice reduced GABA release induced by stress in basolateral amygdala (BLA) and passive coping in the Forced Swimming Test (FST) (experiment 2). Moreover, prefrontal-amygdala disconnection procedure that combined a selective unilateral 5-HT depletion of mpFC and infusion of an inhibitor of GABA synthesis into the contralateral BLA, thereby to disrupt prefrontal-amygdalar serial connectivity bilaterally, showed that disconnection selectively decreases immobility in the FST. These results point to prefrontal/amygdala connectivity mediated by 5-HT and GABA transmission as a critical neural mechanism in stress-induced behavior.
[Mh] Termos MeSH primário: Adaptação Psicológica/fisiologia
Tonsila do Cerebelo/fisiologia
Córtex Pré-Frontal/fisiologia
Serotonina/metabolismo
Estresse Psicológico/fisiopatologia
Estresse Psicológico/psicologia
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: 5,7-Di-Hidroxitriptamina/administração & dosagem
5,7-Di-Hidroxitriptamina/farmacologia
Adaptação Psicológica/efeitos dos fármacos
Alilglicina/administração & dosagem
Alilglicina/farmacologia
Tonsila do Cerebelo/efeitos dos fármacos
Tonsila do Cerebelo/metabolismo
Animais
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Dopamina/metabolismo
Antagonistas GABAérgicos/farmacologia
Resposta de Imobilidade Tônica/efeitos dos fármacos
Resposta de Imobilidade Tônica/fisiologia
Masculino
Camundongos
Microinjeções
Vias Neurais/efeitos dos fármacos
Vias Neurais/metabolismo
Vias Neurais/fisiologia
Norepinefrina/metabolismo
Córtex Pré-Frontal/efeitos dos fármacos
Córtex Pré-Frontal/metabolismo
Estresse Psicológico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GABA Antagonists); 1069-48-3 (Allylglycine); 31363-74-3 (5,7-Dihydroxytryptamine); 333DO1RDJY (Serotonin); 56-12-2 (gamma-Aminobutyric Acid); VTD58H1Z2X (Dopamine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1403
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130503
[St] Status:MEDLINE
[do] DOI:10.1038/npp.2013.107


  4 / 108 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:23022048
[Au] Autor:Asinof SK; Paine TA
[Ad] Endereço:Department of Neuroscience, Oberlin College, 119 Woodland Street, Oberlin, OH 44074, USA.
[Ti] Título:Inhibition of GABA synthesis in the prefrontal cortex increases locomotor activity but does not affect attention in the 5-choice serial reaction time task.
[So] Source:Neuropharmacology;65:39-47, 2013 Feb.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Attention deficits are a core cognitive symptom of schizophrenia; the neuropathology underlying these deficits is not known. Attention is regulated, at least in part, by the prefrontal cortex (PFC), a brain area in which pathology of γ-aminobutyric acid (GABA) neurons has been consistently observed in post-mortem analysis of the brains of people with schizophrenia. Specifically, expression of the 67-kD isoform of the GABA synthesis enzyme glutamic acid decarboxylase (GAD67) is reduced in parvalbumin-containing fast-spiking GABA interneurons. Thus it is hypothesized that reduced cortical GABA synthesis and release may contribute to the attention deficits in schizophrenia. Here the effect of reducing cortical GABA synthesis with l-allylglycine (LAG) on attention was tested using three different versions of the 5-choice serial reaction time task (5CSRTT). Because 5CSRTT performance can be affected by locomotor activity, we also measured this behavior in an open field. Finally, the expression of Fos protein was used as an indirect measure of reduced GABA synthesis. Intra-cortical LAG (10 µg/0.5 µl/side) infusions increased Fos expression and resulted in hyperactivity in the open field. Intra-cortical LAG infusions did not affect attention in any version of the 5CSRTT. These results suggest that a general decrease in GABA synthesis is not sufficient to cause attention deficits. It remains to be tested whether a selective decrease in GABA synthesis in parvalbumin-containing GABA neurons could cause attention deficits. Decreased cortical GABA synthesis did increase locomotor activity; this may reflect the positive symptoms of schizophrenia.
[Mh] Termos MeSH primário: Atenção/fisiologia
Comportamento de Escolha/fisiologia
Antagonistas GABAérgicos/administração & dosagem
Atividade Motora/fisiologia
Córtex Pré-Frontal/fisiologia
Ácido gama-Aminobutírico/biossíntese
[Mh] Termos MeSH secundário: Alilglicina/administração & dosagem
Animais
Atenção/efeitos dos fármacos
Comportamento de Escolha/efeitos dos fármacos
Infusões Intraventriculares
Masculino
Atividade Motora/efeitos dos fármacos
Córtex Pré-Frontal/efeitos dos fármacos
Desempenho Psicomotor/efeitos dos fármacos
Desempenho Psicomotor/fisiologia
Ratos
Ratos Sprague-Dawley
Tempo de Reação/efeitos dos fármacos
Tempo de Reação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GABA Antagonists); 1069-48-3 (Allylglycine); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1310
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121002
[St] Status:MEDLINE


  5 / 108 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:23022539
[Au] Autor:Chabrol FP; Eglen SJ; Sernagor E
[Ad] Endereço:Institute of Neuroscience, Faculty of Medical Sciences, Newcastle University, Framlington Place, Newcastle upon Tyne NE2 4HH, UK.
[Ti] Título:GABAergic control of retinal ganglion cell dendritic development.
[So] Source:Neuroscience;227:30-43, 2012 Dec 27.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Developing GABAergic neurons mature long before excitatory neurons, and early GABA(A) activity exerts important paracrine effects while neurons extend dendrites and axons and they establish neural connections. One of the unique features of early GABA(A) activity is that it induces membrane depolarization and Ca(2+) influx and it shifts to inhibition when networks mature. Although it has been demonstrated in several systems that early GABA(A) signaling plays a fundamental role in guiding neurite outgrowth, it has never been investigated in the retina. Here we show that chronic GABAergic activity is required for the stabilization and maintenance of newly formed dendritic branches in developing turtle retinal ganglion cells (RGCs) in ovo. Blocking GABA(A) receptors with bicuculline or inhibiting GABA synthesis with l-allylglycine have contrasting effects on dendritic growth and branching in biocytin-labeled RGCs. Dendritic arbor reconstruction shows that bicuculline induces dendritic branch loss without global change in the extent of dendritic fields while l-allylglycine causes the entire tree to shrink. At the same time, multielectrode array recordings and Ca(2+) imaging show that l-allylglycine has similar effects to bicuculline (Leitch et al., 2005) on overall network excitability, preventing the disappearance of immature retinal waves of activity and the GABAergic polarity shift. This study demonstrates for the first time that GABA plays an important role in vivo in stabilizing developing dendrites into mature arbors in the retina. However, the way GABA influences dendritic growth appears to be driven by complex mechanisms that cannot be explained solely on the basis of overall network activity levels.
[Mh] Termos MeSH primário: Dendritos/fisiologia
Retina/citologia
Retina/embriologia
Células Ganglionares da Retina/citologia
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Alilglicina/farmacologia
Animais
Bicuculina/farmacologia
Cálcio/metabolismo
Dendritos/efeitos dos fármacos
Relação Dose-Resposta a Droga
Embrião não Mamífero
Antagonistas de Receptores de GABA-A/farmacologia
Técnicas In Vitro
Lisina/análogos & derivados
Lisina/metabolismo
Análise de Regressão
Células Ganglionares da Retina/efeitos dos fármacos
Tartarugas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GABA-A Receptor Antagonists); 1069-48-3 (Allylglycine); 56-12-2 (gamma-Aminobutyric Acid); G6D6147J22 (biocytin); K3Z4F929H6 (Lysine); SY7Q814VUP (Calcium); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1305
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121002
[St] Status:MEDLINE


  6 / 108 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:22998786
[Au] Autor:Kowalczyk R; Brimble MA; Callon KE; Watson M; Cornish J
[Ad] Endereço:The School of Chemical Sciences, University of Auckland, 23 Symonds St, Auckland 1010, New Zealand.
[Ti] Título:How to blast osteoblasts? Novel dicarba analogues of amylin-(1-8) to treat osteoporosis.
[So] Source:Bioorg Med Chem;20(20):6011-8, 2012 Oct 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:When administered in vivo, amylin (1-8) stimulates osteoblast proliferation increasing bone volume and bone strength. The native cyclic octapeptide amylin (1-8) is unstable, however, it provides an attractive framework for the creation of more stable, orally active synthetic analogues using various peptidomimetic techniques. On-resin ring closing metathesis (RCM) on the olefinic side chains of allylglycine residues and lysine moieties functionalized with an allyloxycarbonyl (Alloc) group, was used to prepare novel carba-bridged surrogates of the disulfide bridge between Cys/2 and Cys/7 in amylin-(1-8). Commercially available N(α)-Fmoc N(ε)-Alloc protected lysine was used as a convenient substrate for Grubbs' ring closing metathesis. Analogues of amylin-(1-8) prepared by cyclization of allylglycine residues that also contained proline residues at either position 4 or 6, or both, were also prepared to investigate the effect of proline as a 'kink-inducing' residue on the efficiency of the RCM reaction. Of the nine novel alkene-bridged analogues prepared, five showed promising biological activity in a proliferation study in primary foetal rat osteoblasts at physiological concentrations. Two of these analogues were chosen for further in vivo evaluation.
[Mh] Termos MeSH primário: Polipeptídeo Amiloide das Ilhotas Pancreáticas/química
[Mh] Termos MeSH secundário: Alilglicina/química
Sequência de Aminoácidos
Animais
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Ciclização
Dissulfetos/química
Polipeptídeo Amiloide das Ilhotas Pancreáticas/farmacologia
Polipeptídeo Amiloide das Ilhotas Pancreáticas/uso terapêutico
Dados de Sequência Molecular
Osteoblastos/citologia
Osteoporose/tratamento farmacológico
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Disulfides); 0 (Islet Amyloid Polypeptide); 1069-48-3 (Allylglycine)
[Em] Mês de entrada:1302
[Cu] Atualização por classe:121001
[Lr] Data última revisão:
121001
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120925
[St] Status:MEDLINE


  7 / 108 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:21964521
[Au] Autor:Saigusa T; Aono Y; Sekino R; Uchida T; Takada K; Oi Y; Koshikawa N; Cools AR
[Ad] Endereço:Department of Pharmacology, Nihon University School of Dentistry, 1-8-13, Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan. saigusa@dent.nihon-u.ac.jp
[Ti] Título:In vivo neurochemical evidence that newly synthesised GABA activates GABA(B), but not GABA(A), receptors on dopaminergic nerve endings in the nucleus accumbens of freely moving rats.
[So] Source:Neuropharmacology;62(2):907-13, 2012 Feb.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:GABA released from accumbal GABAergic interneurons plays an inhibitory role in the regulation of dopamine efflux through GABA(B) and GABA(A) receptors located on accumbal dopaminergic nerve endings. The cytosolic newly synthesised GABA alters vesicular GABA levels and, accordingly, the amount of GABA released from the neuron. Therefore, we hypothesised that glutamic acid decarboxylase (GAD) which generates GABA in accumbal GABAergic neurons, at least partly determines the GABA receptor subtype-mediated GABAergic tonus. To (in)validate this hypothesis, in vivo microdialysis was used to study the effects of an intra-accumbal infusion of the GAD inhibitor l-allylglycine (allylglycine) on the accumbal dopamine efflux of freely moving rats. The intra-accumbal infusion of allylglycine (50.0, 250.0 and 500.0 nmol) dose-dependently increased the accumbal dopamine levels. The co-administration of tetrodotoxin (720 pmol) suppressed the allylglycine (500.0 nmol)-induced dopamine efflux. The intra-accumbal infusion of GABA(B) receptor agonist baclofen (2.5 and 5.0 nmol) inhibited the allylglycine (500.0 nmol)-induced dopamine efflux. The baclofen's effects were counteracted by GABA(B) receptor antagonist saclofen (10.0 nmol). Neither GABA(A) receptor agonist (muscimol: 25.0 and 250.0 pmol) nor antagonist (bicuculline: 50.0 pmol) altered the allylglycine (250.0 and 500.0 nmol)-induced dopamine efflux. The present study provides in vivo neurochemical evidence that newly synthesised GABA that exerts an inhibitory tonus on the accumbal dopaminergic activity, acts at the level of GABA(B) receptors, but not GABA(A) receptors. The present study also shows that there is an allylglycine-insensitive GABA pool that release GABA exerting an inhibitory control of the accumbal dopaminergic activity, at the level of GABA(A) receptors. This article is part of a Special Issue entitled 'Post-Traumatic Stress Disorder'.
[Mh] Termos MeSH primário: Neurônios Dopaminérgicos/metabolismo
Terminações Nervosas/metabolismo
Núcleo Accumbens/metabolismo
Receptores de GABA-A/metabolismo
Receptores de GABA-B/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Alilglicina/farmacologia
Animais
Baclofeno/farmacologia
Dopamina/metabolismo
Neurônios Dopaminérgicos/efeitos dos fármacos
Relação Dose-Resposta a Droga
Antagonistas GABAérgicos/farmacologia
Agonistas de Receptores de GABA-A/farmacologia
Agonistas dos Receptores de GABA-B/farmacologia
Masculino
Microdiálise
Muscimol/farmacologia
Terminações Nervosas/efeitos dos fármacos
Núcleo Accumbens/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GABA Antagonists); 0 (GABA-A Receptor Agonists); 0 (GABA-B Receptor Agonists); 0 (Receptors, GABA-A); 0 (Receptors, GABA-B); 1069-48-3 (Allylglycine); 2763-96-4 (Muscimol); 56-12-2 (gamma-Aminobutyric Acid); H789N3FKE8 (Baclofen); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1207
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111004
[St] Status:MEDLINE
[do] DOI:10.1016/j.neuropharm.2011.09.021


  8 / 108 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:21214240
[Au] Autor:Baron A; Verdié P; Martinez J; Lamaty F
[Ad] Endereço:Institut des Biomolécules Max Mousseron, UMR CNRS, Université Montpellier, France.
[Ti] Título:cis-Apa: a practical linker for the microwave-assisted preparation of cyclic pseudopeptides via RCM cyclative cleavage.
[So] Source:J Org Chem;76(3):766-72, 2011 Feb 04.
[Is] ISSN:1520-6904
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A new linker cis-5-aminopent-3-enoic acid (cis-Apa) was prepared for the synthesis of cyclic pseudopeptides by cyclization-cleavage by using ring-closing methatesis (RCM). We developed a new synthetic pathway for the preparation of the cis-Apa linker that was tested in the cyclization-cleavage process of different RGD peptide sequences. Different macrocyclic peptidomimetics were prepared by using this integrated microwave-assisted method, showing that the readily available cis-Apa amino acid is well adapted as a linker in the cyclization-cleavage process.
[Mh] Termos MeSH primário: Alilglicina/química
Peptídeos Cíclicos/química
Peptídeos Cíclicos/síntese química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Ciclização
Espectroscopia de Ressonância Magnética
Micro-Ondas
Estrutura Molecular
Estereoisomerismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Peptides, Cyclic); 1069-48-3 (Allylglycine)
[Em] Mês de entrada:1105
[Cu] Atualização por classe:110131
[Lr] Data última revisão:
110131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110111
[St] Status:MEDLINE
[do] DOI:10.1021/jo101629v


  9 / 108 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:20023007
[Au] Autor:Tumurkhuu G; Koide N; Hiwasa T; Ookoshi M; Dagvadorj J; Abu Shadat Mohammod Noman; Iftakhar-E-Khuda I; Naiki Y; Komatsu T; Yoshida T; Yokochi T
[Ad] Endereço:Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.
[Ti] Título:ONO 3403, a synthetic serine protease inhibitor, inhibits lipopolysaccharide-induced tumor necrosis factor-{alpha} and nitric oxide production and protects mice from lethal endotoxic shock.
[So] Source:Innate Immun;17(1):97-105, 2011 Feb.
[Is] ISSN:1753-4267
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ONO 3403, a new synthetic serine protease inhibitor, is a derivative of camostat mesilate and has a higher protease-inhibitory activity. The effect of ONO 3403 on lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α and nitric oxide (NO) production in RAW 264.7 macrophage-like cells was examined. ONO 3403 significantly inhibited LPS-induced TNF-α production at a lower concentration than camostat mesilate. It also inhibited LPS-induced NO production. Their inhibition was responsible for the reduced mRNA expression of TNF-α and inducible NO synthase. In LPS-stimulated cells, ONO 3403 prevented the augmentation of MyD88 expression and inhibited the phosphorylation of IκB-α, stress-activated protein kinase (SAPK) and IRF-3, and the production of interferon-ß. ONO 3403 abolished the elevation of the extracellular serine protease activity in response to LPS. Further, it reduced the circulating TNF-α level, hepatic injury and mortality in mice receiving an injection of D-galactosamine and LPS. ONO 3403 was suggested to inhibit LPS-induced inflammatory responses via inactivation of MyD88-dependent and independent pathways.
[Mh] Termos MeSH primário: Alilglicina/análogos & derivados
Benzamidinas/farmacologia
Benzamidinas/uso terapêutico
Lipopolissacarídeos/farmacologia
Macrófagos/metabolismo
Óxido Nítrico/metabolismo
Choque Séptico/prevenção & controle
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Alilglicina/farmacologia
Alilglicina/uso terapêutico
Animais
Linhagem Celular Tumoral
Meios de Cultivo Condicionados/metabolismo
Feminino
Gabexato/análogos & derivados
Gabexato/farmacologia
Expressão Gênica/efeitos dos fármacos
Expressão Gênica/genética
Proteínas I-kappa B/metabolismo
Fator Regulador 3 de Interferon/metabolismo
Interferon gama/sangue
Interleucina-6/metabolismo
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Fígado/efeitos dos fármacos
Fígado/patologia
Macrófagos/efeitos dos fármacos
Macrófagos Peritoneais/efeitos dos fármacos
Macrófagos Peritoneais/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Fator 88 de Diferenciação Mieloide/metabolismo
Inibidor de NF-kappaB alfa
Óxido Nítrico Sintase Tipo II/genética
Óxido Nítrico Sintase Tipo II/metabolismo
Fosforilação/efeitos dos fármacos
Serina Proteases/metabolismo
Inibidores de Serino Proteinase/farmacologia
Inibidores de Serino Proteinase/uso terapêutico
Choque Séptico/sangue
Choque Séptico/patologia
Transdução de Sinais/efeitos dos fármacos
Receptor 4 Toll-Like/metabolismo
Fator de Necrose Tumoral alfa/sangue
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzamidines); 0 (Culture Media, Conditioned); 0 (I-kappa B Proteins); 0 (Interferon Regulatory Factor-3); 0 (Interleukin-6); 0 (Irf3 protein, mouse); 0 (Lipopolysaccharides); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (Nfkbia protein, mouse); 0 (Serine Proteinase Inhibitors); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); 0 (ethyl N-allyl-N-(2-methyl-3-(4-(4-amidinophenoxycarbonyl)phenyl)propenoyl)aminoacetate methanesulfonate); 0FD207WKDU (camostat); 1069-48-3 (Allylglycine); 139874-52-5 (NF-KappaB Inhibitor alpha); 31C4KY9ESH (Nitric Oxide); 4V7M9137X9 (Gabexate); 82115-62-6 (Interferon-gamma); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 3.4.- (Serine Proteases)
[Em] Mês de entrada:1106
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:091222
[St] Status:MEDLINE
[do] DOI:10.1177/1753425909353641


  10 / 108 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:20666508
[Au] Autor:Song W; Wang Y; Yu Z; Vera CI; Qu J; Lin Q
[Ad] Endereço:Department of Chemistry, State University of New York at Buffalo, 14260, USA.
[Ti] Título:A metabolic alkene reporter for spatiotemporally controlled imaging of newly synthesized proteins in Mammalian cells.
[So] Source:ACS Chem Biol;5(9):875-85, 2010 Sep 17.
[Is] ISSN:1554-8937
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The nonsymmetrical spatial distribution of newly synthesized proteins in animal cells plays a central role in many cellular processes. Here, we report that a simple alkene tag, homoallylglycine (HAG), was co-translationally incorporated into a recombinant protein as well as endogenous, newly synthesized proteins in mammalian cells with high efficiency. In conjunction with a photoinduced tetrazole-alkene cycloaddition reaction ("photoclick chemistry"), this alkene tag further served as a bioorthogonal chemical reporter both for the selective protein functionalization in vitro and for a spatiotemporally controlled imaging of the newly synthesized proteins in live mammalian cells. This two-step metabolic alkene tagging-photocontrolled chemical functionalization approach may offer a potentially useful tool to study the role of spatiotemporally regulated protein synthesis in mammalian cells.
[Mh] Termos MeSH primário: Alilglicina/análise
Alilglicina/metabolismo
Biossíntese de Proteínas
Proteínas/análise
Proteínas/metabolismo
[Mh] Termos MeSH secundário: Alilglicina/química
Sequência de Aminoácidos
Animais
Citometria de Fluxo
Células HeLa
Seres Humanos
Microscopia de Fluorescência
Dados de Sequência Molecular
Proteínas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proteins); 1069-48-3 (Allylglycine)
[Em] Mês de entrada:1101
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100730
[St] Status:MEDLINE
[do] DOI:10.1021/cb100193h



página 1 de 11 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