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  1 / 922 MEDLINE  
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[PMID]:28121009
[Au] Autor:Kamaleddin MA
[Ad] Endereço:Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada.
[Ti] Título:Molecular, biophysical, and pharmacological properties of calcium-activated chloride channels.
[So] Source:J Cell Physiol;233(2):787-798, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Calcium-activated chloride channels (CaCCs) are a family of anionic transmembrane ion channels. They are mainly responsible for the movement of Cl and other anions across the biological membranes, and they are widely expressed in different tissues. Since the Cl flow into or out of the cell plays a crucial role in hyperpolarizing or depolarizing the cells, respectively, the impact of intracellular Ca concentration on these channels is attracting a lot of attentions. After summarizing the molecular, biophysical, and pharmacological properties of CaCCs, the role of CaCCs in normal cellular functions will be discussed, and I will emphasize how dysregulation of CaCCs in pathological conditions can account for different diseases. A better understanding of CaCCs and a pivotal regulatory role of Ca can shed more light on the therapeutic strategies for different neurological disorders that arise from chloride dysregulation, such as asthma, cystic fibrosis, and neuropathic pain.
[Mh] Termos MeSH primário: Canais de Cloreto/efeitos dos fármacos
Canais de Cloreto/metabolismo
Cloretos/metabolismo
Moduladores de Transporte de Membrana/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Asma/tratamento farmacológico
Asma/metabolismo
Cálcio/metabolismo
Canais de Cloreto/química
Canais de Cloreto/genética
Fibrose Cística/tratamento farmacológico
Fibrose Cística/metabolismo
Seres Humanos
Ativação do Canal Iônico/efeitos dos fármacos
Potenciais da Membrana
Neuralgia/tratamento farmacológico
Neuralgia/metabolismo
Conformação Proteica
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chloride Channels); 0 (Chlorides); 0 (Membrane Transport Modulators); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25823


  2 / 922 MEDLINE  
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[PMID]:28768770
[Au] Autor:Wu Y; Fortin DA; Cochrane VA; Chen PC; Shyng SL
[Ad] Endereço:From the Department of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland, Oregon 97239 and.
[Ti] Título:NMDA receptors mediate leptin signaling and regulate potassium channel trafficking in pancreatic ß-cells.
[So] Source:J Biol Chem;292(37):15512-15524, 2017 Sep 15.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NMDA receptors (NMDARs) are Ca -permeant, ligand-gated ion channels activated by the excitatory neurotransmitter glutamate and have well-characterized roles in the nervous system. The expression and function of NMDARs in pancreatic ß-cells, by contrast, are poorly understood. Here, we report a novel function of NMDARs in ß-cells. Using a combination of biochemistry, electrophysiology, and imaging techniques, we now show that NMDARs have a key role in mediating the effect of leptin to modulate ß-cell electrical activity by promoting AMP-activated protein kinase (AMPK)-dependent trafficking of K and Kv2.1 channels to the plasma membrane. Blocking NMDAR activity inhibited the ability of leptin to activate AMPK, induce K and Kv2.1 channel trafficking, and promote membrane hyperpolarization. Conversely, activation of NMDARs mimicked the effect of leptin, causing Ca influx, AMPK activation, and increased trafficking of K and Kv2.1 channels to the plasma membrane, and triggered membrane hyperpolarization. Moreover, leptin potentiated NMDAR currents and triggered NMDAR-dependent Ca influx. Importantly, NMDAR-mediated signaling was observed in rat insulinoma 832/13 cells and in human ß-cells, indicating that this pathway is conserved across species. The ability of NMDARs to regulate potassium channel surface expression and thus, ß-cell excitability provides mechanistic insight into the recently reported insulinotropic effects of NMDAR antagonists and therefore highlights the therapeutic potential of these drugs in managing type 2 diabetes.
[Mh] Termos MeSH primário: Células Secretoras de Insulina/metabolismo
Canais KATP/metabolismo
Leptina/metabolismo
Receptores de N-Metil-D-Aspartato/agonistas
Canais de Potássio Shab/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/antagonistas & inibidores
Proteínas Quinases Ativadas por AMP/metabolismo
Adulto
Animais
Biotinilação
Sinalização do Cálcio/efeitos dos fármacos
Linhagem Celular Tumoral
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Células Cultivadas
Seres Humanos
Insulina/secreção
Células Secretoras de Insulina/citologia
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/secreção
Ligantes
Moduladores de Transporte de Membrana/farmacologia
Transporte Proteico/efeitos dos fármacos
Ratos
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Receptores de N-Metil-D-Aspartato/metabolismo
Transdução de Sinais/efeitos dos fármacos
Propriedades de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (KATP Channels); 0 (KCNB1 protein, human); 0 (Kcnb1 protein, rat); 0 (Leptin); 0 (Ligands); 0 (Membrane Transport Modulators); 0 (Receptors, N-Methyl-D-Aspartate); 0 (Shab Potassium Channels); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.802249


  3 / 922 MEDLINE  
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[PMID]:28731329
[Au] Autor:Schenck S; Kunz L; Sahlender D; Pardon E; Geertsma ER; Savtchouk I; Suzuki T; Neldner Y; Stefanic S; Steyaert J; Volterra A; Dutzler R
[Ad] Endereço:Department of Biochemistry, University of Zurich , Winterthurerstrasse 190, 8057 Zurich, Switzerland.
[Ti] Título:Generation and Characterization of Anti-VGLUT Nanobodies Acting as Inhibitors of Transport.
[So] Source:Biochemistry;56(30):3962-3971, 2017 Aug 01.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The uptake of glutamate by synaptic vesicles is mediated by vesicular glutamate transporters (VGLUTs). The central role of these transporters in excitatory neurotransmission underpins their importance as pharmacological targets. Although several compounds inhibit VGLUTs, highly specific inhibitors were so far unavailable, thus limiting applications to in vitro experiments. Besides their potential in pharmacology, specific inhibitors would also be beneficial for the elucidation of transport mechanisms. To overcome this shortage, we generated nanobodies (Nbs) by immunization of a llama with purified rat VGLUT1 and subsequent selection of binders from a phage display library. All identified Nbs recognize cytosolic epitopes, and two of the binders greatly reduced the rate of uptake of glutamate by reconstituted liposomes and subcellular fractions enriched with synaptic vesicles. These Nbs can be expressed as functional green fluorescent protein fusion proteins in the cytosol of HEK cells for intracellular applications as immunocytochemical and biochemical agents. The selected binders thus provide valuable tools for cell biology and neuroscience.
[Mh] Termos MeSH primário: Depressores do Sistema Nervoso Central/farmacologia
Córtex Cerebral/efeitos dos fármacos
Moduladores de Transporte de Membrana/farmacologia
Modelos Moleculares
Proteínas do Tecido Nervoso/antagonistas & inibidores
Neurônios/efeitos dos fármacos
Anticorpos de Domínio Único/farmacologia
Proteína Vesicular 1 de Transporte de Glutamato/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Transporte Biológico/efeitos dos fármacos
Camelídeos Americanos
Células Cultivadas
Depressores do Sistema Nervoso Central/química
Depressores do Sistema Nervoso Central/metabolismo
Córtex Cerebral/citologia
Córtex Cerebral/metabolismo
Embrião de Mamíferos/citologia
Ácido Glutâmico/metabolismo
Proteínas de Fluorescência Verde/química
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Células HEK293
Seres Humanos
Moduladores de Transporte de Membrana/química
Moduladores de Transporte de Membrana/metabolismo
Camundongos
Proteínas do Tecido Nervoso/química
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Neurônios/citologia
Neurônios/metabolismo
Biblioteca de Peptídeos
Ratos
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Anticorpos de Domínio Único/química
Anticorpos de Domínio Único/genética
Anticorpos de Domínio Único/metabolismo
Transmissão Sináptica/efeitos dos fármacos
Vesículas Sinápticas/efeitos dos fármacos
Vesículas Sinápticas/metabolismo
Proteína Vesicular 1 de Transporte de Glutamato/química
Proteína Vesicular 1 de Transporte de Glutamato/genética
Proteína Vesicular 1 de Transporte de Glutamato/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Central Nervous System Depressants); 0 (Membrane Transport Modulators); 0 (Nerve Tissue Proteins); 0 (Peptide Library); 0 (Recombinant Fusion Proteins); 0 (Single-Domain Antibodies); 0 (Slc17a7 protein, rat); 0 (Vesicular Glutamate Transport Protein 1); 147336-22-9 (Green Fluorescent Proteins); 3KX376GY7L (Glutamic Acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00436


  4 / 922 MEDLINE  
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[PMID]:28682870
[Au] Autor:Li J; Gong Y; Li C; Lu Y; Liu Y; Shao Y
[Ad] Endereço:aDepartment of Geriatric Endocrinology bOutpatient Department, Chinese PLA General Hospital, Beijing 100853, China.
[Ti] Título:Long-term efficacy and safety of sodium-glucose cotransporter-2 inhibitors as add-on to metformin treatment in the management of type 2 diabetes mellitus: A meta-analysis.
[So] Source:Medicine (Baltimore);96(27):e7201, 2017 Jul.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Drug intensification is often required for patients with type 2 diabetes mellitus on stable metformin therapy. Among the potential candidates for a combination therapy, sodium-glucose transporter-2 (SGLT2) inhibitors have shown promising outcomes. This meta-analysis was performed to compare the efficacy and safety of SGLT2 inhibitors with non-SGLT2 combinations as add-on treatment to metformin. METHODS: Literature search was carried out in multiple electronic databases for the acquisition of relevant randomized controlled trials (RCTs) by following a priori eligibility criteria. After the assessment of quality of the included RCTs, meta-analyses of mean differences or odds ratios (OR) were performed to achieve overall effect sizes of the changes from baseline in selected efficacy and safety endpoints reported in the individual studies. Between-studies heterogeneity was estimated with between-studies statistical heterogeneity (I) index. RESULTS: Six RCTs fulfilled the eligibility criteria. SGLT2 inhibitors as add-on to metformin treatment reduced % HbA1c significantly more than non-SGLT2 combinations after 52 weeks (P = .002) as well as after 104 weeks (P < .00001). Among other endpoints, SGLT2 inhibitors also reduced fasting plasma glucose levels, body weight, systolic, and diastolic blood pressures after 52 weeks and 104 weeks significantly (P < .00001) more than non-SGLT2 combinations. Incidence of hypoglycemia was significantly lower (P = .02) but incidence of suspected or confirmed genital tract infections was significantly higher (P < .00001) in SGLT2 inhibitors treated in comparison with non-SGLT2 combinations. CONCLUSION: As add-on to metformin treatment, SGLT2 inhibitors are found significantly more efficacious than non-SGLT2 inhibitor combinations in the management of type 2 diabetes mellitus, although, SGLT2 inhibitor therapy is associated with significantly higher incidence of suspected or confirmed genital tract infections.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Hipoglicemiantes/uso terapêutico
Moduladores de Transporte de Membrana/uso terapêutico
Metformina/uso terapêutico
Transportador 2 de Glucose-Sódio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Quimioterapia Combinada
Seres Humanos
Hipoglicemiantes/efeitos adversos
Moduladores de Transporte de Membrana/efeitos adversos
Ensaios Clínicos Controlados Aleatórios como Assunto
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Membrane Transport Modulators); 0 (SLC5A2 protein, human); 0 (Sodium-Glucose Transporter 2); 9100L32L2N (Metformin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007201


  5 / 922 MEDLINE  
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[PMID]:28600454
[Au] Autor:Smith CO; Nehrke K; Brookes PS
[Ad] Endereço:Department of Biochemistry, University of Rochester Medical Center, Rochester, NY, U.S.A.
[Ti] Título:The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection.
[So] Source:Biochem J;474(12):2067-2094, 2017 Jun 09.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondria play an important role in tissue ischemia and reperfusion (IR) injury, with energetic failure and the opening of the mitochondrial permeability transition pore being the major causes of IR-induced cell death. Thus, mitochondria are an appropriate focus for strategies to protect against IR injury. Two widely studied paradigms of IR protection, particularly in the field of cardiac IR, are ischemic preconditioning (IPC) and volatile anesthetic preconditioning (APC). While the molecular mechanisms recruited by these protective paradigms are not fully elucidated, a commonality is the involvement of mitochondrial K channel opening. In the case of IPC, research has focused on a mitochondrial ATP-sensitive K channel (mitoK ), but, despite recent progress, the molecular identity of this channel remains a subject of contention. In the case of APC, early research suggested the existence of a mitochondrial large-conductance K (BK, big conductance of potassium) channel encoded by the gene, although more recent work has shown that the channel that underlies APC is in fact encoded by In this review, we discuss both the pharmacologic and genetic evidence for the existence and identity of mitochondrial K channels, and the role of these channels both in IR protection and in regulating normal mitochondrial function.
[Mh] Termos MeSH primário: Alostase
Mitocôndrias Cardíacas/metabolismo
Modelos Biológicos
Isquemia Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/metabolismo
Canais de Potássio/metabolismo
[Mh] Termos MeSH secundário: Animais
Cardiotônicos/farmacologia
Seres Humanos
Ativação do Canal Iônico/efeitos dos fármacos
Precondicionamento Isquêmico Miocárdico
Canais KATP/agonistas
Canais KATP/antagonistas & inibidores
Canais KATP/genética
Canais KATP/metabolismo
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/agonistas
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/antagonistas & inibidores
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/genética
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/metabolismo
Moduladores de Transporte de Membrana/farmacologia
Mitocôndrias Cardíacas/efeitos dos fármacos
Isquemia Miocárdica/terapia
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Bloqueadores dos Canais de Potássio/farmacologia
Canais de Potássio/agonistas
Canais de Potássio/química
Canais de Potássio/genética
Isoformas de Proteínas/agonistas
Isoformas de Proteínas/antagonistas & inibidores
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Terminologia como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cardiotonic Agents); 0 (KATP Channels); 0 (KCNMA1 protein, human); 0 (KCNT2 protein, human); 0 (Large-Conductance Calcium-Activated Potassium Channel alpha Subunits); 0 (Membrane Transport Modulators); 0 (Potassium Channel Blockers); 0 (Potassium Channels); 0 (Protein Isoforms)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170611
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20160623


  6 / 922 MEDLINE  
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[PMID]:28403877
[Au] Autor:Cha SA; Park YM; Yun JS; Lim TS; Song KH; Yoo KD; Ahn YB; Ko SH
[Ad] Endereço:Department of Internal Medicine, Division of Endocrinology and Metabolism, College of Medicine, The Catholic University of Korea, St. Vincent's Hospital, 93 Jungbu - daero, Paldal - gu, Suwon, Gyeonggi - do, Seoul, 442-723, Republic of Korea.
[Ti] Título:A comparison of effects of DPP-4 inhibitor and SGLT2 inhibitor on lipid profile in patients with type 2 diabetes.
[So] Source:Lipids Health Dis;16(1):58, 2017 Apr 13.
[Is] ISSN:1476-511X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Previous studies suggest that dipeptidyl peptidase-4 (DPP-4) inhibitors and sodium glucose cotransporter 2 (SGLT2) inhibitors have different effects on the lipid profile in patients with type 2 diabetes. We investigated the effects of DPP-4 inhibitors and SGLT2 inhibitors on the lipid profile in patients with type 2 diabetes. METHODS: From January 2013 to December 2015, a total of 228 patients with type 2 diabetes who were receiving a DPP-4 inhibitor or SGLT2 inhibitor as add-on therapy to metformin and/or a sulfonylurea were consecutively enrolled. We compared the effects of DPP-4 inhibitors and SGLT2 inhibitors on the lipid profile at baseline and after 24 weeks of treatment. To compare lipid parameters between the two groups, we used the analysis of covariance (ANCOVA). RESULTS: A total of 184 patients completed follow-up (mean age: 53.1 ± 6.9 years, mean duration of diabetes: 7.1 ± 5.7 years). From baseline to 24 weeks, HDL-cholesterol (HDL-C) levels were increased by 0.5 (95% CI, -0.9 to 2.0) mg/dl with a DPP-4 inhibitor and by 5.1 (95% CI, 3.0 to 7.1) mg/dl with an SGLT2 inhibitor (p = 0.001). LDL-cholesterol (LDL-C) levels were reduced by 8.4 (95% CI, -14.0 to -2.8) mg/dl with a DPP-4 inhibitor, but increased by 1.3 (95% CI, -5.1 to 7.6) mg/dl with an SGLT2 inhibitor (p = 0.046). There was no significant difference in the mean hemoglobin A1c (8.3 ± 1.1 vs. 8.0 ± 0.9%, p = 0.110) and in the change of total cholesterol (TC) (p = 0.836), triglyceride (TG) (p = 0.867), apolipoprotein A (p = 0.726), apolipoprotein B (p = 0.660), and lipoprotein (a) (p = 0.991) between the DPP-4 inhibitor and the SGLT2 inhibitor. CONCLUSIONS: The SGLT2 inhibitor was associated with a significant increase in HDL-C and LDL-C after 24 weeks of SGLT2 inhibitor treatment in patients with type 2 diabetes compared with those with DPP-4 inhibitor treatment in this study. TRIAL REGISTRATION: This study was conducted by retrospective medical record review.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/prevenção & controle
Diabetes Mellitus Tipo 2/tratamento farmacológico
Angiopatias Diabéticas/prevenção & controle
Cardiomiopatias Diabéticas/prevenção & controle
Inibidores da Dipeptidil Peptidase IV/uso terapêutico
Moduladores de Transporte de Membrana/uso terapêutico
Transportador 2 de Glucose-Sódio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Compostos Benzidrílicos/efeitos adversos
Compostos Benzidrílicos/uso terapêutico
Doenças Cardiovasculares/complicações
Doenças Cardiovasculares/epidemiologia
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/complicações
Diabetes Mellitus Tipo 2/metabolismo
Angiopatias Diabéticas/epidemiologia
Cardiomiopatias Diabéticas/epidemiologia
Inibidores da Dipeptidil Peptidase IV/efeitos adversos
Quimioterapia Combinada/efeitos adversos
Feminino
Seguimentos
Glucosídeos/efeitos adversos
Glucosídeos/uso terapêutico
Hemoglobina A Glicada/análise
Seres Humanos
Hiperglicemia/prevenção & controle
Hiperlipidemias/complicações
Hiperlipidemias/epidemiologia
Hiperlipidemias/prevenção & controle
Linagliptina/efeitos adversos
Linagliptina/uso terapêutico
Masculino
Moduladores de Transporte de Membrana/efeitos adversos
Meia-Idade
Piperidonas/efeitos adversos
Piperidonas/uso terapêutico
Pirimidinas/efeitos adversos
Pirimidinas/uso terapêutico
República da Coreia/epidemiologia
Estudos Retrospectivos
Fatores de Risco
Transportador 2 de Glucose-Sódio/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (2-(3-(4-ethoxybenzyl)-4-chlorophenyl)-6-hydroxymethyltetrahydro-2H-pyran-3,4,5-triol); 0 (Benzhydryl Compounds); 0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Glucosides); 0 (Glycated Hemoglobin A); 0 (LC15-0444); 0 (Membrane Transport Modulators); 0 (Piperidones); 0 (Pyrimidines); 0 (Sodium-Glucose Transporter 2); 0 (hemoglobin A1c protein, human); 3X29ZEJ4R2 (Linagliptin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1186/s12944-017-0443-4


  7 / 922 MEDLINE  
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[PMID]:28330845
[Au] Autor:Praetorius J; Damkier HH
[Ad] Endereço:Department of Biomedicine, Health, Aarhus University, Aarhus, Denmark; and jp@biomed.au.dk.
[Ti] Título:Transport across the choroid plexus epithelium.
[So] Source:Am J Physiol Cell Physiol;312(6):C673-C686, 2017 Jun 01.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The choroid plexus epithelium is a secretory epithelium par excellence. However, this is perhaps not the most prominent reason for the massive interest in this modest-sized tissue residing inside the brain ventricles. Most likely, the dominant reason for extensive studies of the choroid plexus is the identification of this epithelium as the source of the majority of intraventricular cerebrospinal fluid. This finding has direct relevance for studies of diseases and conditions with deranged central fluid volume or ionic balance. While the concept is supported by the vast majority of the literature, the implication of the choroid plexus in secretion of the cerebrospinal fluid was recently challenged once again. Three newer and promising areas of current choroid plexus-related investigations are as follows: ) the choroid plexus epithelium as the source of mediators necessary for central nervous system development, ) the choroid plexus as a route for microorganisms and immune cells into the central nervous system, and ) the choroid plexus as a potential route for drug delivery into the central nervous system, bypassing the blood-brain barrier. Thus, the purpose of this review is to highlight current active areas of research in the choroid plexus physiology and a few matters of continuous controversy.
[Mh] Termos MeSH primário: Líquido Cefalorraquidiano/fisiologia
Plexo Corióideo/fisiologia
Epitélio/fisiologia
Canais Iônicos/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
Transporte Biológico
Barreira Hematoencefálica
Plexo Corióideo/ultraestrutura
Expressão Gênica
Seres Humanos
Concentração de Íons de Hidrogênio
Molécula 1 de Adesão Intercelular/líquido cefalorraquidiano
Molécula 1 de Adesão Intercelular/genética
Canais Iônicos/antagonistas & inibidores
Canais Iônicos/genética
Moduladores de Transporte de Membrana/farmacologia
Molécula 1 de Adesão de Célula Vascular/líquido cefalorraquidiano
Molécula 1 de Adesão de Célula Vascular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (ICAM1 protein, human); 0 (Ion Channels); 0 (Membrane Transport Modulators); 0 (Vascular Cell Adhesion Molecule-1); 126547-89-5 (Intercellular Adhesion Molecule-1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00041.2017


  8 / 922 MEDLINE  
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[PMID]:28298475
[Au] Autor:Toussaint F; Pierman B; Bertin A; Lévy D; Boutry M
[Ad] Endereço:Institut des Sciences de la Vie, Université catholique de Louvain, B-1348 Louvain-la-Neuve, Belgium.
[Ti] Título:Purification and biochemical characterization of NpABCG5/NpPDR5, a plant pleiotropic drug resistance transporter expressed in BY-2 suspension cells.
[So] Source:Biochem J;474(10):1689-1703, 2017 May 04.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pleiotropic drug resistance (PDR) transporters belong to the ABCG subfamily of ATP-binding cassette (ABC) transporters and are involved in the transport of various molecules across plasma membranes. During evolution, genes appeared independently in fungi and in plants from a duplication of a half-size ABC gene. The enzymatic properties of purified PDR transporters from yeast have been characterized. This is not the case for any plant PDR transporter, or, incidentally, for any purified plant ABC transporter. Yet, plant PDR transporters play important roles in plant physiology such as hormone signaling or resistance to pathogens or herbivores. Here, we describe the expression, purification, enzymatic characterization and 2D analysis by electron microscopy of NpABCG5/NpPDR5 from , which has been shown to be involved in the plant defense against herbivores. We constitutively expressed NpABCG5/NpPDR5, provided with a His-tag in a homologous system: suspension cells from (Bright Yellow 2 line). NpABCG5/NpPDR5 was targeted to the plasma membrane and was solubilized by dodecyl maltoside and purified by Ni-affinity chromatography. The ATP-hydrolyzing specific activity (27 nmol min mg ) was stimulated seven-fold in the presence of 0.1% asolectin. Electron microscopy analysis indicated that NpABCG5/NpPDR5 is monomeric and with dimensions shorter than those of known ABC transporters. Enzymatic data (optimal pH and sensitivity to inhibitors) confirmed that plant and fungal PDR transporters have different properties. These data also show that suspension cells are a convenient host for the purification and biochemical characterization of ABC transporters.
[Mh] Termos MeSH primário: Membro 5 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo
Proteínas de Plantas/metabolismo
Tabaco/metabolismo
[Mh] Termos MeSH secundário: Membro 5 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/química
Membro 5 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/genética
Membro 5 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/isolamento & purificação
Adenosina Trifosfatases/química
Adenosina Trifosfatases/genética
Adenosina Trifosfatases/isolamento & purificação
Adenosina Trifosfatases/metabolismo
Trifosfato de Adenosina/metabolismo
Técnicas de Cultura Celular por Lotes
Reatores Biológicos
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Membrana Celular/ultraestrutura
Células Cultivadas
Cromatografia de Afinidade
Detergentes/química
Glucosídeos/química
Concentração de Íons de Hidrogênio
Processamento de Imagem Assistida por Computador
Moduladores de Transporte de Membrana/farmacologia
Microscopia Eletrônica
Peso Molecular
Fosfatidilcolinas/química
Proteínas de Plantas/química
Proteínas de Plantas/genética
Proteínas de Plantas/isolamento & purificação
Conformação Proteica
Transporte Proteico/efeitos dos fármacos
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/isolamento & purificação
Proteínas Recombinantes de Fusão/metabolismo
Solubilidade
Tabaco/citologia
Tabaco/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP Binding Cassette Transporter, Sub-Family G, Member 5); 0 (Detergents); 0 (Glucosides); 0 (Membrane Transport Modulators); 0 (Phosphatidylcholines); 0 (Plant Proteins); 0 (Recombinant Fusion Proteins); 69227-93-6 (dodecyl maltoside); 69279-91-0 (asolectin); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.1.- (Adenosine Triphosphatases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20170108


  9 / 922 MEDLINE  
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[PMID]:28286997
[Au] Autor:Salata C; Calistri A; Parolin C; Baritussio A; Palù G
[Ad] Endereço:a Department of Molecular Medicine , University of Padova , Padova , Italy.
[Ti] Título:Antiviral activity of cationic amphiphilic drugs.
[So] Source:Expert Rev Anti Infect Ther;15(5):483-492, 2017 May.
[Is] ISSN:1744-8336
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Emerging and reemerging viral infections represent a major concern for human and veterinary public health and there is an urgent need for the development of broad-spectrum antivirals. Areas covered: A recent strategy in antiviral research is based on the identification of molecules targeting host functions required for infection of multiple viruses. A number of FDA-approved drugs used to treat several human diseases are cationic amphiphilic drugs (CADs) that have the ability to accumulate inside cells affecting several structures/functions hijacked by viruses during infection. In this review we summarized the CADs' chemical properties and effects on the cells and reported the main FDA-approved CADs that have been identified so far as potential antivirals in drug repurposing studies. Expert commentary: Although there have been concerns regarding the efficacy and the possible side effects of the off-label use of CADs as antivirals, they seem to represent a promising starting point for the development of broad-spectrum antiviral strategies. Further knowledge about their mechanism of action is required to improve their antiviral activity and to reduce the risk of side effects.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Reposicionamento de Medicamentos
Interações Hospedeiro-Patógeno/efeitos dos fármacos
Uso Off-Label
Tensoativos/uso terapêutico
Viroses/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antiarrítmicos/uso terapêutico
Antimaláricos/uso terapêutico
Seres Humanos
Moduladores de Transporte de Membrana/uso terapêutico
Inibidores de Proteínas Quinases/uso terapêutico
Psicotrópicos/uso terapêutico
Viroses/virologia
Vírus/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Antimalarials); 0 (Antiviral Agents); 0 (Membrane Transport Modulators); 0 (Protein Kinase Inhibitors); 0 (Psychotropic Drugs); 0 (Surface-Active Agents)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE
[do] DOI:10.1080/14787210.2017.1305888


  10 / 922 MEDLINE  
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[PMID]:28274820
[Au] Autor:Andersson R; Galter D; Papadia D; Fisahn A
[Ad] Endereço:Neuronal Oscillations Laboratory, Neurogeriatrics Division, Center for Alzheimer Research, Dept. of Neurobiology, Care Sciences and Society, Karolinska Institutet, 14186 Stockholm, Sweden.
[Ti] Título:Histamine induces KCNQ channel-dependent gamma oscillations in rat hippocampus via activation of the H1 receptor.
[So] Source:Neuropharmacology;118:13-25, 2017 May 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Histamine is an aminergic neurotransmitter, which regulates wakefulness, arousal and attention in the central nervous system. Histamine receptors have been the target of efforts to develop pro-cognitive drugs to treat disorders such as Alzheimer's disease and schizophrenia. Cognitive functions including attention are closely associated with gamma oscillations, a rhythmical electrical activity pattern in the 30-80 Hz range, which depends on the synchronized activity of excitatory pyramidal cells and inhibitory fast-spiking interneurons. We set out to explore whether histamine has a role in promoting gamma oscillations in the hippocampus. Using in-situ hybridization we demonstrate that histamine receptor subtypes 1, 2 and 3 are expressed in stratum pyramidale of area CA3 in rats. We show that both pyramidal cells and fast-spiking interneurons depolarize and increase action potential firing in response to histamine in vitro. The activation of histamine receptors generates dose-dependent, transient gamma oscillations in area CA3 of the hippocampus - the locus of the gamma rhythm generator. We also demonstrate that this histamine effect is independent of muscarinic receptors. Using specific antagonists we provide evidence that histamine gamma rhythmogenesis specifically depends on the H1 receptor. Histamine also depolarized both pyramidal cells and fast-spiking interneurons and increased membrane resistance in pyramidal cells. The increased membrane resistance is potentially mediated by the inhibition of potassium channels because application of the KCNQ channel opener ICA110381 abolished the oscillations. Taken together our data demonstrate a novel and physiological mechanism for generating gamma oscillations in hippocampus and suggest a role for KCNQ channels in this cognition-relevant brain activity.
[Mh] Termos MeSH primário: Ritmo Gama/efeitos dos fármacos
Hipocampo
Histamínicos/farmacologia
Histamina/farmacologia
Canais de Potássio KCNQ/metabolismo
Receptores Histamínicos/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Animais Recém-Nascidos
Benzamidas/farmacologia
Glutamato Descarboxilase/metabolismo
Hipocampo/citologia
Hipocampo/efeitos dos fármacos
Hipocampo/fisiologia
Técnicas In Vitro
Masculino
Moduladores de Transporte de Membrana/farmacologia
Rede Nervosa/efeitos dos fármacos
Rede Nervosa/fisiologia
Neurônios/efeitos dos fármacos
Neurotransmissores/farmacologia
Piridinas/farmacologia
Ratos
Ratos Sprague-Dawley
Ubiquitina Tiolesterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-chloro-N-(6-chloropyridin-3-yl)benzamide); 0 (Benzamides); 0 (Histamine Agents); 0 (KCNQ Potassium Channels); 0 (Membrane Transport Modulators); 0 (Neurotransmitter Agents); 0 (Pyridines); 0 (Receptors, Histamine); 820484N8I3 (Histamine); EC 3.4.19.12 (Ubiquitin Thiolesterase); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE



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