Search results for "ACIDS"

showing 10 items of 3520 documents

Histone deacetylase inhibitors: apoptotic effects and clinical implications (Review).

2008

It has been shown that epigenetic modifications play an important role in tumorigenesis. Thus, affecting epigenetic tumorigenic alterations can represent a promising strategy for anticancer targeted therapy. Among the key chromatin modifying enzymes which influence gene expression, histone acetyltransferases (HATs) and histone deacetylases (HDACs) have recently attracted interest because of their impact on tumor development and progression. Increased expression of HDACs and disrupted activities of HATs have been found in several tumor types, with a consequent hypoacetylated state of chromatin that can be strictly correlated with low expression of either tumor suppressor or pro-apoptotic gen…

Cancer Researchmedicine.drug_classAntineoplastic AgentsApoptosisBiologyHydroxamic AcidsModels BiologicalRomidepsinEpigenesis Geneticchemistry.chemical_compoundDepsipeptidesNeoplasmsSettore BIO/10 - BiochimicamedicineHumansEpigeneticsVorinostatSulfonamidesVorinostatHistone deacetylase inhibitorHDACI apoptosisChromatinChromatinProtein Structure TertiaryGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsHistoneOncologychemistryModels ChemicalCancer researchbiology.proteinHistone deacetylaseBelinostatmedicine.drug
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Beyond cholesterol reduction, the pleiotropic effects of statins: is their use in cancer prevention hype or hope?

2013

ISSN 1758-4299 10.2217/CLP.13.29 © 2013 Future Medicine Ltd Clin. Lipidol. (2013) 8(3), 273–277 Pleiotropic effects of statins Millions of patients worldwide are currently tak­ ing prescribed statins. Clinical trials have dem­ onstrated that statins reduce the risk of cardio­ vascular disease [1]. Statins are well known to reduce cholesterol levels through the inhibition of 3­hydroxy­methylglutaryl CoA reductase [2]. However, great interest has recently been paid to the mechanisms beyond cholesterol reduc­ tion (pleiotropic effects) by which statins exert their action. Indeed, statins are associated with plaque stabilization and improvement of endo­ thelial function, as well as anti­inflamm…

Cancer preventionIsoprenoid synthesisbusiness.industryCholesterolEndocrinology Diabetes and Metabolismnutritional and metabolic diseasesContext (language use)Pharmacologyanticancer drugs cancer chemotherapeutics statins tumorchemistry.chemical_compoundchemistryAntithromboticMedicinelipids (amino acids peptides and proteins)cardiovascular diseasesCardiology and Cardiovascular MedicinebusinessClinical Lipidology
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Interacciones dieta-genotipo entre el consumo de grasas y polimorfismos comunes determinando el metabolismo lipídico

2009

Las recomendaciones dietéticas actuales referentes al consumo de grasas en la dieta han sido realizadas sin tener en cuenta las posibles diferencias genéticas de las personas que podrían ser las responsables de las diferentes respuestas interindividuales que frecuentemente se observan ante la misma dieta. La presencia de variabilidad genética ha sido puesta de manifiesto para todos los genes relacionados con el metabolismo lipídico, por lo que existe un ingente número de genes y de variantes genéticas para ser incluidas en los estudios sobre interacciones dieta-genotipo en el ámbito específico del consumo de grasas y aceites. Se revisarán algunos ejemplos sobre interacciones grasa-genotipo.…

Candidate genemedicine.medical_specialtyInteractionPopulationNutrigenéticalcsh:TX341-641BiologyDieta; Genes; Interacción; Lípidos; Nutrigenética; PolimorfismosLípidosNutrigeneticsInteracciónNutrigenéticaInternal medicineAPOA1 GenemedicineTX341-641PPARA GeneGenetic variabilityeducationNutrigeneticsGeneticseducation.field_of_studyNutrition. Foods and food supplyOrganic ChemistryPolimorfismosLipid metabolism:CIENCIAS MÉDICAS [UNESCO]LipidsDietEndocrinologyNutrigenomicsGenesInteracciónUNESCO::CIENCIAS MÉDICASLípidoslipids (amino acids peptides and proteins)DietaPolymorphismslcsh:Nutrition. Foods and food supplyFood Science
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Anti-inflammatory lipoxin A4 is an endogenous allosteric enhancer of CB1 cannabinoid receptor.

2012

Allosteric modulation of G-protein–coupled receptors represents a key goal of current pharmacology. In particular, endogenous allosteric modulators might represent important targets of interventions aimed at maximizing therapeutic efficacy and reducing side effects of drugs. Here we show that the anti-inflammatory lipid lipoxin A 4 is an endogenous allosteric enhancer of the CB 1 cannabinoid receptor. Lipoxin A 4 was detected in brain tissues, did not compete for the orthosteric binding site of the CB 1 receptor (vs. 3 H-SR141716A), and did not alter endocannabinoid metabolism (as opposed to URB597 and MAFP), but it enhanced affinity of anandamide at the CB1 receptor, thereby potentiating …

Cannabinoid receptorAllosteric regulationAnti-Inflammatory AgentsSpatial BehaviorEndogenyAmyloidogenic ProteinsMice TransgenicBiologyPharmacologyReceptors G-Protein-Coupled03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineReceptor Cannabinoid CB1In vivoMemoryCommentariesAnimalsReceptor030304 developmental biologyInflammationMice Knockout0303 health sciencesMultidisciplinarymusculoskeletal neural and ocular physiologyBrainAnandamideURB597Biological SciencesEndocannabinoid system3. Good healthLipoxinsMice Inbred C57BLKineticsNeuroprotective Agentschemistrynervous systemlipids (amino acids peptides and proteins)030217 neurology & neurosurgerypsychological phenomena and processesAllosteric SiteEndocannabinoidsProceedings of the National Academy of Sciences of the United States of America
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The Endocannabinoid System Promotes Astroglial Differentiation by Acting on Neural Progenitor Cells

2006

Endocannabinoids exert an important neuromodulatory role via presynaptic cannabinoid CB1receptors and may also participate in the control of neural cell death and survival. The function of the endocannabinoid system has been extensively studied in differentiated neurons, but its potential role in neural progenitor cells remains to be elucidated. Here we show that the CB1receptor and the endocannabinoid-inactivating enzyme fatty acid amide hydrolase are expressed, bothin vitroandin vivo, in postnatal radial glia (RC2+cells) and in adult nestin type I (nestin+GFAP+) neural progenitor cells. Cell culture experiments show that CB1receptor activation increases progenitor proliferation and differ…

Cannabinoid receptorCellular differentiationMorpholinesApoptosisNerve Tissue ProteinsBiologyNaphthalenesHippocampusAmidohydrolasesNestinMiceIntermediate Filament ProteinsReceptor Cannabinoid CB1Cannabinoid Receptor ModulatorsGlial Fibrillary Acidic ProteinAnimalsProgenitor cellEnzyme InhibitorsNeural cellCells CulturedProgenitorMice KnockoutNeuronsCannabinoidsmusculoskeletal neural and ocular physiologyGeneral NeuroscienceStem CellsCell DifferentiationArticlesNestinEndocannabinoid systemNeural stem cellBenzoxazinesRatsnervous systemAstrocytesBenzamideslipids (amino acids peptides and proteins)CarbamatesNeurosciencepsychological phenomena and processesEndocannabinoids
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The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB(1)).

2012

Endocannabinoids exert numerous effects in the CNS under physiological and pathological conditions. The aim of the present study was to examine whether the endocannabinoid N-arachidonoyldopamine (NADA) may protect neurons in excitotoxically lesioned organotypic hippocampal slice cultures (OHSC). OHSC were excitotoxically lesioned by application of N-methyl-d-aspartate (NMDA, 50 μM) for 4 h and subsequently treated with different NADA concentrations (0.1 pM-50 μM) alone or in combination with cannabinoid receptor antagonists. NADA protected dentate gyrus granule cells and caused a slight reduction in the number of microglial cells. The number of degenerated neurons significantly decreased be…

Cannabinoid receptorDopamineTRPV1Arachidonic AcidsPharmacologyNeuroprotectionHippocampusCellular and Molecular NeuroscienceMicePiperidinesReceptor Cannabinoid CB1Neuronal damageAnimalsRats WistarCells CulturedPharmacologyNeuronsChemistryDentate gyrusExcitatory Postsynaptic PotentialsEndocannabinoid systemRatsNeuroprotective Agentsnervous systemNerve DegenerationCannabinoid receptor antagonistNMDA receptorPyrazolesNeuropharmacology
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Cannabinoid CB1 receptors regulate neuronal TNF-α effects in experimental autoimmune encephalomyelitis.

2011

Abstract Cannabinoid CB1 receptors (CB1Rs) regulate the neurodegenerative damage of experimental autoimmune encephalomyelitis (EAE) and of multiple sclerosis (MS). The mechanism by which CB1R stimulation exerts protective effects is still unclear. Here we show that pharmacological activation of CB1Rs dampens the tumor necrosis factor α (TNFα)-mediated potentiation of striatal spontaneous glutamate-mediated excitatory postsynaptic currents (EPSCs), which is believed to cogently contribute to the inflammation-induced neurodegenerative damage observed in EAE mice. Furthermore, mice lacking CB1Rs showed a more severe clinical course and, in parallel, exacerbated alterations of sEPSC duration af…

Cannabinoid receptorEncephalomyelitis Autoimmune ExperimentalPolyunsaturated Alkamidesmedicine.medical_treatmentImmunologyExcitotoxicityGlutamic AcidArachidonic AcidsPharmacologyBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateReceptors Tumor Necrosis FactorAmidohydrolasesEtanerceptBehavioral Neurosciencechemistry.chemical_compoundMiceReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid Receptor ModulatorsmedicineAnimalsDronabinolReceptors AMPA6-Cyano-7-nitroquinoxaline-23-dioneMice KnockoutNeuronsEndocrine and Autonomic SystemsTumor Necrosis Factor-alphaNeurodegenerationExperimental autoimmune encephalomyelitisExcitatory Postsynaptic PotentialsAnandamidemedicine.diseaseEndocannabinoid systemCorpus StriatumMice Inbred C57BLchemistryImmunoglobulin GImmunologyNerve DegenerationSettore MED/26 - NeurologiaFemaleCannabinoidDizocilpine MaleateEndocannabinoidsBrain, behavior, and immunity
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Subsynaptic Distribution, Lipid Raft Targeting and G Protein-Dependent Signalling of the Type 1 Cannabinoid Receptor in Synaptosomes from the Mouse H…

2021

Numerous studies have investigated the roles of the type 1 cannabinoid receptor (CB1) in glutamatergic and GABAergic neurons. Here, we used the cell-type-specific CB1 rescue model in mice to gain insight into the organizational principles of plasma membrane targeting and Gαi/o protein signalling of the CB1 receptor at excitatory and inhibitory terminals of the frontal cortex and hippocampus. By applying biochemical fractionation techniques and Western blot analyses to synaptosomal membranes, we explored the subsynaptic distribution (pre-, post-, and extra-synaptic) and CB1 receptor compartmentalization into lipid and non-lipid raft plasma membrane microdomains and the signalling properties.…

Cannabinoid receptorG proteinhippocampusPharmaceutical ScienceHippocampusOrganic chemistryanti-CB1 antibodyGTP-Binding Protein alpha Subunits Gi-GoInhibitory postsynaptic potentialArticlerescue modelAnalytical ChemistryGlutamatergicMiceQD241-441Membrane MicrodomainsReceptor Cannabinoid CB1Drug Discoverytype 1 cannabinoid receptor CB1AnimalsPhysical and Theoretical ChemistryLipid raftMice KnockoutChemistryfrontal cortexmusculoskeletal neural and ocular physiologyfood and beveragescholesterolsynaptosomesEndocannabinoid systemCell biologyFrontal Lobenervous systemChemistry (miscellaneous)SynapsesMolecular MedicineGABAergiclipids (amino acids peptides and proteins)psychological phenomena and processesSignal TransductionMolecules (Basel, Switzerland)
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Neuron-type specific cannabinoid-mediated G protein signalling in mouse hippocampus

2013

Type 1 cannabinoid receptor (CB1) is expressed in different neuronal populations in the mammalian brain. In particular, CB1 on GABAergic or glutamatergic neurons exerts different functions and display different pharmacological properties in vivo. This suggests the existence of neuron-type specific signalling pathways activated by different subpopulations of CB1. In this study, we analysed CB1 expression, binding and signalling in the hippocampus of conditional mutant mice, bearing CB1 deletion in GABAergic (GABA-CB1-KO mice) or cortical glutamatergic neurons (Glu-CB1-KO mice). Compared to their wild-type littermates, Glu-CB1-KO displayed a small decrease of CB1 mRNA amount, immunoreactivity…

Cannabinoid receptorG proteinmedicine.medical_treatmentHippocampusBiologyHippocampal formationHippocampusBiochemistryMice03 medical and health sciencesCellular and Molecular NeuroscienceGlutamatergic0302 clinical medicineGTP-binding protein regulatorsReceptor Cannabinoid CB1GTP-Binding ProteinsmedicineAnimalsGABAergic Neurons030304 developmental biologyMice Knockout0303 health sciencesCannabinoidsmusculoskeletal neural and ocular physiologyfood and beveragesMice Inbred C57BLnervous systemGABAergiclipids (amino acids peptides and proteins)CannabinoidNeurosciencepsychological phenomena and processes030217 neurology & neurosurgeryProtein BindingSignal TransductionJournal of Neurochemistry
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Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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