Search results for "Membrane Transport"

showing 10 items of 215 documents

Chemical probes to potently and selectively inhibit endocannabinoid cellular reuptake

2017

The extracellular effects of the endocannabinoids anandamide and 2-arachidonoyl glycerol are terminated by enzymatic hydrolysis after crossing cellular membranes by facilitated diffusion. The lack of potent and selective inhibitors for endocannabinoid transport has prevented the molecular characterization of this process, thus hindering its biochemical investigation and pharmacological exploitation. Here, we report the design, chemical synthesis, and biological profiling of natural product-derived N-substituted 2,4-dodecadienamides as a selective endocannabinoid uptake inhibitor. The highly potent (IC50 = 10 nM) inhibitor N-(3,4-dimethoxyphenyl)ethyl amide (WOBE437) exerted pronounced canna…

0301 basic medicinePolyunsaturated Alkamidesmedicine.drug_classmedicine.medical_treatmentAnti-Inflammatory AgentsArachidonic AcidsPharmacologyDepolarization-induced suppression of inhibitionAnxiolyticGlyceridesReuptakeMice03 medical and health scienceschemistry.chemical_compoundCell Line TumorExtracellularmedicineAnimalsHumansReceptors Cannabinoid610 Medicine & healthMice Inbred BALB CMultidisciplinaryHydrolysismusculoskeletal neural and ocular physiologyCell MembraneBrainBiological TransportU937 CellsAnandamideMembrane transportEndocannabinoid systemMice Inbred C57BL030104 developmental biologynervous systemPNAS PlusAnti-Anxiety AgentschemistryBiophysics570 Life sciences; biologylipids (amino acids peptides and proteins)Cannabinoidpsychological phenomena and processesEndocannabinoidsProceedings of the National Academy of Sciences
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Permeating disciplines: Overcoming barriers between molecular simulations and classical structure-function approaches in biological ion transport

2017

Ion translocation across biological barriers is a fundamental requirement for life. In many cases, controlling this process-for example with neuroactive drugs-demands an understanding of rapid and reversible structural changes in membrane-embedded proteins, including ion channels and transporters. Classical approaches to electrophysiology and structural biology have provided valuable insights into several such proteins over macroscopic, often discontinuous scales of space and time. Integrating these observations into meaningful mechanistic models now relies increasingly on computational methods, particularly molecular dynamics simulations, while surfacing important challenges in data manage…

0301 basic medicineProtein ConformationComputer sciencemedia_common.quotation_subjectData managementBiophysicsContext (language use)Molecular Dynamics SimulationBiochemistryIon ChannelsArticleStructure-Activity Relationship03 medical and health sciencesAnimalsHumansFunction (engineering)Biological sciencesClassical structureIon transportermedia_commonIon Transportbusiness.industryMembrane Transport ProteinsCell BiologyData science030104 developmental biologyStructural biologybusinessIon Channel GatingProtein BindingBiochimica et Biophysica Acta (BBA) - Biomembranes
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A new “sudden fright paradigm” to explore the role of (epi)genetic modulations of the DAT gene in fear-induced avoidance behavior

2020

Alterations in dopamine (DA) reuptake are involved in several psychiatric disorders whose symptoms can be investigated in knock out rats for the DA transporter (DAT-KO). Recent studies evidenced the role of epigenetic DAT modulation in depressive-like behavior. Accordingly, we used heterozygous (HET) rats born from both HET parents (termed MIX-HET), compared to HET rats born from WT-mother and KO-father (MAT-HET), implementing the role of maternal care on DAT modulation. We developed a "sudden fright" paradigm (based on dark-light test) to study reaction to fearful inputs in the DAT-KO, MAT-HET, MIX-HET, and WT groups. Rats could freely explore the whole 3-chambers apparatus; then, they wer…

0301 basic medicineanimal structuresEmotionsStimulus (physiology)Epigenesis GeneticReuptakechoice behavior03 medical and health sciencesBehavioral Neuroscience0302 clinical medicineDopamineDAT-KO ratAvoidance LearningGeneticsmedicineAnimalsFear conditioningEpigeneticsprefrontal cortex.Prefrontal cortexdopamine transporterDopamine transporterDopamine Plasma Membrane Transport ProteinsBehavior AnimalbiologyFearfear conditioningRatsDisease Models Animal030104 developmental biologyNeurologyAttention Deficit Disorder with Hyperactivitybiology.proteinSettore BIO/14 - Farmacologiaconditioned preferenceHistone deacetylaseNeuroscience030217 neurology & neurosurgerymedicine.drug
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Brothers in arms: proBDNF/BDNF and sAPPα/Aβ-signaling and their common interplay with ADAM10, TrkB, p75NTR, sortilin, and sorLA in the progression of…

2021

Abstract Brain-derived neurotrophic factor (BDNF) is an important modulator for a variety of functions in the central nervous system (CNS). A wealth of evidence, such as reduced mRNA and protein level in the brain, cerebrospinal fluid (CSF), and blood samples of Alzheimer’s disease (AD) patients implicates a crucial role of BDNF in the progression of this disease. Especially, processing and subcellular localization of BDNF and its receptors TrkB and p75 are critical determinants for survival and death in neuronal cells. Similarly, the amyloid precursor protein (APP), a key player in Alzheimer’s disease, and its cleavage fragments sAPPα and Aβ are known for their respective roles in neuropro…

ADAM10Clinical BiochemistryNerve Tissue ProteinsTropomyosin receptor kinase BReceptors Nerve Growth FactorBiochemistryNeuroprotectionADAM10 ProteinAmyloid beta-Protein PrecursorNeurotrophic factorsAlzheimer DiseaseAmyloid precursor proteinHumansReceptor trkBMolecular BiologyLDL-Receptor Related ProteinsAmyloid beta-PeptidesMembrane GlycoproteinsbiologyBrain-Derived Neurotrophic FactorMembrane ProteinsMembrane Transport ProteinsAdaptor Proteins Vesicular Transportnervous systembiology.proteinSignal transductionAmyloid Precursor Protein SecretasesNeuroscienceAmyloid precursor protein secretaseNeurotrophinBiological chemistryReferences
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Influence of gamma-aminobutyric acid on baclofen intestinal absorption.

1994

Since previous studies suggested that baclofen absorption in the rat middle intestine was inhibited by beta-alanine and therefore mediated, at least in part, by the beta-aminoacid carrier, we focused our new studies on the analysis of the possible inhibition of the drug by a gamma-aminoacid model compound, gamma-aminobutyric acid (GABA). A rat jejunum in situ study was undertaken in order to evaluate the effect of GABA on baclofen absorption and to establish the inhibition model. Assays using isotonic perfusion solutions of 0.5 mM baclofen with starting GABA concentrations ranging from 0 to 100 mM are reported. The results show that the absorption rate pseudoconstants of the drug decrease a…

Absorption (pharmacology)MaleBaclofenPharmaceutical ScienceIn Vitro TechniquesMichaelis–Menten kineticsAminobutyric acidModels BiologicalIntestinal absorptionchemistry.chemical_compoundNon-competitive inhibitionmedicineAnimalsPharmacology (medical)Rats WistarChromatography High Pressure Liquidgamma-Aminobutyric AcidPharmacologyGeneral MedicineMembrane transportSmall intestineRatsPerfusionBaclofenmedicine.anatomical_structurenervous systemchemistryBiochemistryIntestinal AbsorptionBiophysicsBiopharmaceuticsdrug disposition
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Intestinal absorption pathway of gamma-aminobutyric acid in rat small intestine.

1994

Intestinal absorption of gamma-aminobutyric acid (GABA), as a model compound for gamma-aminoacids, has not been extensively studied from the kinetic viewpoint. Since data from our laboratory suggested that some competition arises between intestinal absorption of beta-alanine and GABA and since our intent was to maintain the aqueous stagnant diffusion layer in order to approach absorption tests to in vivo physiological conditions, a rat jejunum in situ study was undertaken in order to gain an insight into the mechanism of GABA absorption. In the present paper, results from assays using isotonic perfusion solutions with starting GABA concentrations ranging from 1 to 50 mM are reported. They s…

Absorption (pharmacology)MalePharmaceutical ScienceMichaelis–Menten kineticsAminobutyric acidIntestinal absorptionDiffusionNon-competitive inhibitionBody WaterIn vivoIntestine SmallmedicineAnimalsPharmacology (medical)Rats WistarChromatography High Pressure Liquidgamma-Aminobutyric AcidPharmacologyAlanineChemistryGeneral MedicineMembrane transportSmall intestineRatsmedicine.anatomical_structureSpectrometry FluorescenceBiochemistryIntestinal AbsorptionBiophysicsBiopharmaceuticsdrug disposition
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Endometrial gene expression in the window of implantation is altered in obese women especially in association with polycystic ovary syndrome

2010

Objective To determine whether luteal phase endometrial transcriptome is altered in obese women during the window of implantation (WOI), considering the presence of infertility, fat distribution and association with polycystic ovary syndrome (PCOS). Design Prospective study. Setting University-affiliated infertility clinic, between May 2007 and March 2009. Patient(s) One control group of women with normal weight (n = 4), and four study groups of obese women (n = 6 each one) according to the association with infertility, PCOS, and ovarian stimulation. Intervention(s) The endometrium was biopsied 7 days after LH surge or hCG administration in 28 women. Main Outcome Measure(s) Endometrial gene…

AdultInfertilitymedicine.medical_specialtyTime FactorsAdolescentMicroarrayBiopsyLuteal PhaseLuteal phasePeptide receptor activityBiologyEndometriumEndometriumYoung AdultOvulation InductionInternal medicinemedicineCluster AnalysisHumansEmbryo ImplantationObesityProspective StudiesOligonucleotide Array Sequence AnalysisUnexplained infertilityPrincipal Component AnalysisGene Expression ProfilingObstetrics and GynecologyFertility Agents Femalemedicine.diseasePolycystic ovarymedicine.anatomical_structureEndocrinologyGene Expression RegulationReproductive MedicineSpainCase-Control StudiesFemaleTransmembrane transporter activityInfertility FemalePolycystic Ovary SyndromeFertility and Sterility
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Mutations in the gene encoding the basal body protein RPGRIP1L, a nephrocystin-4 interactor, cause Joubert syndrome.

2007

Peters, T.A./0000-0001-8443-5500; van Beersum, Sylvia E.C./0000-0002-4552-2908; Cremers, Frans/0000-0002-4954-5592; Roepman, Ronald/0000-0002-5178-8163 WOS: 000247619800019 PubMed: 17558407 Protein- protein interaction analyses have uncovered a ciliary and basal body protein network that, when disrupted, can result in nephronophthisis ( NPHP), Leber congenital amaurosis, Senior- Loken syndrome ( SLSN) or Joubert syndrome ( JBTS)(1-6). However, details of the molecular mechanisms underlying these disorders remain poorly understood. RPGRIP1- like protein ( RPGRIP1L) is a homolog of RPGRIP1 ( RPGR-interacting protein 1), a ciliary protein defective in Leber congenital amaurosis(7,8). We show t…

AdultMaleHealth aging / healthy living [IGMD 5]Eye DiseasesGenetics and epigenetic pathways of disease [NCMLS 6]TMEM67Molecular Sequence DataMembrane transport and intracellular motility [NCMLS 5]Biologymedicine.disease_causeJoubert syndromeCell LineGenomic disorders and inherited multi-system disorders [IGMD 3]NephronophthisisCerebellar DiseasesGeneticsmedicinePerception and Action [DCN 1]Basal bodyAnimalsHumansNeurosensory disorders [UMCN 3.3]CiliaAdaptor Proteins Signal TransducingRenal disorder [IGMD 9]GeneticsMutationCiliumCiliary transition zoneProteinsSyndromemedicine.diseasePedigreeRatsCytoskeletal ProteinsGenetic defects of metabolism [UMCN 5.1]RPGRIP1LFemaleKidney DiseasesFunctional Neurogenomics [DCN 2]Ciliary Motility Disorders
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Genome-wide association data provide further support for an association between 5-HTTLPR and major depressive disorder.

2013

Abstract Background Dysfunctions of serotonergic neurotransmission are supposed to be involved in the pathogenesis of psychiatric disorders such as major depressive disorder (MDD). The concentration of serotonin (5-hydroxytryptamine, 5-HT) in the synaptic cleft is essentially regulated by the 5-HT transporter (5-HTT). A length polymorphism repeat in the 5-HTT promoter region, termed 5-HTTLPR, has been commonly investigated for an association with psychiatric disorders. Methods Genotyping of the 5-HTTLPR is time-consuming and technically challenging. Recently, a two-SNP haplotype was identified that tags the 5-HTTLPR at r 2 =0.775. This allows extraction of 5-HTTLPR genotype information from…

AdultMaleLinkage disequilibriumSynaptic cleftGenotypeSingle-nucleotide polymorphismGenome-wide association studyPolymorphism Single NucleotideGermanygenetics [Haplotypes]mental disordersGenotypegenetics [Serotonin Plasma Membrane Transport Proteins]medicineHumansGenetic Predisposition to Diseaseddc:610GeneticsSerotonin Plasma Membrane Transport ProteinsDepressive Disorder MajorSLC6A4 protein humanHaplotypegenetics [Depressive Disorder Major]Middle Agedmedicine.diseasePsychiatry and Mental healthClinical PsychologyHaplotypes5-HTTLPRCase-Control Studiesgenetics [Polymorphism Single Nucleotide]Major depressive disorderFemalePsychologyClinical psychologyGenome-Wide Association StudyJournal of affective disorders
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REEP1 mutation spectrum and genotype/phenotype correlation in hereditary spastic paraplegia type 31.

2008

Contains fulltext : 71291.pdf (Publisher’s version ) (Closed access) Mutations in the receptor expression enhancing protein 1 (REEP1) have recently been reported to cause autosomal dominant hereditary spastic paraplegia (HSP) type SPG31. In a large collaborative effort, we screened a sample of 535 unrelated HSP patients for REEP1 mutations and copy number variations. We identified 13 novel and 2 known REEP1 mutations in 16 familial and sporadic patients by direct sequencing analysis. Twelve out of 16 mutations were small insertions, deletions or splice site mutations. These changes would result in shifts of the open-reading-frame followed by premature termination of translation and haploins…

AdultMaleMutation rateAdolescentGenotypeHereditary spastic paraplegiaDNA Mutational AnalysisBiologymedicine.disease_causeArticleCognitive neurosciences [UMCN 3.2]Gene duplicationGenotypemedicinePerception and Action [DCN 1]HumansCopy-number variationAge of OnsetMutation frequencyChildAgedAged 80 and overGeneticsMutationHereditary cancer and cancer-related syndromes [ONCOL 1]Spastic Paraplegia HereditaryInfantMembrane Transport ProteinsMiddle Agedmedicine.diseasePedigreePhenotypeChild PreschoolMutationFemaleNeurology (clinical)HaploinsufficiencyFunctional Neurogenomics [DCN 2]
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