Search results for "Transport"

showing 10 items of 4457 documents

Ticket to Ride: Targeting Proteins to Exosomes for Brain Delivery.

2017

Exosomes represent an attractive vehicle for the delivery of biomolecules. However, mechanisms for loading functional molecules into exosomes are relatively unexplored. Here we report the use of the evolutionarily conserved late-domain (L-domain) pathway as a mechanism for loading exogenous proteins into exosomes. We demonstrate that labeling of a target protein, Cre recombinase, with a WW tag leads to recognition by the L-domain-containing protein Ndfip1, resulting in ubiquitination and loading into exosomes. Our results show that Ndfip1 expression acts as a molecular switch for exosomal packaging of WW-Cre that can be suppressed using the exosome inhibitor GW4869. When taken up by floxed …

0301 basic medicineBiocompatibilityRecombinant Fusion ProteinsGene ExpressionComputational biologyBiologyExosomesPermeabilityCell LineExtracellular VesiclesMice03 medical and health sciencesDrug Delivery SystemsDrug DiscoveryGeneticsAnimalsMolecular BiologyPharmacologyIntegrasesbusiness.industryImmunogenicityMembrane ProteinsRNABrainProteinsMicrovesiclesBiotechnologyProtein Transport030104 developmental biologyTargeted drug deliveryBlood-Brain BarrierCommentaryMolecular MedicineOriginal ArticleNasal AbsorptionCarrier ProteinsGenetic EngineeringbusinessMolecular therapy : the journal of the American Society of Gene Therapy
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Haploinsufficiency of the Primary Familial Brain Calcification Gene SLC20A2 Mediated by Disruption of a Regulatory Element

2020

OBJECTIVE Primary familial brain calcification (PFBC) is a rare cerebral microvascular calcifying disorder with diverse neuropsychiatric expression. Five genes were reported as PFBC causative when carrying pathogenic variants. Haploinsufficiency of SLC20A2, which encodes an inorganic phosphate importer, is a major cause of autosomal-dominant PFBC. However, PFBC remains genetically unexplained in a proportion of patients, suggesting the existence of additional genes or cryptic mutations. We analyzed exome sequencing data of 71 unrelated, genetically unexplained PFBC patients with the aim to detect copy number variations that may disrupt the expression of core PFBC-causing genes. METHODS Afte…

0301 basic medicineBrain DiseasesDNA Copy Number VariationsSodium-Phosphate Cotransporter Proteins Type IIIHEK 293 cellsBrainHaploinsufficiencyBiologyMolecular biologyReverse transcriptase03 medical and health sciencesHEK293 Cells030104 developmental biology0302 clinical medicineNeurologyMutationHumansNeurology (clinical)Copy-number variationAlleleHaploinsufficiencyEnhancerGene030217 neurology & neurosurgeryExome sequencingMovement Disorders
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Deregulated Lipid Sensing by Intestinal CD36 in Diet-Induced Hyperinsulinemic Obese Mouse Model

2016

International audience; The metabolic syndrome (MetS) greatly increases risk of cardiovascular disease and diabetes and is generally associated with abnormally elevated postprandial triglyceride levels. We evaluated intestinal synthesis of triglyceride-rich lipoproteins (TRL) in a mouse model of the MetS obtained by feeding a palm oil-rich high fat diet (HFD). By contrast to control mice, MetS mice secreted two populations of TRL. If the smaller size population represented 44% of total particles in the beginning of intestinal lipid absorption in MetS mice, it accounted for only 17% after 4 h due to the secretion of larger size TRL. The MetS mice displayed accentuated postprandial hypertrigl…

0301 basic medicineCD36 Antigens[SDV]Life Sciences [q-bio]lcsh:Medicine030204 cardiovascular system & hematologyLipoprotein MetabolismMice0302 clinical medicineIntestinal mucosaHyperinsulinemiaIntestinal Mucosalcsh:ScienceMetabolic Syndromeeducation.field_of_studyMultidisciplinaryIntestinal lipid absorption3. Good healthPostprandialChain Fatty-Acidslipids (amino acids peptides and proteins)Research ArticleNonfasting Triglyceridesmedicine.medical_specialtyPopulationTransportDistal IntestineBiologyDiet High-FatAbsorption03 medical and health sciencesInsulin resistanceInternal medicineHyperinsulinismmedicineAnimalsCholesterol UptakeObesityeducationSecretion[ SDV ] Life Sciences [q-bio]Insulin-Resistancelcsh:RHypertriglyceridemiaLipid metabolismmedicine.diseaseLipid MetabolismDisease Models Animal030104 developmental biologyEndocrinologyGene Expression Regulationlcsh:Q[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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The role of Plasma Membrane Calcium ATPases (PMCAs) in neurodegenerative disorders

2017

Selective degeneration of differentiated neurons in the brain is the unifying feature of neurodegenerative disorders such as Parkinson's disease (PD) or Alzheimer's disease (AD). A broad spectrum of evidence indicates that initially subtle, but temporally early calcium dysregulation may be central to the selective neuronal vulnerability observed in these slowly progressing, chronic disorders. Moreover, it has long been evident that excitotoxicity and its major toxic effector mechanism, neuronal calcium overload, play a decisive role in the propagation of secondary neuronal death after acute brain injury from trauma or ischemia. Under physiological conditions, neuronal calcium homeostasis is…

0301 basic medicineCalcium pumpExcitotoxicitychemistry.chemical_elementCalciumProtein oxidationmedicine.disease_causeProtein Structure SecondaryPlasma Membrane Calcium-Transporting ATPases03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansPhylogenyCalcium metabolismMembrane potentialChemistryGeneral NeuroscienceNeurodegenerationNeurodegenerative Diseasesmedicine.diseaseCytosol030104 developmental biologyNeuroscience030217 neurology & neurosurgeryNeuroscience Letters
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Cationic Amino Acid Transporter-1-Mediated Arginine Uptake Is Essential for Chronic Lymphocytic Leukemia Cell Proliferation and Viability

2019

Interfering with tumor metabolism by specifically restricting the availability of extracellular nutrients is a rapidly emerging field of cancer research. A variety of tumor entities depend on the uptake of the amino acid arginine since they have lost the ability to synthesize it endogenously, that is they do not express the rate limiting enzyme for arginine synthesis, argininosuccinate synthase (ASS). Arginine transport through the plasma membrane of mammalian cells is mediated by eight different transporters that belong to two solute carrier (SLC) families. In the present study we found that the proliferation of primary as well as immortalized chronic lymphocytic leukemia (CLL) cells depen…

0301 basic medicineCancer ResearchArginineArgininosuccinate synthaseargininelcsh:RC254-282amino acid transporter03 medical and health sciences0302 clinical medicineDownregulation and upregulationhemic and lymphatic diseasesAmino acid transporterViability assayOriginal Researchchemistry.chemical_classificationnutrient restrictionArginine transportbiologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAmino acidSolute carrier familyCell biology030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisbiology.proteinchronic lymphocytic leukemiatumor metabolismFrontiers in Oncology
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2-Methoxyestradiol Affects Mitochondrial Biogenesis Pathway and Succinate Dehydrogenase Complex Flavoprotein Subunit A in Osteosarcoma Cancer Cells.

2017

Background/aim Dysregulation of mitochondrial pathways is implicated in several diseases, including cancer. Notably, mitochondrial respiration and mitochondrial biogenesis are favored in some invasive cancer cells, such as osteosarcoma. Hence, the aim of the current work was to investigate the effects of 2-methoxyestradiol (2-ME), a potent anticancer agent, on the mitochondrial biogenesis of osteosarcoma cells. Materials and methods Highly metastatic osteosarcoma 143B cells were treated with 2-ME separately or in combination with L-lactate, or with the solvent (non-treated control cells). Protein levels of α-syntrophin and peroxisome proliferator-activated receptor gamma, coactivator 1 alph…

0301 basic medicineCancer ResearchSIRT3Protein subunitSDHAMuscle ProteinsAntineoplastic AgentsMolecular Dynamics SimulationBiochemistryElectron Transport Complex IV03 medical and health sciences0302 clinical medicineGeneticSettore BIO/10 - BiochimicaCell Line TumorSirtuin 3CoactivatorGeneticsHumansMolecular BiologyOsteosarcomaOrganelle BiogenesisbiologyEstradiolSettore BIO/16 - Anatomia UmanaChemistryElectron Transport Complex IICalcium-Binding ProteinsMembrane ProteinsPeroxisomeMitochondrial biogenesiPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biology2-MethoxyestradiolMitochondriaSuccinate dehydrogenaseMolecular Docking Simulation030104 developmental biologyMitochondrial biogenesisSettore CHIM/03 - Chimica Generale E Inorganica030220 oncology & carcinogenesisSirtuinCancer cellbiology.proteinResearch ArticleCancer genomicsproteomics
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Lack of a peroxiredoxin suppresses the lethality of cells devoid of electron donors by channelling electrons to oxidized ribonucleotide reductase

2017

The thioredoxin and glutaredoxin pathways are responsible of recycling several enzymes which undergo intramolecular disulfide bond formation as part of their catalytic cycles such as the peroxide scavengers peroxiredoxins or the enzyme ribonucleotide reductase (RNR). RNR, the rate-limiting enzyme of deoxyribonucleotide synthesis, is an essential enzyme relying on these electron flow cascades for recycling. RNR is tightly regulated in a cell cycle-dependent manner at different levels, but little is known about the participation of electron donors in such regulation. Here, we show that cytosolic thioredoxins Trx1 and Trx3 are the primary electron donors for RNR in fission yeast. Unexpectedly,…

0301 basic medicineCancer ResearchThioredoxin reductaseSynthesis PhaseYeast and Fungal ModelsBiochemistryElectron DonorsSchizosaccharomyces PombeThioredoxinsGlutaredoxinCell Cycle and Cell DivisionGenetics (clinical)Chemical ReactionsOxidesPeroxidesNucleic acidsChemistryRibonucleotide reductaseBiochemistryExperimental Organism SystemsCell ProcessesSchizosaccharomyces pombePhysical SciencesSynthesis phaseThioredoxinOxidation-ReductionResearch ArticleDNA Replicationlcsh:QH426-470DNA transcriptionElectron donorsBiologyDNA replicationResearch and Analysis MethodsCatalysisElectron Transport03 medical and health sciencesModel OrganismsSchizosaccharomycesRibonucleotide ReductasesOxidationGeneticsMolecular BiologyEcology Evolution Behavior and SystematicsGlutaredoxinsCell growthDNA replicationChemical CompoundsOrganismsFungiBiology and Life SciencesCell BiologyDNAPeroxiredoxinsbiology.organism_classificationYeastCell cycle and cell divisionCheckpoint Kinase 2lcsh:Genetics030104 developmental biologySchizosaccharomyces pombeGene expressionSchizosaccharomyces pombe ProteinsPeroxiredoxin
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Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

2018

Objective— Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N -acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-α (peroxisome proliferator-activated receptors α) and the orphan receptor GPR55. Palmitoylethanolamide exerts potent anti-inflammatory actions but its physiological role and promise as a therapeutic agent in chronic arterial inflammation, such as atherosclerosis remain unexplored. Approach and Results— First, the polarization of mouse primary macrophages towards a proinflammatory phenotype was found to reduce N -acyl phosphatidylethanolamine phospholipase D expression …

0301 basic medicineCannabinoid receptorTime FactorsMice Knockout ApoECHOLESTEROL TRANSPORTAnti-Inflammatory AgentsPhospholipaseProto-Oncogene Maschemistry.chemical_compoundCannabinoid receptor type 2Receptors CannabinoidAortachemistry.chemical_classificationMARROW-DERIVED CELLSAPOPTOTIC CELL ACCUMULATIONPlaque AtheroscleroticCell biologymacrophagesDENSITY-LIPOPROTEIN RECEPTORPhenotypeREDUCES INFLAMMATIONCB2 RECEPTOREthanolaminesFemaleCardiology and Cardiovascular MedicineSCAVENGER RECEPTORAortic DiseasesPalmitic Acidsta3111fatty acidsCell Line03 medical and health sciencesMediatorPhagocytosisPhospholipase DAnimalsHumansScavenger receptorCANNABINOID RECEPTORPhosphatidylethanolaminePalmitoylethanolamidec-Mer Tyrosine KinaseFatty acidcholesterolta3121AmidesRatsMice Inbred C57BLDisease Models Animal030104 developmental biologychemistryinflammationRECEPTOR CLASS-BatherosclerosisCONTACT ALLERGIC DERMATITISArteriosclerosis Thrombosis and Vascular Biology
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C 4 -Dicarboxylate Utilization in Aerobic and Anaerobic Growth

2016

C 4 -dicarboxylates and the C 4 -dicarboxylic amino acid l -aspartate support aerobic and anaerobic growth of Escherichia coli and related bacteria. In aerobic growth, succinate, fumarate, D - and L -malate, L -aspartate, and L -tartrate are metabolized by the citric acid cycle and associated reactions. Because of the interruption of the citric acid cycle under anaerobic conditions, anaerobic metabolism of C 4 -dicarboxylates depends on fumarate reduction to succinate (fumarate respiration). In some related bacteria (e.g., Klebsiella ), utilization of C 4 -dicarboxylates, such as tartrate, is independent of fumarate respiration and uses a Na + -dependent membrane-bound oxaloacetate decarbo…

0301 basic medicineCarboxy-LyasesCitric Acid Cycle030106 microbiologySuccinic AcidContext (language use)medicine.disease_causeMicrobiology03 medical and health sciencesFumaratesKlebsiellaEscherichia colimedicineHumansDicarboxylic AcidsAnaerobiosisEscherichia coliDicarboxylic Acid TransportersbiologyEscherichia coli ProteinsMembrane Transport ProteinsBiological TransportGene Expression Regulation BacterialMetabolismFumarate reductasebiology.organism_classificationAerobiosisCitric acid cycle030104 developmental biologyOxaloacetate decarboxylaseBiochemistryAnaerobic exerciseBacteriaEcoSal Plus
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mRNA-binding protein tristetraprolin is essential for cardiac response to iron deficiency by regulating mitochondrial function

2018

Cells respond to iron deficiency by activating iron-regulatory proteins to increase cellular iron uptake and availability. However, it is not clear how cells adapt to conditions when cellular iron uptake does not fully match iron demand. Here, we show that the mRNA-binding protein tristetraprolin (TTP) is induced by iron deficiency and degrades mRNAs of mitochondrial Fe/S-cluster-containing proteins, specifically Ndufs1 in complex I and Uqcrfs1 in complex III, to match the decrease in Fe/S-cluster availability. In the absence of TTP, Uqcrfs1 levels are not decreased in iron deficiency, resulting in nonfunctional complex III, electron leakage, and oxidative damage. Mice with deletion of Ttp …

0301 basic medicineCardiac responseCardiac function curveIron-Sulfur ProteinsTristetraprolinMitochondria HeartCell Line03 medical and health sciencesElectron Transport Complex IIIMiceTristetraprolinmedicineAnimalschemistry.chemical_classificationMice KnockoutReactive oxygen speciesMultidisciplinaryNDUFS1MyocardiumNADH DehydrogenaseIron deficiencyIron Deficienciesmedicine.diseaseCell biology030104 developmental biologychemistryPNAS PlusCoenzyme Q – cytochrome c reductaseOxidation-ReductionFunction (biology)
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