Search results for "SNARE Proteins"

showing 10 items of 14 documents

Tissue expression of the vesicle protein pantophysin

1999

The cell-type restricted expression of cytoplasmic microvesicle membrane protein isoforms may be a consequence of the functional adaptation of these vesicles to the execution of specialized processes in cells of different specialization. To characterize the expression of the vesicle protein pantophysin, an isoform of the synaptic vesicle proteins synaptophysin and synaptoporin, we have prepared and characterized antibodies useful for the immunological detection of pantophysin in vitro and in situ. Using these reagents, we show by immunoblot analyses that pantophysin expression is not homogeneous but differs significantly between various bovine tissues. Furthermore, these differences are not…

Vesicle-associated membrane protein 8Membrane GlycoproteinsHistologySynaptobrevinMicrovesicleMembrane ProteinsSNAP25Cell BiologySynaptoporinBiologyCytoplasmic GranulesMolecular biologyPathology and Forensic MedicineCell biologyR-SNARE ProteinsVesicle-associated membrane proteinMembrane proteinOrgan SpecificitySynaptophysinbiology.proteinAnimalsProtein IsoformsCattleCarrier ProteinsFluorescent Antibody Technique IndirectCell and Tissue Research
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Fertility and Polarized Cell Growth Depends on eIF5A for Translation of Polyproline-Rich Formins in Saccharomyces cerevisiae

2014

eIF5A is an essential and evolutionary conserved translation elongation factor, which has recently been proposed to be required for the translation of proteins with consecutive prolines. The binding of eIF5A to ribosomes occurs upon its activation by hypusination, a modification that requires spermidine, an essential factor for mammalian fertility that also promotes yeast mating. We show that in response to pheromone, hypusinated eIF5A is required for shmoo formation, localization of polarisome components, induction of cell fusion proteins, and actin assembly in yeast. We also show that eIF5A is required for the translation of Bni1, a proline-rich formin involved in polarized growth during …

TranslationSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiaePeptide Chain Elongation TranslationalForminsRNA-binding proteinSaccharomyces cerevisiaeInvestigationsPeptide Initiation FactorsMorphogenesisGeneticsQc-SNARE ProteinsPolyproline helixPolarisomeGeneticsMatingbiologyMicrofilament ProteinsMembrane ProteinsRNA-Binding ProteinsTranslation (biology)Polarized growthbiology.organism_classificationActinsProtein Structure TertiaryCell biologyCytoskeletal ProteinsMating of yeastForminsMutationbiology.proteinEIF5APeptidesRibosomesEIF5A
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Stx5 is a novel interactor of VLDL-R to affect its intracellular trafficking and processing

2012

We identified syntaxin 5 (Stx5), a protein involved in intracellular vesicle trafficking, as a novel interaction partner of the very low density lipoprotein (VLDL)-receptor (VLDL-R), a member of the LDL-receptor family. In addition, we investigated the effect of Stx5 on VLDL-R maturation, trafficking and processing. Here, we demonstrated mutual association of both proteins using several in vitro approaches. Furthermore, we detected a special maturation phenotype of VLDL-R resulting from Stx5 overexpression. We found that Stx5 prevented advanced Golgi-maturation of VLDL-R, but did not cause accumulation of the immature protein in ER, ER to Golgi compartments, or cis-Golgi ribbon, the main ex…

Low-density lipoprotein receptor-related protein 8Very Low-Density Lipoprotein ReceptorCHO CellsSTX5Biologysymbols.namesakeCricetulusCricetinaeAnimalsHumansSyntaxinSecretory PathwayQa-SNARE ProteinsCell Membranenutritional and metabolic diseasesIntracellular vesicleHep G2 CellsCell BiologyGolgi apparatusCell biologyProtein TransportHEK293 CellsReceptors LDLLDL receptorsymbolslipids (amino acids peptides and proteins)Protein Processing Post-TranslationalIntracellularProtein Bindingtrans-Golgi NetworkExperimental Cell Research
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ROP, the Drosophila Sec1 homolog, interacts with syntaxin and regulates neurotransmitter release in a dosage-dependent manner.

1998

The Sec1 family of proteins is thought to function in both non-neuronal and neuronal secretion, although the precise role of this protein family has not been defined. Here, we study the function of ROP, the Drosophila Sec1 homolog, in neurotransmitter release. Electrophysiological analyses of transgenic lines overexpressing ROP and syntaxin, a presynaptic membrane protein, indicate that ROP interacts with syntaxin in vivo. Characterization of four point mutations in ROP shows that they fall into two phenotypic classes. Two mutations cause a dramatic reduction in both evoked and spontaneous neurotransmitter release. In contrast, the other two mutations reveal an increase in evoked neurotrans…

Munc18 Proteinscongenital hereditary and neonatal diseases and abnormalitiesProtein familyNerve Tissue ProteinsNeurotransmissionBiologySynaptic TransmissionGeneral Biochemistry Genetics and Molecular BiologySyntaxin bindingExocytosischemistry.chemical_compoundSyntaxinAnimalsDrosophila ProteinsNeurotransmitterMolecular BiologyNeurotransmitter AgentsGeneral Immunology and MicrobiologyQa-SNARE ProteinsGeneral NeuroscienceMembrane ProteinsSyntaxin 3eye diseasesCell biologychemistryDrosophilaResearch ArticleThe EMBO journal
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A single mutation in the recombinant light chain of tetanus toxin abolishes its proteolytic activity and removes the toxicity seen after reconstituti…

1994

Specific proteolysis by the tetanus toxin light chain of a vesicle-associated membrane protein (VAMP) involved in exocytosis is thought to underlie its intracellular blockade of neurotransmitter release. To substantiate this mechanism, recombinant light chain was expressed as a maltose binding protein-light chain fusion product in Escherichia coli. After purification of affinity chromatography and cleavage with factor Xa, the resultant light chain was isolated and its identity confirmed by Western blotting and N-terminal sequencing. It exhibited activity similar to that of the native light chain in proteolyzing its target in isolated bovine small synaptic vesicles and in hydrolyzing a 62-re…

medicine.medical_treatmentRecombinant Fusion ProteinsMolecular Sequence DataNeurotoxinsGlutamic AcidMaltose bindingNerve Tissue ProteinsIn Vitro TechniquesImmunoglobulin light chainBiochemistrySynaptic vesicleExocytosislaw.inventionR-SNARE ProteinsMiceStructure-Activity RelationshipAffinity chromatographyGlutamatesTetanus ToxinlawThermolysinEndopeptidasesmedicineEscherichia coliAnimalsAmino Acid SequenceProteaseBase SequenceChemistryMembrane ProteinsMolecular biologyPeptide FragmentsRecombinant DNAMutagenesis Site-DirectedCattleBiochemistry
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β1-Integrin– and K(V)1.3 channel–dependent signaling stimulates glutamate release from Th17 cells

2020

Although the impact of Th17 cells on autoimmunity is undisputable, their pathogenic effector mechanism is still enigmatic. We discovered soluble N-ethylmaleimide–sensitive factor attachment receptor (SNARE) complex proteins in Th17 cells that enable a vesicular glutamate release pathway that induces local intracytoplasmic calcium release and subsequent damage in neurons. This pathway is glutamine dependent and triggered by binding of β1-integrin to vascular cell adhesion molecule 1 (VCAM-1) on neurons in the inflammatory context. Glutamate secretion could be blocked by inhibiting either glutaminase or K(V)1.3 channels, which are known to be linked to integrin expression and highly expressed…

0301 basic medicineMultiple SclerosisGlutamic AcidVascular Cell Adhesion Molecule-1Cell Communication03 medical and health sciencesMice0302 clinical medicineAnimalsHumansChannel blockerReceptorNeuroinflammationMice KnockoutKv1.3 Potassium ChannelGlutamate secretionChemistryGlutaminaseCell adhesion moleculeIntegrin beta1Glutamate receptorGeneral MedicineCell biologyGlutamine030104 developmental biology030220 oncology & carcinogenesisTh17 CellsSNARE ProteinsResearch ArticleSignal Transduction
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Mutations in the Neuronal Vesicular SNARE VAMP2 Affect Synaptic Membrane Fusion and Impair Human Neurodevelopment

2019

VAMP2 encodes the vesicular SNARE protein VAMP2 (also called synaptobrevin-2). Together with its partners syntaxin-1A and synaptosomal-associated protein 25 (SNAP25), VAMP2 mediates fusion of synaptic vesicles to release neurotransmitters. VAMP2 is essential for vesicular exocytosis and activity-dependent neurotransmitter release. Here, we report five heterozygous de novo mutations in VAMP2 in unrelated individuals presenting with a neurodevelopmental disorder characterized by axial hypotonia (which had been present since birth), intellectual disability, and autistic features. In total, we identified two single-amino-acid deletions and three non-synonymous variants affecting conserved resid…

MaleHeterozygoteAdolescentVesicle-Associated Membrane Protein 2neuronal exocytosisynaptopathyautismsynaptobrevinMembrane FusionExocytosisR-SNARE ProteinsProtein DomainsReportIntellectual DisabilityGeneticsHumansAutistic DisorderChildGenetics (clinical)NeuronsNeurotransmitter Agentsneurodevelopmental disordersvesicle fusionBrainautism; epilepsy; movement disorders; neurodevelopmental disorders; neuronal exocytosis; SNARE; synaptobrevin; synaptopathy; VAMP2; vesicle fusionneuronal exocytosisLipidsMagnetic Resonance Imagingneurodevelopmental disorderautism epilepsy movement disorders neurodevelopmental disorders neuronal exocytosis SNARE synaptobrevin synaptopathy VAMP2 vesicle fusion Genetics Genetics (clinical)Phenotypeautism; epilepsy; movement disorders; neurodevelopmental disorders; neuronal exocytosis; SNARE; synaptobrevin; synaptopathy; VAMP2; vesicle fusion; Genetics; Genetics (clinical)VAMP2SNAREChild PreschoolMutationSynapsesMuscle Hypotoniaepilepsymovement disordersFemalesense organsmovement disorder
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Comprehensive analysis of expression, subcellular localization, and cognate pairing of SNARE proteins in oligodendrocytes

2009

Oligodendrocytes form the central nervous system myelin sheath by spiral wrapping of their plasma membrane around axons, necessitating a high rate of exocytic membrane addition to the growing myelin membrane. Membrane fusion is mediated by soluble N-ethylmaleimide-sensitive factor attachment protein receptor proteins (SNAREs), which act by specific pairing of vesicle (R)- and target (Q)-SNAREs. To characterize oligodendroglial SNAREs and their trafficking pathways, we performed a detailed expression analysis of SNAREs in differentiating cultured oligodendrocytes and myelin and determined their subcellular localization. Expression of the plasma membrane Q-SNAREs syntaxin 3, syntaxin 4, SNAP2…

Central Nervous SystemMaleVesicle-Associated Membrane Protein 3SynaptobrevinGolgi ApparatusBiologyMembrane FusionR-SNARE ProteinsMiceCellular and Molecular NeuroscienceSNAP23AnimalsSyntaxinQc-SNARE ProteinsTransport VesiclesCells CulturedMyelin SheathR-SNARE ProteinsQa-SNARE ProteinsVesicleCell MembraneLipid bilayer fusionQb-SNARE ProteinsSyntaxin 3Cell CompartmentationTransport proteinCell biologyOligodendrogliaProtein Transportnervous systemFemalebiological phenomena cell phenomena and immunitySNARE ProteinsDimerizationJournal of Neuroscience Research
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Transport of the major myelin proteolipid protein is directed by VAMP3 and VAMP7.

2011

CNS myelination by oligodendrocytes requires directed transport of myelin membrane components and a timely and spatially controlled membrane expansion. In this study, we show the functional involvement of the R-solubleN-ethylmaleimide-sensitive factor attachment protein receptor (R-SNARE) proteins VAMP3/cellubrevin and VAMP7/TI-VAMP in myelin membrane trafficking. VAMP3 and VAMP7 colocalize with the major myelin proteolipid protein (PLP) in recycling endosomes and late endosomes/lysosomes, respectively. Interference with VAMP3 or VAMP7 function using small interfering RNA-mediated silencing and exogenous expression of dominant-negative proteins diminished transport of PLP to the oligodendro…

MaleProteolipid protein 1Vesicle-Associated Membrane Protein 3MESH: Myelin SheathMESH: R-SNARE Proteins[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyR-SNARE ProteinsMiceMyelin0302 clinical medicineMESH: Microscopy ImmunoelectronMESH: Genetic VectorsImage Processing Computer-AssistedMESH: AnimalsMicroscopy ImmunoelectronMESH: Myelin Proteolipid ProteinCells CulturedMyelin SheathMESH: Vesicle-Associated Membrane Protein 3VAMP30303 health sciencesMESH: ExocytosisGeneral NeuroscienceMESH: Enzyme-Linked Immunosorbent AssayArticlesImmunohistochemistryMESH: Image Processing Computer-AssistedMyelin proteolipid proteinCell biologymedicine.anatomical_structureElectrophoresis Polyacrylamide GelFemaleRNA InterferenceMESH: Cells CulturedEndosomeGenetic VectorsMESH: RNA InterferenceBiological Transport ActiveEnzyme-Linked Immunosorbent AssayEndosomesBiologyTransfectionExocytosisExocytosis03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsSecretionMyelin Proteolipid ProteinMESH: MiceSecretory pathway030304 developmental biologyMESH: TransfectionCell MembraneMESH: ImmunohistochemistryMESH: MaleMice Inbred C57BLnervous systemMESH: EndosomesMESH: Biological Transport ActiveLysosomesMESH: Female030217 neurology & neurosurgeryMESH: LysosomesMESH: Cell MembraneMESH: Electrophoresis Polyacrylamide Gel
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Syntaxin13 expression is regulated by mammalian target of rapamycin (mTOR) in injured neurons to promote axon regeneration.

2014

Injured peripheral neurons successfully activate intrinsic signaling pathways to enable axon regeneration. We have previously shown that dorsal root ganglia (DRG) neurons activate the mammalian target of rapamycin (mTOR) pathway following injury and that this activity enhances their axon growth capacity. mTOR plays a critical role in protein synthesis, but the mTOR-dependent proteins enhancing the regenerative capacity of DRG neurons remain unknown. To identify proteins whose expression is regulated by injury in an mTOR-dependent manner, we analyzed the protein composition of DRGs from mice in which we genetically activated mTOR and from mice with or without a prior nerve injury. Quantitati…

ProteomicsAxon; Proteomics; Regeneration; SNARE Proteins; mTORSNARE Proteinmedicine.medical_treatmentInbred C57BLRegenerative MedicineBiochemistryMedical and Health SciencesMiceNeurobiologyGanglia SpinalAxonCells CulturedMice KnockoutGene knockdownCulturedQa-SNARE ProteinsTOR Serine-Threonine KinasesAxotomyBiological SciencesSciatic NerveCell biologymedicine.anatomical_structureNeurologicalmTORFemaleAxotomySignal transductionmedicine.symptomSNARE ProteinsBiochemistry & Molecular BiologyPhysical Injury - Accidents and Adverse EffectsSpinalSensory Receptor CellsCellsKnockout1.1 Normal biological development and functioningBiologyAxonUnderpinning researchmedicineAnimalsRegenerationMolecular BiologyPI3K/AKT/mTOR pathwayRegeneration (biology)NeurosciencesProteomicCell BiologyNerve injuryAxonsNerve RegenerationMice Inbred C57BLnervous systemChemical SciencesAxoplasmic transportGanglia
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