Search results for " Immunoelectron"

showing 10 items of 64 documents

Localization of the cannabinoid type-1 receptor in subcellular astrocyte compartments of mutant mouse hippocampus

2018

Astroglial type‐1 cannabinoid (CB1) receptors are involved in synaptic transmission, plasticity and behavior by interfering with the so‐called tripartite synapse formed by pre‐ and post‐synaptic neuronal elements and surrounding astrocyte processes. However, little is known concerning the subcellular distribution of astroglial CB1 receptors. In particular, brain CB1 receptors are mostly localized at cells' plasmalemma, but recent evidence indicates their functional presence in mitochondrial membranes. Whether CB1 receptors are present in astroglial mitochondria has remained unknown. To investigate this issue, we included conditional knock‐out mice lacking astroglial CB1 receptor expression …

0301 basic medicineCannabinoid receptormedicine.medical_treatmentImmunoelectron microscopyNeurotransmissionBiologyHippocampusImmunoenzyme Techniques03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineReceptor Cannabinoid CB1Glial Fibrillary Acidic ProteinTripartite synapsemedicineAnimalsMicroscopy ImmunoelectronReceptorMice KnockoutGlial fibrillary acidic proteinmusculoskeletal neural and ocular physiologyfood and beveragesMitochondriaCell biology030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyAstrocytesbiology.proteinlipids (amino acids peptides and proteins)Cannabinoidpsychological phenomena and processes030217 neurology & neurosurgeryAstrocyte
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Complexity of gap junctions between horizontal cells of the carp retina.

2016

In the vertebrate retina, horizontal cells (HCs) reveal homologous coupling by gap junctions (gj), which are thought to consist of different connexins (Cx). However, recent studies in mouse, rabbit and zebrafish retina indicate that individual HCs express more than one connexin. To provide further insights into the composition of gj connecting HCs and to determine whether HCs express multiple connexins, we examined the molecular identity and distribution of gj between HCs of the carp retina. We have cloned four carp connexins designated Cx49.5, Cx55.5, Cx52.6 and Cx53.8 with a close relationship to connexins previously reported in HCs of mouse, rabbit and zebrafish, respectively. Using in s…

0301 basic medicineFish ProteinsCarpsImmunoelectron microscopyBlotting WesternConnexinIn situ hybridizationRetinal Horizontal Cellsbehavioral disciplines and activitiesPolymerase Chain ReactionConnexins03 medical and health sciencesMice0302 clinical medicineCell Line TumormedicineAnimalsProtein IsoformsElectrical synapseAmino Acid SequenceCarpMicroscopy ImmunoelectronZebrafishIn Situ HybridizationRetinabiologyGeneral NeuroscienceGap junctionGap JunctionsAnatomyDendritesbiology.organism_classificationImmunohistochemistryAxonsCell biology030104 developmental biologymedicine.anatomical_structureembryonic structuressense organsSequence Alignment030217 neurology & neurosurgeryNeuroscience
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Antibody trapping: A novel mechanism of parasite immune evasion by the trematode Echinostoma caproni

2017

Background Helminth infections are among the most prevalent neglected tropical diseases, causing an enormous impact in global health and the socioeconomic growth of developing countries. In this context, the study of helminth biology, with emphasis on host-parasite interactions, appears as a promising approach for developing new tools to prevent and control these infections. Methods/Principal findings The role that antibody responses have on helminth infections is still not well understood. To go in depth into this issue, work on the intestinal helminth Echinostoma caproni (Trematoda: Echinostomatidae) has been undertaken. Adult parasites were recovered from infected mice and cultured in vi…

0301 basic medicineMalePhysiologyAntibody ResponsePathogenesisPathology and Laboratory MedicineBiochemistryMiceImmune PhysiologyEchinostomaMedicine and Health SciencesParasite hostingEnzyme-Linked ImmunoassaysMicroscopy ImmunoelectronImmune ResponseEchinostomiasisImmune System Proteinsbiologylcsh:Public aspects of medicineProteases030108 mycology & parasitologyEnzymesInfectious DiseasesHelminth InfectionsHost-Pathogen InteractionsTrematodaAntibodyEchinostomaCellular Structures and OrganellesResearch ArticleProtein BindingProteaseslcsh:Arctic medicine. Tropical medicinelcsh:RC955-962ImmunologyAntibodies HelminthContext (language use)Research and Analysis MethodsAntibodies03 medical and health sciencesImmune systemParasitic DiseasesAnimalsSecretionVesiclesImmunoassaysImmune EvasionPublic Health Environmental and Occupational HealthBiology and Life SciencesProteinslcsh:RA1-1270Cell Biologybiology.organism_classificationVirologyDisease Models Animal030104 developmental biologyMicroscopy FluorescenceProteolysisbiology.proteinImmunologic TechniquesEnzymologyPLoS Neglected Tropical Diseases
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Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction

2016

Myelination of axons facilitates rapid impulse propagation in the nervous system. The axon/myelin-unit becomes impaired in myelin-related disorders and upon normal aging. However, the molecular cause of many pathological features, including the frequently observed myelin outfoldings, remained unknown. Using label-free quantitative proteomics, we find that the presence of myelin outfoldings correlates with a loss of cytoskeletal septins in myelin. Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that extend longitudinally along myelinated axons. By confoca…

0301 basic medicineNervous systemCentral Nervous SystemProteomicsScaffoldMouseProteomeNeural ConductionSeptinNerve Fibers MyelinatedMyelinGene Knockout TechniquesMiceContractile ProteinsAxonBiology (General)CytoskeletonMicroscopy ImmunoelectronCytoskeletonMyelin SheathMicroscopy ConfocalGeneral NeuroscienceQRGeneral MedicineAnatomyCell biologyglial cellsmedicine.anatomical_structureGene TargetingMedicineResearch ArticleQH301-705.5ScienceCentral nervous systemmyelinated axonsmacromolecular substancesBiologyGeneral Biochemistry Genetics and Molecular Biologymyelin structure03 medical and health sciencesSeptin/anillin filaments; central nervous system; myelinlabel-free proteomicsmedicineAnimalsneuropathologyGeneral Immunology and Microbiology030104 developmental biologynervous systemseptin cytoskeletonProtein MultimerizationSeptinsSeptin cytoskeletonNeuroscienceeLife
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Usherin defects lead to early-onset retinal dysfunction in zebrafish

2018

Mutations in USH2A are the most frequent cause of Usher syndrome and autosomal recessive nonsyndromic retinitis pigmentosa. To unravel the pathogenic mechanisms underlying USH2A-associated retinal degeneration and to evaluate future therapeutic strategies that could potentially halt the progression of this devastating disorder, an animal model is needed. The available Ush2a knock-out mouse model does not mimic the human phenotype, because it presents with only a mild and late-onset retinal degeneration. Using CRISPR/Cas9-technology, we introduced protein-truncating germline lesions into the zebrafish ush2a gene (ush2a(rmc1): c.2337_2342delinsAC; p.Cys780GlnfsTer32 and ush2a(b1245): c.15520_…

0301 basic medicineRetinal degenerationGenotyping TechniquesUsher syndrome2804 Cellular and Molecular NeuroscienceApoptosis030105 genetics & heredityBiologyArticleRetinaGermlineSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Gene Knockout Techniques03 medical and health sciencesCellular and Molecular NeuroscienceUSH2 complex2809 Sensory SystemsAll institutes and research themes of the Radboud University Medical CenterRetinitis pigmentosaElectroretinographymedicineotorhinolaryngologic diseasesJournal ArticleAnimalsMicroscopy ImmunoelectronZebrafishZebrafishExtracellular Matrix ProteinsRetinal DegenerationMembrane ProteinsZebrafish ProteinsRetinal Photoreceptor Cell Outer Segmentmedicine.diseasebiology.organism_classification2731 OphthalmologySensory Systems10124 Institute of Molecular Life SciencesCell biologyDisease Models AnimalOphthalmology030104 developmental biologyGene Expression RegulationEctodomainMutation570 Life sciences; biologyXenotropic and Polytropic Retrovirus ReceptorUsher SyndromesErg
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Immunohistological and immunoelectron microscopic identification of TNF alpha in normal human and murine epidermis.

1992

The presence, distribution and cellular localization of tumour necrosis factor-alpha (TNF alpha) were investigated in normal human and murine epidermis using immunohistological and immunoelectron microscopic methods with monoclonal and polyclonal antibodies. The immunostaining revealed an intercellular plasma membrane and cytoplasmic labelling of the epidermal keratinocytes, but no labelling of Langerhans cells, melanocytes and Merkel cells. Large amounts of TNF alpha were regularly found in the sebaceous glands. These findings demonstrate that epidermal keratinocytes and especially sebocytes produce and release TNF alpha and that this keratinocyte-derived cytokine may be important for the …

AdultMalePathologymedicine.medical_specialtyImmunoelectron microscopymedicine.medical_treatmentDermatologyMicemedicineAnimalsHumansMicroscopy ImmunoelectronCellular localizationMice Inbred BALB Cintegumentary systemEpidermis (botany)biologyTumor Necrosis Factor-alphaGeneral MedicineMiddle AgedMolecular biologyImmunohistochemistryCytokinemedicine.anatomical_structurePolyclonal antibodiesbiology.proteinImmunohistochemistryFemaleEpidermisMerkel cellImmunostainingArchives of dermatological research
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Clinical, histological and genetic characterization of reducing body myopathy caused by mutations in FHL1

2008

We recently identified the X-chromosomal four and a half LIM domain gene FHL1 as the causative gene for reducing body myopathy, a disorder characterized by progressive weakness and intracytoplasmic aggregates in muscle that exert reducing activity on menadione nitro-blue-tetrazolium (NBT). The mutations detected in FHL1 affected highly conserved zinc coordinating residues within the second LIM domain and lead to the formation of aggregates when transfected into cells. Our aim was to define the clinical and morphological phenotype of this myopathy and to assess the mutational spectrum of FHL1 mutations in reducing body myopathy in a larger cohort of patients. Patients were ascertained via th…

AdultMaleWeaknessPathologymedicine.medical_specialtyMutation MissenseMuscle ProteinsBiologymedicine.disease_causeMuscular DiseasesBiopsymedicineHumansGenetic Predisposition to DiseaseMyopathyChildMicroscopy ImmunoelectronMuscle SkeletalMutationMuscle biopsymedicine.diagnostic_testIntracellular Signaling Peptides and ProteinsInfantGenetic Diseases X-LinkedOriginal ArticlesLIM Domain Proteinsmedicine.diseaseCongenital myopathyFHL1PedigreeChild PreschoolFemaleNeurology (clinical)medicine.symptomProgressive disease
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Inducible nitric oxide synthase in skeletal muscle of patients with chronic heart failure

1998

Abstract Objectives. The expression and localization of inducible nitric oxide (NO) synthase (NOS II) was evaluated as a source of NO which has been shown to affect muscle contraction. Background. Advanced stages of chronic heart failure are associated with systemic activation of cytokines which have been shown to stimulate the expression of NOS II in various cell types, including myocytes. We hypothesized that systemic cytokine activation could lead to expression of NOS II in skeletal muscle of patients with chronic heart failure. Methods. Skeletal muscle specimens were obtained by percutaneous needle biopsy in six normal volunteers and eight patients with heart failure (New York Heart Ass…

Adultmedicine.medical_specialtyHeart diseaseGene ExpressionNitric Oxide Synthase Type IIPolymerase Chain ReactionNitric oxidechemistry.chemical_compoundInternal medicineGene expressionmedicineHumansMyocyteRNA MessengerMicroscopy ImmunoelectronMuscle SkeletalHeart Failurebiologybusiness.industrySkeletal muscleRNA-Directed DNA PolymeraseMiddle Agedmedicine.diseaseNitric oxide synthaseEndocrinologymedicine.anatomical_structurechemistryHeart failureChronic Diseasebiology.proteinNitric Oxide Synthasemedicine.symptombusinessCardiology and Cardiovascular MedicineMuscle contractionJournal of the American College of Cardiology
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Infantile intranuclear rod myopathy.

1997

This report concerns three unrelated floppy infants, two girls and one boy, each biopsied at the age of 1 month. They were hypotonic since birth and required artificial ventilation. The two girls died at the ages of 4 and 3½ months, respectively, the boy is still alive at the age of 2 years, but requires assisted ventilation. Each of the three infants showed, by muscle biopsy, abundant intranuclear rods, the boy and one girl also had sarcoplasmic rods, which were not present in the other girl's muscle. Absence of sarcoplasmic rods, but the presence of intranuclear rods could also be documented in her autopsied muscle. Using an antibody against α-actinin, immunoelectron microscopy showed re…

Artificial ventilationMalePediatricsmedicine.medical_specialtygenetic structuresmedicine.medical_treatmentBiopsyMyosinsMyopathies Nemaline03 medical and health sciences0302 clinical medicineFatal Outcome030225 pediatricsmedicineHumansEndotheliumFloppy InfantMicroscopy ImmunoelectronMuscle SkeletalCell Nucleusbusiness.industryInfant NewbornPediatrics Perinatology and Child HealthFemalesense organsNeurology (clinical)Intranuclear Rod Myopathybusiness030217 neurology & neurosurgeryJournal of child neurology
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Different roles for KIF17 and kinesin II in photoreceptor development and maintenance.

2009

Kinesin 2 family members are involved in transport along ciliary microtubules. In Caenorhabditis elegans channel cilia, kinesin II and OSM-3 cooperate along microtubule doublets of the axoneme middle segment, whereas OSM-3 alone works on microtubule singlets to elongate the distal segment. Among sensory cilia, vertebrate photoreceptors share a similar axonemal structure with C. elegans channel cilia, and deficiency in either kinesin II or KIF17, the homologue of OSM-3, results in disruption of photoreceptor organization. However, direct comparison of the two effects is confounded by the use of different species and knockdown strategies in prior studies. Here, we directly compare the effects…

AxonemeEmbryo NonmammalianBlotting WesternKinesinsBiologyArticleMiceMicroscopy Electron TransmissionMicrotubuleCiliogenesisAnimalsImmunoprecipitationKinesin 8Microscopy ImmunoelectronZebrafishZebrafishKIF17CiliumfungiZebrafish Proteinsbiology.organism_classificationImmunohistochemistryCell biologyRetinal Cone Photoreceptor CellsKinesinsense organsDevelopmental BiologyDevelopmental dynamics : an official publication of the American Association of Anatomists
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