Search results for "APLP1"

showing 4 items of 4 documents

Structure and Synaptic Function of Metal Binding to the Amyloid Precursor Protein and its Proteolytic Fragments

2017

Alzheimer’s disease (AD) is ultimately linked to the Amyloid Precursor Protein (APP). However, current research reveals an important synaptic function of APP and APP-like proteins (APLP1 and 2). In this context various neurotrophic and neuroprotective functions have been reported for the APP proteolytic fragments sAPPα, sAPPβ, and the monomeric amyloid-beta peptide (Aβ). APP is a metalloprotein and binds copper and zinc ions. Synaptic activity correlates with a release of these ions into the synaptic cleft and dysregulation of their homeostasis is linked to different neurodegenerative diseases. Metal binding to APP or its fragments affects its structure and its proteolytic cleavage and ther…

0301 basic medicineSynaptic cleftamyloid precursor protein (APP)Context (language use)ReviewNeurotransmission03 medical and health sciencesCellular and Molecular Neurosciencemental disordersAmyloid precursor proteinsynaptic transmissionAPLP1Molecular BiologybiologyChemistryzincP3 peptideCell biologyBiochemistry of Alzheimer's disease030104 developmental biologyAlpha secretaseBiochemistrycopperbiology.proteinAlzheimer’s diseaseNeuroscienceFrontiers in Molecular Neuroscience
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Amyloid Precursor-like Protein 1 Influences Endocytosis and Proteolytic Processing of the Amyloid Precursor Protein

2005

Ectodomain shedding of the amyloid precursor protein (APP) is a key regulatory step in the generation of the Alzheimer disease amyloid beta peptide (Abeta). The molecular mechanisms underlying the control of APP shedding remain little understood but are in part dependent on the low density lipoprotein receptor-related protein (LRP), which is involved in APP endocytosis. Here, we show that the APP homolog APLP1 (amyloid precursor-like protein 1) influences APP shedding. In human embryonic kidney 293 cells expression of APLP1 strongly activated APP shedding by alpha-secretase and slightly reduced beta-secretase cleavage. As revealed by domain deletion analysis, the increase in APP shedding re…

CytoplasmTime FactorsRecombinant Fusion ProteinsAmino Acid MotifsBlotting WesternGenetic VectorsEndocytic cycleCHO CellsTransfectionEndocytosisBiochemistryCell LineAmyloid beta-Protein PrecursorGenes ReporterCricetinaeChlorocebus aethiopsEndopeptidasesmental disordersAmyloid precursor proteinAnimalsAspartic Acid EndopeptidasesHumansImmunoprecipitationAPLP1Molecular BiologyModels GeneticbiologyChemistryHEK 293 cellsP3 peptideCell BiologyEndocytosisProtein Structure TertiaryMicroscopy FluorescenceBiochemistryAlpha secretaseEctodomainCOS Cellsbiology.proteinAmyloid Precursor Protein SecretasesPeptidesGene DeletionPlasmidsJournal of Biological Chemistry
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Loss of all three APP family members during development impairs synaptic function and plasticity, disrupts learning, and causes an autism-like phenot…

2021

The key role of APP for Alzheimer pathogenesis is well established. However, perinatal lethality of germline knockout mice lacking the entire APP family has so far precluded the analysis of its physiological functions for the developing and adult brain. Here, we generated conditional APP/APLP1/APLP2 triple KO (cTKO) mice lacking the APP family in excitatory forebrain neurons from embryonic day 11.5 onwards. NexCre cTKO mice showed altered brain morphology with agenesis of the corpus callosum and disrupted hippocampal lamination. Further, NexCre cTKOs revealed reduced basal synaptic transmission and drastically reduced long-term potentiation that was associated with reduced dendritic length …

Male10017 Institute of AnatomyLong-Term PotentiationHippocampal formationSynaptic TransmissionAmyloid beta-Protein Precursor0302 clinical medicine2400 General Immunology and MicrobiologyAmyloid precursor proteinMolecular Biology of DiseaseAutism spectrum disorderMice KnockoutNeurons0303 health sciencesbiologyBehavior AnimalGeneral NeuroscienceBrain2800 General NeuroscienceLong-term potentiationArticlesPhenotype10076 Center for Integrative Human PhysiologyKnockout mouseFemalelearning and memory610 Medicine & healthGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesProsencephalon1300 General Biochemistry Genetics and Molecular Biologymental disorders1312 Molecular BiologyAnimalsLearningAPLP1Autistic DisorderSocial BehaviorMolecular BiologyAPLP2CA1 Region Hippocampal030304 developmental biologysynaptic plasticityGeneral Immunology and MicrobiologyAmyloid precursor proteinSynaptic plasticityForebrainSynapsesbiology.proteinAlzheimer570 Life sciences; biologyNeuroscience030217 neurology & neurosurgeryNeuroscienceThe EMBO journal
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Single cell 3’UTR analysis identifies changes in alternative polyadenylation throughout neuronal differentiation and in autism

2020

SUMMARYAutism spectrum disorder (ASD) is a neurodevelopmental disease affecting social behavior. Many of the high-confident ASD risk genes relate to mRNA translation. Specifically, many of these genes are involved in regulation of gene expression for subcellular compartmentalization of proteins1. Cis-regulatory motifs that often localize to 3’- and 5’-untranslated regions (UTRs) offer an additional path for posttranscriptional control of gene expression. Alternative cleavage and polyadenylation (APA) affect 3’UTR length thereby influencing the presence or absence of regulatory elements. However, APA has not yet been addressed in the context of neurodevelopmental disorders. Here we used sing…

Regulation of gene expressionNeuroblastPolyadenylationThree prime untranslated regionmental disordersGene expressionAPLP1BiologyGeneNeural stem cellCell biology
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