Search results for "BINDING PROTEIN"

showing 10 items of 1292 documents

Beyond the Transport Function of Import Receptors: What’s All the FUS about?

2018

Nuclear import receptors are central players in transporting protein cargoes into the nucleus. Moving beyond this role, four newly published articles describe a function in regulating supramolecular assemblies by fine-tuning the phase separating properties of RNA-binding proteins, which has implications for a variety of devastating neurodegenerative disorders.

0301 basic medicineProteomeActive Transport Cell NucleusReceptors Cytoplasmic and NuclearBiologyKaryopherinsModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesmedicineAnimalsHumansReceptorRNA metabolismCell NucleusAmyotrophic Lateral SclerosisRNA-Binding ProteinsNeurodegenerative Diseases3. Good healthCell biologyDNA-Binding ProteinsCell nucleus030104 developmental biologymedicine.anatomical_structureRNARNA-Binding Protein FUSNuclear transportNucleusFunction (biology)Cell
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Human R1441C LRRK2 regulates the synaptic vesicle proteome and phosphoproteome in a Drosophila model of Parkinson's disease

2016

International audience; Mutations in leucine-rich repeat kinase 2 (LRRK2) cause late-onset, autosomal dominant familial Parkinsons disease (PD) and variation at the LRRK2 locus contributes to the risk for idiopathic PD. LRRK2 can function as a protein kinase and mutations lead to increased kinase activity. To elucidate the pathophysiological mechanism of the R1441C mutation in the GTPase domain of LRRK2, we expressed human wild-type or R1441C LRRK2 in dopaminergic neurons of Drosophila and observe reduced locomotor activity, impaired survival and an age-dependent degeneration of dopaminergic neurons thereby creating a new PD-like model. To explore the function of LRRK2 variants in vivo, we …

0301 basic medicineProteomerab3 GTP-Binding Proteinsalpha-synucleindomainSyntaxin 1Interactomedopaminergic-neuronsAnimals Genetically Modifiedchemistry.chemical_compound0302 clinical medicinemicrotubule stabilityDrosophila ProteinsProtein Interaction MapsGenetics (clinical)LRRK2 GeneKinasephosphorylationBrainParkinson DiseaseArticlesGeneral Medicineautosomal-dominant parkinsonismLRRK2Drosophila melanogasterSynaptotagmin IProteomePhosphorylationSynaptic VesiclesNerve Tissue ProteinsBiologyLeucine-Rich Repeat Serine-Threonine Protein Kinase-203 medical and health sciencesGeneticsAnimalsHumansKinase activitygeneMolecular BiologyAlpha-synucleingtp-bindingDopaminergic Neuronsrepeat kinase 2Molecular biologyPhosphoric Monoester Hydrolasesnervous system diseasesDisease Models Animal030104 developmental biologyGene Expression Regulationchemistrymutation030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Small Rab GTPases in Intracellular Vesicle Trafficking: The Case of Rab3A/Raphillin-3A Complex in the Kidney

2021

Small Rab GTPases, the largest group of small monomeric GTPases, regulate vesicle trafficking in cells, which are integral to many cellular processes. Their role in neurological diseases, such as cancer and inflammation have been extensively studied, but their implication in kidney disease has not been researched in depth. Rab3a and its effector Rabphillin-3A (Rph3A) expression have been demonstrated to be present in the podocytes of normal kidneys of mice rats and humans, around vesicles contained in the foot processes, and they are overexpressed in diseases with proteinuria. In addition, the Rab3A knockout mice model induced profound cytoskeletal changes in podocytes of high glucose fed a…

0301 basic medicineQH301-705.5Kidney Glomerulus030232 urology & nephrologyVesicular Transport ProteinsNerve Tissue ProteinsGTPaseReviewBiologyKidneyRabphilin-3ACatalysisInorganic Chemistry03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansPhysical and Theoretical ChemistryBiology (General)CytoskeletonMolecular BiologyQD1-999SpectroscopyAdaptor Proteins Signal TransducingKidneyEffectorPodocytesVesicleOrganic ChemistryRab3AIntracellular vesicleEpithelial CellsGeneral Medicinerab3A GTP-Binding ProteinComputer Science ApplicationsCell biologyChemistry030104 developmental biologymedicine.anatomical_structurerab GTP-Binding ProteinsRab proteinsKnockout mouseRabInternational Journal of Molecular Sciences
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Radial Glial Fibers Promote Neuronal Migration and Functional Recovery after Neonatal Brain Injury.

2018

Radial glia (RG) are embryonic neural stem cells (NSCs) that produce neuroblasts and provide fibers that act as a scaffold for neuroblast migration during embryonic development. Although they normally disappear soon after birth, here we found that RG fibers can persist in injured neonatal mouse brains and act as a scaffold for postnatal ventricular-subventricular zone (V-SVZ)-derived neuroblasts that migrate to the lesion site. This injury-induced maintenance of RG fibers has a limited time window during post-natal development and promotes directional saltatory movement of neuroblasts via N-cadherin-mediated cell-cell contacts that promote RhoA activation. Transplanting an N-cadherin-contai…

0301 basic medicineRHOAanimal structuresventricular-subventricular zoneBiology03 medical and health sciences0302 clinical medicinegait behaviorNeuroblastCell MovementNeuroblast migrationLateral VentriclesGeneticsmedicineAnimalsreproductive and urinary physiologyN-cadherinNeuronsneuronal migrationneuronal regenerationneonatal brain injuryCadherinEmbryogenesisfungiCell Biologypostnatal neurogenesisRecovery of FunctionCadherinsEmbryonic stem cellNeural stem cellRadial glial cell030104 developmental biologymedicine.anatomical_structurenervous systemAnimals NewbornBrain Injuriesbiology.proteinMolecular MedicinerhoA GTP-Binding ProteinNeuroscienceNeuroglia030217 neurology & neurosurgeryradial glial cellCell stem cell
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The RAB GTPase RAB18 modulates macroautophagy and proteostasis

2017

Macroautophagy is a conserved degradative pathway and its deterioration is linked to disturbances in cellular proteostasis and multiple diseases. Here, we show that the RAB GTPase RAB18 modulates autophagy in primary human fibroblasts. The knockdown of RAB18 results in a decreased autophagic activity, while its overexpression enhances the degradative pathway. Importantly, this function of RAB18 is dependent on RAB3GAP1 and RAB3GAP2, which might act as RAB GEFs and stimulate the activity of the RAB GTPase. Moreover, the knockdown of RAB18 deteriorates proteostasis and results in the intracellular accumulation of ubiquitinated degradation-prone proteins. Thus, the RAB GTPase RAB18 is a positi…

0301 basic medicineRecombinant Fusion Proteinsrab3 GTP-Binding ProteinsPrimary Cell CultureBiophysicsGTPaseBiochemistry03 medical and health sciencesUbiquitinGenes ReporterAutophagyHumansRNA Small InterferingMolecular BiologyGene knockdownbiologyProtein StabilityChemistryfungiAutophagyCell BiologyFibroblastsCell biologyLuminescent Proteins030104 developmental biologyProteostasisGene Expression Regulationrab GTP-Binding ProteinsProteolysisbiology.proteinCancer researchRabSignal transductionRAB18Signal TransductionBiochemical and Biophysical Research Communications
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Nucleocytoplasmic transport of the RNA-binding protein CELF2 regulates neural stem cell fates.

2020

The development of the cerebral cortex requires balanced expansion and differentiation of neural stem/progenitor cells (NPCs), which rely on precise regulation of gene expression. Because NPCs often exhibit transcriptional priming of cell-fate-determination genes, the ultimate output of these genes for fate decisions must be carefully controlled in a timely fashion at the post-transcriptional level, but how that is achieved is poorly understood. Here, we report that de novo missense variants in an RNA-binding protein CELF2 cause human cortical malformations and perturb NPC fate decisions in mice by disrupting CELF2 nucleocytoplasmic transport. In self-renewing NPCs, CELF2 resides in the cyt…

0301 basic medicineRegulation of gene expressionNeurogenesisRNA-Binding ProteinsTranslation (biology)RNA-binding proteinCell DifferentiationNerve Tissue ProteinsBiologyCell fate determinationGeneral Biochemistry Genetics and Molecular BiologyNeural stem cellCell biology03 medical and health sciences030104 developmental biology0302 clinical medicineNeural Stem CellsNucleocytoplasmic TransportCELF ProteinsHumansProgenitor cell030217 neurology & neurosurgeryCell reports
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Functional impacts of 5-hydroxymethylcytosine, 5-formylcytosine, and 5-carboxycytosine at a single hemi-modified CpG dinucleotide in a gene promoter

2017

Abstract Enzymatic oxidation of 5-methylcytosine (5-mC) in the CpG dinucleotides to 5-hydroxymethylcytosine (5-hmC), 5-formylcytosine (5-fC) and 5-carboxycytosine (5-caC) has central role in the process of active DNA demethylation and epigenetic reprogramming in mammals. However, it is not known whether the 5-mC oxidation products have autonomous epigenetic or regulatory functions in the genome. We used an artificial upstream promoter constituted of one cAMP response element (CRE) to measure the impact of 5-mC in a hemi-methylated CpG on the promoter activity and further explored the consequences of 5-hmC, 5-fC, and 5-caC in the same system. All modifications induced mild impairment of the …

0301 basic medicineResponse elementCREB03 medical and health sciencesCytosine0302 clinical medicineGeneticsAnimalsHumansCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticRegulation of gene expressionbiologyBase SequenceGene regulation Chromatin and EpigeneticsPromoterDNADNA MethylationThymine DNA GlycosylaseCell biology030104 developmental biologyDNA demethylationCpG siteGene Expression RegulationDNA glycosylaseDNA methylationbiology.protein5-MethylcytosineCpG Islands030217 neurology & neurosurgeryProtein BindingNucleic Acids Research
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Progressive Characterization of Visual Phenotype in Bardet-Biedl Syndrome Mutant Mice

2019

Purpose Bardet-Biedl syndrome (BBS) is an archetypical ciliopathy caused by defective ciliary trafficking and consequent function. Insights gained from BBS mouse models are applicable to other syndromic and nonsyndromic retinal diseases. This progressive characterization of the visual phenotype in three BBS mouse models sets a baseline for testing therapeutic interventions. Methods Longitudinal acquisition of electroretinograms, optical coherence tomography scans, and visual acuity using the optomotor reflex in Bbs6/Mkks, Bbs8/Ttc8, and Bbs5 knockout mice. Gene and protein expression analysis in vivo and in vitro. Results Complete loss of BBS5, BBS6, or BBS8 leads to different rates of reti…

0301 basic medicineRetinal degenerationAgingBBSomeGenotyping Techniquesgenetic structuresBlotting WesternGroup II ChaperoninsBBS5030105 genetics & heredityBiologyReal-Time Polymerase Chain ReactionRetinaMKKSMice03 medical and health sciencesBardet–Biedl syndromeElectroretinographymedicineAnimalsBardet-Biedl SyndromeVision OcularMice Knockoutmedicine.diagnostic_testRetinal DegenerationPhosphate-Binding Proteinsmedicine.diseaseImmunohistochemistryMice Mutant StrainsCytoskeletal ProteinsDisease Models AnimalCiliopathyPhenotype030104 developmental biologyKnockout mouseCarrier ProteinsMicrotubule-Associated ProteinsNeuroscienceTomography Optical CoherenceSignal TransductionElectroretinographyInvestigative Opthalmology & Visual Science
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Structure-Based Discovery of Small Molecules Binding to RNA

2017

Ribonucleic acids (RNAs) constitute attractive drug targets. The wealth of structural information about RNAs is steadily increasing making it possible to use this information for the design of new ligands. Two methods that make heavy use of structural knowledge for ligand discovery are molecular docking and fragment screening. In molecular docking the structure of the binding site is used as a template for the design of new ligands using computational methods whereas in fragment screening biophysical methods are used for the detection of weak binding ligands which are subsequently elaborated into tighter binding molecules. In this chapter, we give an overview of both methods in the context …

0301 basic medicineRiboswitch010405 organic chemistryChemistryLigandBinding proteinRNAComputational biology01 natural sciencesSmall molecule0104 chemical sciences03 medical and health sciences030104 developmental biologyDocking (molecular)Structure basedBinding site
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SPEN haploinsufficiency causes a neurodevelopmental disorder overlapping proximal 1p36 deletion syndrome with an episignature of X chromosomes in fem…

2021

Contains fulltext : 231702.pdf (Publisher’s version ) (Closed access) Deletion 1p36 (del1p36) syndrome is the most common human disorder resulting from a terminal autosomal deletion. This condition is molecularly and clinically heterogeneous. Deletions involving two non-overlapping regions, known as the distal (telomeric) and proximal (centromeric) critical regions, are sufficient to cause the majority of the recurrent clinical features, although with different facial features and dysmorphisms. SPEN encodes a transcriptional repressor commonly deleted in proximal del1p36 syndrome and is located centromeric to the proximal 1p36 critical region. Here, we used clinical data from 34 individuals…

0301 basic medicineSHARPMaleobesitygenotype-phenotype correlationsAutism Spectrum DisorderPROTEINChromosome DisordersHaploinsufficiencyRNA-Binding ProteinPHENOTYPE CORRELATIONS1p36; distal 1p36 deletion syndrome; DNA methylome analysis; episignature; genotype-phenotype correlations; neurodevelopmental disorder; obesity; proximal 1p36 deletion syndrome; SPEN; X chromosome; Adolescent; Autism Spectrum Disorder; Child; Child Preschool; Chromosome Deletion; Chromosome Disorders; Chromosomes Human Pair 1; Chromosomes Human X; DNA Methylation; DNA-Binding Proteins; Epigenesis Genetic; Female; Haploinsufficiency; Humans; Intellectual Disability; Male; Neurodevelopmental Disorders; Phenotype; RNA-Binding Proteins; Young AdultEpigenesis GeneticX chromosome0302 clinical medicineNeurodevelopmental disorderNeurodevelopmental DisorderIntellectual disabilityMOLECULAR CHARACTERIZATIONdistal 1p36 deletion syndromeChildGenetics (clinical)X chromosomeGeneticsXDNA methylome analysiRNA-Binding ProteinsSPLIT-ENDSHypotoniaDNA-Binding ProteinsPhenotypeAutism spectrum disorderChromosomes Human Pair 1Child PreschoolDNA methylome analysisMONOSOMY 1P36Pair 1SPENFemalemedicine.symptomChromosome DeletionHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]HumanAdolescentDNA-Binding ProteinBiologygenotype-phenotype correlationChromosomes03 medical and health sciencesYoung AdultGeneticSDG 3 - Good Health and Well-beingReportIntellectual DisabilityREVEALSGeneticsmedicineHumansEpigeneticsPreschoolChromosomes Human XNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]1p361p36 deletion syndromeIDENTIFICATIONMUTATIONSproximal 1p36 deletion syndromeDNA Methylationmedicine.diseaseneurodevelopmental disorderGENEepisignature030104 developmental biologyChromosome DisorderNeurodevelopmental Disorders030217 neurology & neurosurgeryEpigenesis
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