Search results for "MUTATION"

showing 10 items of 2830 documents

Junctophilin-1 is a modifier gene of GDAP1-related Charcot-Marie-Tooth disease.

2014

Mutations in the GDAP1 gene cause different forms of Charcot-Marie-Tooth (CMT) disease, and the primary clinical expression of this disease is markedly variable in the dominant inheritance form (CMT type 2K; CMT2K), in which carriers of the GDAP1 p.R120W mutation can display a wide range of clinical severity. We investigated the JPH1 gene as a genetic modifier of clinical expression variability because junctophilin-1 (JPH1) is a good positional and functional candidate. We demonstrated that the JPH1-GDAP1 cluster forms a paralogon and is conserved in vertebrates. Moreover, both proteins play a role in Ca(2+) homeostasis, and we demonstrated that JPH1 is able to restore the store-operated Ca…

Nerve Tissue ProteinsDiseaseMitochondrionBiologyCell LineEvolution MolecularMiceCharcot-Marie-Tooth DiseaseGeneticsAnimalsHumansGenetic Predisposition to DiseaseStromal Interaction Molecule 1Molecular BiologyGeneGenetics (clinical)PhylogenyGenes ModifierActivator (genetics)Endoplasmic reticulumMembrane ProteinsSTIM1General MedicinePhenotypeMolecular biologyMitochondriaNeoplasm ProteinsMutationCalciumHomeostasisHuman molecular genetics
researchProduct

Cell expression of GDAP1 in the nervous system and pathogenesis of Charcot-Marie-Tooth type 4A disease

2007

Abstract Mutations in the mitochondrial protein GDAP1 are the cause of Charcot-Marie-Tooth type 4A disease (CMT4A), a severe form of peripheral neuropathy associated with either demyelinating, axonal or intermediate pheno-types. GDAP1 is located in the outer mitochondrial membrane and it seems that may be related with the mitochondrial network dynamics. We are interested to define cell expression in the nervous system and the effect of mutations in mitochondrial morphology and pathogenesis of the disease. We investigated GDAP1 expression in the nervous system and dorsal root ganglia (DRG) neuron cultures. GDAP1 is expressed in motor and sensory neurons of the spinal cord and other large neu…

Nervous systemCMT4A mutations and pathogenesisPathologymedicine.medical_specialtyperipheral neuropathyCharcot-Marie-Tooth type 4A diseaseMutation MissenseGene ExpressionImages in Cellular / Molecular MedicineNerve Tissue ProteinsGDAP1MitochondrionBiologymedicine.disease_causeNervous SystemPathogenesisMicePurkinje CellsCharcot-Marie-Tooth DiseaseInterneuronsGanglia SpinalChlorocebus aethiopsmedicineAnimalsHumansNeurons AfferentCells CulturedMotor NeuronsMutationfusion and fission pathwayPyramidal CellsCell Biologymedicine.diseaseSpinal cordImmunohistochemistrymitochondrial dynamicsCell biologyOlfactory bulbRatsmedicine.anatomical_structurePeripheral neuropathynervous systemAnimals NewbornSpinal CordCOS CellsMolecular MedicineNeuronHeLa CellsJournal of Cellular and Molecular Medicine
researchProduct

The columnar gene vnd is required for tritocerebral neuromere formation during embryonic brain development of Drosophila.

2006

International audience; In Drosophila, evolutionarily conserved transcription factors are required for the specification of neural lineages along the anteroposterior and dorsoventral axes, such as Hox genes for anteroposterior and columnar genes for dorsoventral patterning. In this report, we analyse the role of the columnar patterning gene ventral nervous system defective (vnd) in embryonic brain development. Expression of vnd is observed in specific subsets of cells in all brain neuromeres. Loss-of-function analysis focussed on the tritocerebrum shows that inactivation of vnd results in regionalized axonal patterning defects, which are comparable with the brain phenotype caused by mutatio…

Nervous systemMutantApoptosis0302 clinical medicineMESH: Gene Expression Regulation DevelopmentalDrosophila ProteinsMESH: AnimalsAxonHox geneMESH: MelatoninGenetics0303 health sciencesMESH: Pineal GlandBrainGene Expression Regulation DevelopmentalMESH: Transcription FactorsNeuromerePhenotypeBiological EvolutionCell biologymedicine.anatomical_structureDrosophila melanogasterPhenotypeMESH: Photic StimulationMESH: Body PatterningMESH: MutationMESH: Drosophila ProteinsBiologyMESH: PhenotypeMESH: Drosophila melanogaster03 medical and health sciencesMESH: BrainNeuroblastMESH: EvolutionMESH: Homeodomain ProteinsmedicineAnimalsMESH: Circadian RhythmMolecular Biology030304 developmental biologyBody PatterningHomeodomain ProteinsMESH: HumansMESH: ApoptosisEmbryogenesis[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMESH: LightMutationMESH: SerotoninMESH: Seasons030217 neurology & neurosurgeryDevelopmental BiologyTranscription Factors
researchProduct

FLRT structure: Balancing repulsion and cell adhesion in cortical and vascular development

2014

Summary FLRTs are broadly expressed proteins with the unique property of acting as homophilic cell adhesion molecules and as heterophilic repulsive ligands of Unc5/Netrin receptors. How these functions direct cell behavior and the molecular mechanisms involved remain largely unclear. Here we use X-ray crystallography to reveal the distinct structural bases for FLRT-mediated cell adhesion and repulsion in neurons. We apply this knowledge to elucidate FLRT functions during cortical development. We show that FLRTs regulate both the radial migration of pyramidal neurons, as well as their tangential spread. Mechanistically, radial migration is controlled by repulsive FLRT2-Unc5D interactions, wh…

Nervous systemNeuroscience(all)CellBiologyCrystallography X-RayArticle03 medical and health sciencesMice0302 clinical medicineddc:570NetrinmedicineCell AdhesionAnimalsHumansCell adhesionReceptor030304 developmental biologyGlycosaminoglycansNeurons0303 health sciencesCell adhesion moleculeGeneral NeuroscienceMembrane ProteinsAdhesionCell biologyRatsmedicine.anatomical_structureMembrane proteinMutation030217 neurology & neurosurgery
researchProduct

Characterization of molecular mechanisms underlying the axonal Charcot–Marie–Tooth neuropathy caused by MORC2 mutations

2019

Mutations in MORC2 lead to an axonal form of Charcot-Marie-Tooth (CMT) neuropathy type 2Z. To date, 31 families have been described with mutations in MORC2, indicating that this gene is frequently involved in axonal CMT cases. While the genetic data clearly establish the causative role of MORC2 in CMT2Z, the impact of its mutations on neuronal biology and their phenotypic consequences in patients remains to be clarified. We show that the full-length form of MORC2 is highly expressed in both embryonic and adult human neural tissues and that Morc2 expression is dynamically regulated in both the developing and the maturing murine nervous system. To determine the effect of the most common MORC2…

Nervous systemSensory Receptor CellsCellBiologymedicine.disease_causeNeural Stem CellsCharcot-Marie-Tooth DiseaseGeneticsmedicineAnimalsHumansMolecular BiologyGeneEmbryonic Stem CellsGenetics (clinical)MutationGeneral MedicineFibroblastsPhenotypeEmbryonic stem cellAxonsNeural stem cellPathophysiologyRatsCell biologymedicine.anatomical_structureGene Expression Regulationnervous systemMutationTranscription FactorsHuman Molecular Genetics
researchProduct

Netrins guide migration of distinct glial cells in the Drosophila embryo

2010

Development of the nervous system and establishment of complex neuronal networks require the concerted activity of different signalling events and guidance cues, which include Netrins and their receptors. In Drosophila, two Netrins are expressed during embryogenesis by cells of the ventral midline and serve as attractant or repellent cues for navigating axons. We asked whether glial cells, which are also motile, are guided by similar cues to axons, and analysed the influence of Netrins and their receptors on glial cell migration during embryonic development. We show that in Netrin mutants, two distinct populations of glial cells are affected: longitudinal glia (LG) fail to migrate medially …

Nervous systemanimal structuresCentral nervous systemBiologyNeuroblastCell MovementPrecursor cellGlial cell migrationNetrinmedicineAnimalsNerve Growth FactorsMolecular BiologyTumor Suppressor ProteinsfungiNeurogenesisCell PolarityExonsAnatomyNetrin-1ImmunohistochemistryEmbryonic stem cellCell biologyPhenotypemedicine.anatomical_structurenervous systemMutationDrosophilaCuesNeurogliaSignal TransductionDevelopmental BiologyDevelopment
researchProduct

Defining the role of common variation in the genomic and biological architecture of adult human height

2014

Item does not contain fulltext Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated approximately 2,000, approximately 3,700 and approximately 9,500 SNPs explained approximately 21%, approximately 24% and approximately 29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes…

Netherlands Twin Register (NTR)BIO/12 - BIOCHIMICA CLINICA E BIOLOGIA MOLECOLARE CLINICAElectronic Medical Records and Genomics (eMEMERGEGE) ConsortiumMedizinGenome-wide association studyAdult; Analysis of Variance; Body Height/genetics; European Continental Ancestry Group/genetics; Genetic Variation/genetics; Genetics Population; Genome-Wide Association Study/methods; Humans; Oligonucleotide Array Sequence Analysis; Polymorphism Single Nucleotide/geneticsheritability0302 clinical medicineGenome-wideEuropean Continental Ancestry Group/geneticsSNPSOligonucleotide Array Sequence AnalysissnpsGenetics & Heredityddc:616GeneticsMedical And Health Sciences0303 health scienceseducation.field_of_studyvariantsBody Height/geneticsGENETIC-VARIATIONBiological SciencesPolymorphism Single Nucleotide/geneticsGenetic Variation/geneticsUrological cancers Radboud Institute for Health Sciences [Radboudumc 15]Genome-Wide Association Study/methodsbody heightgenetic-variationLife Sciences & BiomedicineSingle Nucleotide/geneticsHumanAdultEuropean Continental Ancestry GroupPopulationPopulationSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideArticleWhite PeopleNOcomplex traits03 medical and health sciencesGenetic variationheritability adult height/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_GeneticsHumansPolymorphismHuman heightPAGEGE ConsortiumeducationGeneVLAG030304 developmental biologyGlobal NutritionWereldvoedingAnalysis of VarianceGenome-wide; heritability; variantsgenome-wide association studyScience & TechnologyWhitesOligonucleotide Array Sequence AnalysiMUTATIONSCOMPLEX TRAITSta1184Klinisk medicinpopulation geneticsGenetic VariationHeritabilityta3121mutationsGenetic architectureBody HeightGenetics Populationgenetic variationMIGen ConsortiumInflammatory diseases Radboud Institute for Health Sciences [Radboudumc 5]Clinical Medicine030217 neurology & neurosurgeryheightLifeLines Cohort StudyDevelopmental BiologyGenome-Wide Association StudyNature genetics
researchProduct

Psychiatric genome-wide association study analyses implicate neuronal, immune and histone pathways

2015

G.B. and S.N. acknowledge funding support for this work from the National Institute for Health Research (NIHR) Mental Health Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London. P.H.L. is supported by US National Institute of Mental Health (NIMH) grant K99MH101367. Genome-wide association studies (GWAS) of psychiatric disorders have identified multiple genetic associations with such disorders, but better methods are needed to derive the underlying biological mechanisms that these signals indicate. We sought to identify biological pathways in GWAS data from over 60,000 participants from the Psychiatric Genomics Consortium. We developed an an…

Netherlands Twin Register (NTR)Statistical methodsAutismMedizinLOCIGenome-wide association studyheritabilityGenome-wide association studiesHistonesGenètica mèdica0302 clinical medicineHistone methylationDatabases Genetic2.1 Biological and endogenous factorsPsychologyGWASAetiologyPsychiatric geneticsR2Cbipolar disorderPsychiatry0303 health sciencesDisordersLociDepressionGeneral NeuroscienceMental DisordersMedical geneticsMETHYLATIONBrain3rd-DASSerious Mental IllnessPsychiatric Disorders3. Good healthHistoneMental HealthSchizophreniaMental DisorderCognitive Sciences[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]PromotersBDCBURDENRC0321 Neuroscience. Biological psychiatry. NeuropsychiatryHumanSignal Transductionmedicine.medical_specialtyDISORDERSGenomicsNetwork and Pathway Analysis Subgroup of Psychiatric Genomics ConsortiumBurdenBiologyMethylationArticleBiological pathwayPROMOTERS03 medical and health sciencesDatabasesGeneticmedicineGenetics/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_HumansGenetic Predisposition to Diseasehistone methylationBipolar disorderPsiquiatriaAUTISMPsychiatry030304 developmental biologyGenetic associationNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Neurology & NeurosurgeryNeuroscience (all)Human GenomeNeurosciencesmedicine.diseaseBrain DisordersGood Health and Well BeingDE-NOVO MUTATIONSPerturbações do Desenvolvimento Infantil e Saúde MentalRC0321SchizophreniaGenome-wide Association StudiesDe-novo mutationsmajor depressionNeuroscience030217 neurology & neurosurgeryGenome-Wide Association Study
researchProduct

Analysis of KRAS , NRAS , BRAF , PIK3CA and TP53 mutations in a large prospective series of locally advanced rectal cancer patients

2019

Little information is available on the clinical significance of cancer-related genes such as KRAS, NRAS, BRAF, PIK3CA and TP53 in nonmetastatic rectal cancer. We investigated mutations of these genes in a large prospective series of locally advanced rectal cancer (LARC) patients who were recruited into two phase II trials. Mutational analyses were performed with diagnostically validated methods including polymerase chain reaction, capillary electrophoresis single-strand conformational analysis, Sanger sequencing and next-generation sequencing. Associations between single or multiple gene mutations and clinicopathological characteristics and treatment outcomes were explored. Of these 269, 21…

Neuroblastoma RAS viral oncogene homologOncologyCancer Researchmedicine.medical_specialtyendocrine system diseasesColorectal cancerPopulationGene mutationmedicine.disease_cause03 medical and health sciences0302 clinical medicineInternal medicinemedicineeducationneoplasmsUnivariate analysiseducation.field_of_studyCetuximabbusiness.industrymedicine.diseaseOncology030220 oncology & carcinogenesisBiomarker (medicine)KRASbusinessmedicine.drugInternational Journal of Cancer
researchProduct

Molecular Characterization of Relapsed Core-Binding Factor (CBF) Acute Myeloid Leukemia (AML)

2015

Abstract Background: CBF-AML is defined by recurrent genetic abnormalities which encompass t(8;21)(q22;q22), inv(16)(p13.1q22) or less frequently t(16;16)(p13.1;q22). Most frequent secondary chromosome aberrations in t(8;21) AML are del(9q) or loss of a sex chromosome, and in inv(16)/t(16;16) AML trisomy 22 or trisomy 8. At the molecular level mutations involving KIT, FLT3, or NRAS were identified as recurrent lesions in CBF-AML. However, the underlying genetic alterations which might trigger relapse in CBF-AML are not well delineated. Thus, the aim of our study was to characterize the clonal architecture of relapsed CBF-AML. Methods: We performed mutational profiling (KIT, FLT3-ITD, FLT3-T…

Neuroblastoma RAS viral oncogene homologOncologymedicine.medical_specialtybusiness.industryImmunologyMyeloid leukemiaCell BiologyHematologyKit mutationCore binding factorBioinformaticsTrisomy 8medicine.diseaseBiochemistryExonInternal medicineChromosome abnormalityMedicinebusinessTrisomyBlood
researchProduct