Search results for "Phenotype"

showing 10 items of 1875 documents

Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia

2017

Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated me…

0301 basic medicineMalememoriaAginggenetics [Stress Disorders Post-Traumatic]Diseasegenetics [Neuronal Plasticity]BioinformaticsdemenciaStress Disorders Post-TraumaticMice0302 clinical medicineRisk FactorsNews & ViewsAge of OnsetMice KnockoutNeuronal PlasticitybiologyGeneral NeuroscienceMicrofilament ProteinsNuclear Proteinsgenetics [Nuclear Proteins]FearadultoMiddle AgedAlzheimer's diseasephysiology [Aging]Phenotype3. Good healthPhenotypemiedoFormin 2Forminsgenetics [Aging]estres postraumaticoepidemiology [Stress Disorders Post-Traumatic]AdultHDAC inhibidorpsychology [Dementia]alzheimerForminsNerve Tissue Proteinsepidemiology [Dementia]Affect (psychology)General Biochemistry Genetics and Molecular Biology03 medical and health sciencesHDAC inhibitorMemorygenetics [Dementia]ddc:570medicineDementiaAnimalsHumansenvejecimientoMolecular Biologyphysiology [Memory]General Immunology and MicrobiologyPost-traumatic stress disordermedicine.diseaseYoung age030104 developmental biologyformin 2 protein mouseCase-Control StudiesSynaptic plasticitybiology.proteinDementiagenetics [Microfilament Proteins]complications [Stress Disorders Post-Traumatic]030217 neurology & neurosurgeryHomeostasis
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Common genes associated with antidepressant response in mouse and man identify key role of glucocorticoid receptor sensitivity.

2017

Response to antidepressant treatment in major depressive disorder (MDD) cannot be predicted currently, leading to uncertainty in medication selection, increasing costs, and prolonged suffering for many patients. Despite tremendous efforts in identifying response-associated genes in large genome-wide association studies, the results have been fairly modest, underlining the need to establish conceptually novel strategies. For the identification of transcriptome signatures that can distinguish between treatment responders and nonresponders, we herein submit a novel animal experimental approach focusing on extreme phenotypes. We utilized the large variance in response to antidepressant treatmen…

0301 basic medicineMicroarraysPhysiologyGene ExpressionBioinformaticsBiochemistryBiomarkers PharmacologicalTranscriptomeMice0302 clinical medicineGlucocorticoid receptorMedicine and Health SciencesBiology (General)DepressionGeneral NeuroscienceBrainDrugsAntidepressantsPhenotypeAntidepressive Agents3. Good healthBody FluidsParoxetineBioassays and Physiological AnalysisBloodMice Inbred DBAMultigene FamilyMajor depressive disorderAntidepressantDNA microarrayAnatomyGeneral Agricultural and Biological SciencesResearch ArticleQH301-705.5Antidepressant drug therapy ; Blood ; Gene regulation ; Biomarkers ; Depression ; Gene expression ; Microarrays ; AntidepressantsBiologyResearch and Analysis MethodsGeneral Biochemistry Genetics and Molecular BiologyBlood Plasma03 medical and health sciencesReceptors GlucocorticoidMental Health and PsychiatrymedicineGeneticsAnimalsHumansGene RegulationPharmacologyDepressive Disorder MajorGeneral Immunology and MicrobiologyMechanism (biology)Mood DisordersGene Expression ProfilingBiology and Life Sciencesmedicine.diseaseGene expression profiling030104 developmental biologyGene Expression RegulationCorticosterone030217 neurology & neurosurgeryBiomarkersPLoS biology
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First phenotypic and genotypic description of Fasciola hepatica infecting highland cattle in the state of Mexico, Mexico

2018

Abstract Fascioliasis is a plantborne and zoonotic parasitic disease caused by fasciolid liver flukes. Fasciola hepatica is the only fasciolid species described in the Americas. Human fascioliasis endemic areas are mainly located in high altitude areas of the Americas. Given the necessity to characterize F. hepatica populations involved, the phenotypic and genotypic features of fasciolid adults infecting cattle in the highland area of Toluca, State of Mexico, Mexico, were analyzed and compared to fasciolid materials from the Northern Bolivian Altiplano, representing the altiplanic transmission pattern in a hyperendemic scenario. A computer image analysis system (CIAS) was applied on the bas…

0301 basic medicineMicrobiology (medical)FascioliasisGenotypeRange (biology)030231 tropical medicinebiology.animal_breedPopulationCattle DiseasesZoologyDNA RibosomalMicrobiology03 medical and health sciences0302 clinical medicineIntergenic regionHepaticaparasitic diseasesGeneticsAnimalsFasciola hepaticaGeography MedicaleducationMexicoMolecular BiologyRibosomal DNAEcology Evolution Behavior and SystematicsBase Compositioneducation.field_of_studybiologyHighland CattleFasciola hepatica030108 mycology & parasitologyLiver flukebiology.organism_classificationPhenotypeInfectious DiseasesHaplotypesCattleSequence AnalysisInfection, Genetics and Evolution
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The broad phenotypic spectrum of PPP2R1A -related neurodevelopmental disorders correlates with the degree of biochemical dysfunction

2021

PURPOSE: Neurodevelopmental disorders (NDD) caused by protein phosphatase 2A (PP2A) dysfunction have mainly been associated with de novo variants in PPP2R5D and PPP2CA, and more rarely in PPP2R1A. Here, we aimed to better understand the latter by characterizing 30 individuals with de novo and often recurrent variants in this PP2A scaffolding Aα subunit. METHODS: Most cases were identified through routine clinical diagnostics. Variants were biochemically characterized for phosphatase activity and interaction with other PP2A subunits. RESULTS: We describe 30 individuals with 16 different variants in PPP2R1A, 21 of whom had variants not previously reported. The severity of developmental delay …

0301 basic medicineMicrocephaly[SDV]Life Sciences [q-bio]Intellectual disability030105 genetics & heredityBioinformaticsEpilepsyNeurodevelopmental disorderIntellectual disabilityCOREProtein Phosphatase 2SPECIFICITYGenetics (clinical)PROTEIN PHOSPHATASE 2APhenotypeHypotoniaFAMILY3. Good healthPP2A[SDV] Life Sciences [q-bio]PPP2R1APPP2R5DINSIGHTSintellectual disabilityMicrocephalyMuscle Hypotoniamedicine.symptomLanguage delay[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsArticle03 medical and health sciencesNeurodevelopmental disorder[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEpilepsybusiness.industryMacrocephalyDEPHOSPHORYLATIONmedicine.diseaseneurodevelopmental disorder030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsNeurodevelopmental DisordersSUBUNITepilepsyHuman medicineTAUbusinessTranscription Factors
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Re-definition and supporting evidence toward Fanconi Anemia as a mitochondrial disease: Prospects for new design in clinical management

2021

Fanconi anemia (FA) has been investigated since early studies based on two definitions, namely defective DNA repair and proinflammatory condition. The former definition has built up the grounds for FA diagnosis as excess sensitivity of patients' cells to xenobiotics as diepoxybutane and mitomycin C, resulting in typical chromosomal abnormalities. Another line of studies has related FA phenotype to a prooxidant state, as detected by both in vitro and ex vivo studies. The discovery that the FA group G (FANCG) protein is found in mitochondria (Mukhopadhyay et al., 2006) has been followed by an extensive line of studies providing evidence for multiple links between other FA gene products and mi…

0301 basic medicineMitochondrial DNAMitochondrial DiseasesMitomycinMitochondrial diseaseClinical BiochemistryDiepoxybutaneReview ArticleMitochondrionBiologyBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFanconi anemiaFANCGmedicineHumansClastogenCarnitinelcsh:QH301-705.5Coenzyme Q10lcsh:R5-920ProteinOrganic ChemistryMitochondrial nutrientProteinsmedicine.diseaseMitochondrial diseaseFanconi AnemiaPhenotypeClastogens030104 developmental biologylcsh:Biology (General)chemistryProoxidant stateCancer researchMitochondrial nutrientsMitochondrial dysfunctionlcsh:Medicine (General)030217 neurology & neurosurgeryHumanmedicine.drugRedox Biology
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Whole Exome Sequencing Is the Preferred Strategy to Identify the Genetic Defect in Patients With a Probable or Possible Mitochondrial Cause

2018

Mitochondrial disorders, characterized by clinical symptoms and/or OXPHOS deficiencies, are caused by pathogenic variants in mitochondrial genes. However, pathogenic variants in some of these genes can lead to clinical manifestations which overlap with other neuromuscular diseases, which can be caused by pathogenic variants in non-mitochondrial genes as well. Mitochondrial pathogenic variants can be found in the mitochondrial DNA (mtDNA) or in any of the 1,500 nuclear genes with a mitochondrial function. We have performed a two-step next-generation sequencing approach in a cohort of 117 patients, mostly children, in whom a mitochondrial disease-cause could likely or possibly explain the phe…

0301 basic medicineMitochondrial DNANuclear genelcsh:QH426-470DISORDERSMitochondrial diseaseBiologyMOLECULAR DIAGNOSISMtDNA sequencingDNA sequencingDISEASEDiagnostic yield03 medical and health sciencesmedicineGeneticsDNA DELETIONSGenetics(clinical)whole-exome sequencingTRANSFER-RNA-SYNTHETASELACTIC-ACIDOSISGeneGenetics (clinical)Exome sequencingOriginal ResearchGeneticsmtDNA sequencingGenetic heterogeneityMUTATIONSASSEMBLY FACTORSmedicine.diseasePhenotypeMitochondrial diseaselcsh:Geneticsmitochondrial disease030104 developmental biologyHUMAN COMPLEX-IWhole-exome sequencingdiagnostic yieldNext-generation sequencingMolecular Medicinenext-generation sequencingLEIGH-SYNDROMEFrontiers in Genetics
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Total Hemi-overgrowth in Pigmentary Mosaicism of the (Hypomelanosis of) Ito Type: Eight Case Reports.

2016

Abstract Pigmentary mosaicism of the (hypomelanosis of) Ito type is an umbrella term, which includes phenotypes characterized by mosaic hypopigmentation in the form of streaks, whorls, patchy, or more bizarre skin configurations (running along the lines of Blaschko): these cutaneous patterns can manifest as an isolated skin disorder (pigmentary mosaicism of the Ito type) or as a complex malformation syndrome in association with extracutaneous anomalies (most often of the musculoskeletal and/or nervous systems) (hypomelanosis of Ito). Affected individuals are anecdotally reported to have also partial or total body hemi-overgrowth (HOG), which often causes moderate to severe complications. We…

0301 basic medicineModerate to severeAdultMalePathologymedicine.medical_specialtyAdolescentDevelopmental DisabilitiesContext (language use)030105 genetics & heredity03 medical and health sciences0302 clinical medicinemedicineHumansAbnormalities MultipleClinical Case ReportClinical phenotypeChildKyphoscoliosisPigmentation disorderHypopigmentationChromosome AberrationsHypopigmentationbusiness.industryMosaicismFollow up studiesTotal bodyGeneral Medicinemedicine.diseaseMagnetic Resonance Imaging6200Musculoskeletal Abnormalitieshypomelanosis Ito type Pigmentary mosaicism mosaic hypopigmentation childrenPhenotypeItalyChild PreschoolKaryotypingFemalemedicine.symptombusinessPigmentation Disorders030217 neurology & neurosurgeryResearch ArticleFollow-Up StudiesMedicine
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In silico discovery of substituted pyrido[2,3-d]pyrimidines and pentamidine-like compounds with biological activity in myotonic dystrophy models

2016

Myotonic dystrophy type 1 (DM1) is a rare multisystemic disorder associated with an expansion of CUG repeats in mutant DMPK (dystrophia myotonica protein kinase) transcripts; the main effect of these expansions is the induction of pre-mRNA splicing defects by sequestering muscleblind-like family proteins (e.g. MBNL1). Disruption of the CUG repeats and the MBNL1 protein complex has been established as the best therapeutic approach for DM1, hence two main strategies have been proposed: targeted degradation of mutant DMPK transcripts and the development of CUG-binding molecules that prevent MBNL1 sequestration. Herein, suitable CUG-binding small molecules were selected using in silico approach…

0301 basic medicineMolecular biologyPhysiologyMutantMyotonic dystrophyDruggabilitylcsh:Medicine01 natural sciencesBiochemistryPhysical ChemistryMyoblastschemistry.chemical_compoundAnabolic AgentsMedicaments--InteraccióAnimal CellsDrug DiscoveryMedicine and Health SciencesMBNL1Drosophila ProteinsMyotonic Dystrophylcsh:ScienceRNA structureConnective Tissue CellsMultidisciplinaryMolecular StructureOrganic CompoundsStem CellsPhysicsRNA-Binding ProteinsBiological activityPhenotypeClimbingMolecular Docking SimulationNucleic acidsChemistryDrosophila melanogasterBiochemistryGenetic DiseasesConnective TissueRNA splicingPhysical SciencesCellular TypesAnatomyLocomotion57 - BiologiaSignal TransductionResearch ArticleBiotechnologyHydrogen bondingcongenital hereditary and neonatal diseases and abnormalitiesIn silicoPrimary Cell CultureComputational biologyBiology010402 general chemistryMyotonic dystrophyMyotonin-Protein KinaseDrug interactionsSmall Molecule Libraries03 medical and health sciencesStructure-Activity RelationshipmedicineAnimalsHumansRNA MessengerEnllaços d'hidrogenClinical GeneticsChemical PhysicsBiology and life sciencesChemical BondingBiological Locomotionlcsh:ROrganic ChemistryEstructura molecularChemical CompoundsHydrogen BondingCell BiologyFibroblastsmedicine.disease0104 chemical sciencesBenzamidinesAlternative SplicingDisease Models AnimalMacromolecular structure analysis030104 developmental biologyPyrimidinesBiological TissuechemistrySmall MoleculesRNAlcsh:QTrinucleotide Repeat ExpansionMolecular structure
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Assessing Human Genetic Variations in Glucose Transporter SLC2A10 and Their Role in Altering Structural and Functional Properties

2018

Purpose: Demand is increasing for clinical genomic sequencing to provide diagnoses for patients presenting phenotypes indicative of genetic diseases, but for whom routine genetic testing failed to yield a diagnosis. DNA-based testing using high-throughput technologies often identifies variants with insufficient evidence to determine whether they are disease-causal or benign, leading to categorization as variants of uncertain significance (VUS). Methods: We used molecular modeling and simulation to generate specific hypotheses for the molecular effects of variants in the human glucose transporter, GLUT10 (SLC2A10). Similar to many disease-relevant membrane proteins, no experimentally derived…

0301 basic medicineMolecular modellcsh:QH426-470Computational biologyBiology03 medical and health scienceschemistry.chemical_compoundGenetic variationmedicinegeneticsnatural variationGenetics (clinical)Genetic testingOriginal Researchmedicine.diagnostic_testmolecular modelingvariant of uncertain significanceGlucose transporterPrecision medicinePhenotypelcsh:Genetics030104 developmental biologychemistryMembrane proteinATSMolecular MedicineDNAFrontiers in Genetics
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Genomic evolution of bacterial populations under coselection by antibiotics and phage

2017

Bacteria live in dynamic systems where selection pressures can alter rapidly, forcing adaptation to the prevailing conditions. In particular, bacteriophages and antibiotics of anthropogenic origin are major bacterial stressors in many environments. We previously observed that populations of the bacterium Pseudomonas fluorescens SBW25 exposed to the lytic bacteriophage SBW25Φ2 and a noninhibitive concentration of the antibiotic streptomycin (coselection) achieved higher levels of phage resistance compared to populations exposed to the phage alone. In addition, the phage became extinct under coselection while remaining present in the phage alone environment. Further, phenotypic tests indicate…

0301 basic medicineMutation rateantibiotic resistancemedicine.drug_class030106 microbiologyAntibioticsBiologyPseudomonas fluorescensmedicine.disease_causeMicrobiologyEvolution MolecularBacteriophage03 medical and health sciencesAntibiotic resistanceMutation RateDrug Resistance BacterialGeneticsmedicineBacteriophagesexperimental evolutionSelection GeneticEscherichia coliEcology Evolution Behavior and Systematics2. Zero hungerExperimental evolutionta1182biology.organism_classificationsublethal antibiotic concentrationsAnti-Bacterial AgentsPhenotypeLytic cyclephage resistanceStreptomycinta1181phage phi-2Genome BacterialBacteria
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