Search results for "Variants"

showing 10 items of 227 documents

Histones, Their Variants and Post-translational Modifications in Zebrafish Development.

2020

Complex multi-cellular organisms are shaped starting from a single-celled zygote, owing to elaborate developmental programs. These programs involve several layers of regulation to orchestrate the establishment of progressively diverging cell type-specific gene expression patterns. In this scenario, epigenetic modifications of chromatin are central in influencing spatiotemporal patterns of gene transcription. In fact, it is generally recognized that epigenetic changes of chromatin states impact on the accessibility of genomic DNA to regulatory proteins. Several lines of evidence highlighted that zebrafish is an excellent vertebrate model for research purposes in the field of developmental ep…

0301 basic medicineHistone-modifying enzymeshistone posttranslational modificationsMini ReviewMorphogenesisSettore BIO/11 - Biologia Molecolarematernal-to-zygotic transitionComparative biologyComputational biologyhistone03 medical and health sciencesCell and Developmental Biology0302 clinical medicineEpigeneticshistone variantsZebrafishlcsh:QH301-705.5developmentzygotic genome activationbiologyepigeneticsCell Biologybiology.organism_classificationzebrafishChromatinhistone histone posttranslational modifications histone variants epigenetics development maternal-to-zygotic transition zygotic genome activation zebrafish030104 developmental biologyHistonelcsh:Biology (General)030220 oncology & carcinogenesisbiology.proteinMaternal to zygotic transitionDevelopmental BiologyFrontiers in cell and developmental biology
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Missense Mutations of Human Hsp60: A Computational Analysis to Unveil Their Pathological Significance

2020

Two chaperonopathies have been linked to mutations in the human hsp60 (hHsp60; HSPD1) gene, but other existing variants might cause diseases, even if there is no comprehensive information about this possibility. To fill this vacuum, which might be at the basis of misdiagnoses or simply ignorance of chaperonopathies in patients who would benefit by proper identification of their ailments, we searched the sequenced human genomes available in public databases to determine the range of missense mutations in the single hsp60 gene. A total of 224 missense mutations were identified, including those already characterized. Detailed examination of these mutations was carried out to assess their possi…

0301 basic medicineHsp60 gene variantlcsh:QH426-470chaperoning systemMutantunderdiagnosed chaperonopathiesDiseaseBiology03 medical and health sciences0302 clinical medicinehuman genomeGeneticsMissense mutationGeneGenetics (clinical)Hsp60 genetic chaperonopathieOriginal ResearchGeneticschemistry.chemical_classificationHsp60 genetic chaperonopathieshuman genomesHsp60 gene variantsAmino acidlcsh:Genetics030104 developmental biologychemistry030220 oncology & carcinogenesisMolecular MedicineHSP60Human genomeIdentification (biology)Frontiers in Genetics
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Human apolipoprotein A-I Gly26Arg stimulation of inflammatory responses via NF-kB activation: Potential roles in amyloidosis?

2018

The cascade of molecular events leading to Human apolipoprotein A–I (apoA–I) amyloidosis is not completely understood, not even the pathways that determine clinical manifestations associated to systemic protein deposition in organs such as liver, kidney and heart. About twenty natural variants of apoA–I were described as inducing amyloidosis, but the mechanisms driving their aggregation and deposition are still unclear. We previously identified that the mutant Gly26Arg but not Lys107-0 induced the release of cytokines and reactive oxygen species from cultured RAW 264.7 murine macrophages, suggesting that part of the pathogenic pathway could elicit of an inflammatory signal. In this work we …

0301 basic medicineLipopolysaccharideMACROPHAGES ACTIVATIONMutantStimulationInflammationOxidative phosphorylationPathology and Forensic MedicineCiencias Biológicas03 medical and health scienceschemistry.chemical_compoundINFLAMMATIONPhysiology (medical)APOLIPOPROTEIN A-I VARIANTSmedicineNUCLEAR FACTOR-ΚBchemistry.chemical_classificationReactive oxygen speciesAmyloidosisNF-κBBioquímica y Biología Molecularmedicine.diseaseCell biology030104 developmental biologychemistryAMYLOIDOSISlipids (amino acids peptides and proteins)medicine.symptomCIENCIAS NATURALES Y EXACTASPathophysiology
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Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin.

2020

Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, i…

0301 basic medicineMaleDendritic spineGeneral Physics and AstronomyHippocampal formationVARIANTSADULT NEUROGENESIS0302 clinical medicineCognitionhemic and lymphatic diseasesReceptors ErythropoietinHypoxialcsh:ScienceNEURONSMultidisciplinaryNeuronal PlasticityPyramidal CellsNeurogenesisQBrainCell DifferentiationHEMATOPOIETIC PROGENITOR CELLSFemalemedicine.symptomProto-Oncogene Proteins c-fosmedicine.drugEXPRESSIONScienceDendritic SpinesNeurogenesisModels NeurologicalBiologyMotor ActivityGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesParacrine signallingPhysical Conditioning AnimalNeuroplasticitymedicineAnimalsHumansErythropoietinMEMORYCognitive neuroscienceGeneral ChemistryHypoxia (medical)RECOMBINANT-HUMAN-ERYTHROPOIETINCellular neuroscienceErythropoietin receptorMice Inbred C57BLMICE030104 developmental biologyErythropoietinPhysical EnduranceIDENTITYlcsh:QTranscriptomeNeuroscience030217 neurology & neurosurgeryGene Deletion
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New insights into the genetics of primary open-angle glaucoma based on meta-analyses of intraocular pressure and optic disc characteristics

2017

Item does not contain fulltext Primary open-angle glaucoma (POAG), the most common optic neuropathy, is a heritable disease. Siblings of POAG cases have a ten-fold increased risk of developing the disease. Intraocular pressure (IOP) and optic nerve head characteristics are used clinically to predict POAG risk. We conducted a genome-wide association meta-analysis of IOP and optic disc parameters and validated our findings in multiple sets of POAG cases and controls. Using imputation to the 1000 genomes (1000G) reference set, we identified 9 new genomic regions associated with vertical cup-disc ratio (VCDR) and 1 new region associated with IOP. Additionally, we found 5 novel loci for optic ne…

0301 basic medicineMaleIntraocular pressuregenetic structuresOptic diskGlaucomaPROTEINGenome-wide association studyIDENTIFIES 5Sensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Optic neuropathyOptic Nerve DiseasesPROSTATEGenetics (clinical)RISKAssociation Studies ArticlesCOMMON VARIANTSGeneral MedicineMiddle AgedCANCER3. Good healthmedicine.anatomical_structureOptic nerveFemaleGlaucoma Open-AngleOptic discCyclin-Dependent Kinase Inhibitor p21medicine.medical_specialtyOpen angle glaucomaSUSCEPTIBILITY LOCIOptic Disk610 Medicine & healthBiology03 medical and health sciencesTonometry OcularOphthalmologyGeneticsmedicineHumansGENOME-WIDE ASSOCIATIONMolecular BiologyIntraocular PressureHomeodomain ProteinsP53Genome HumanPOPULATION-BASED EPIDEMIOLOGYZebrafish Proteinsmedicine.diseaseeye diseases030104 developmental biologysense organsGenome-Wide Association StudyHuman Molecular Genetics
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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Characterization of the Clinical and Immunologic Phenotype and Management of 157 Individuals with 56 Distinct Heterozygous NFKB1 Mutations

2020

Contains fulltext : 229571.pdf (Publisher’s version ) (Closed access) BACKGROUND: An increasing number of NFKB1 variants are being identified in patients with heterogeneous immunologic phenotypes. OBJECTIVE: To characterize the clinical and cellular phenotype as well as the management of patients with heterozygous NFKB1 mutations. METHODS: In a worldwide collaborative effort, we evaluated 231 individuals harboring 105 distinct heterozygous NFKB1 variants. To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling. RESU…

0301 basic medicineMaleNF-KAPPA-BMedizinlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Fluorescent Antibody TechniqueAutoimmunityDiseaseNUCLEAR-FACTORKaplan-Meier Estimatemedicine.disease_causeHypogammaglobulinemia0302 clinical medicineNFKB1 variants and mutations; autosomal dominant inheritance; common variable immunodeficiency; reduced penetrance; variable expressivityHDE PEDImmunology and Allergyvariants and mutationsNF-κB1-related phenotypeImmunodeficiencyIMMUNODEFICIENCY*NF-?B1-related phenotypeNFKB1 variants and mutations1184 Genetics developmental biology physiologycommon variable immunodeficiencyDisease ManagementMiddle AgedNF-kappa B1-related phenotypereduced penetrancePrognosisPenetranceImmunohistochemistryMagnetic Resonance Imaging3. Good healthPhenotypeNFKB1 variant*NFKB1 variant*common variable immunodeficiencyFemaleHaploinsufficiency*reduced penetranceNFKB1 mutationAdultHeterozygote*NFKB1 mutationImmunologyHAPLOINSUFFICIENCYArticle03 medical and health sciencesvariable expressivityautosomal dominantmedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesAgedbusiness.industryCommon variable immunodeficiencyNF-kappa B p50 SubunitNF-KAPPA-B1Immune dysregulationmedicine.diseaseautosomal dominant inheritance030104 developmental biologyBiological Variation PopulationImmunologyCELLSMutation*autosomal dominantPrimary immunodeficiency3111 BiomedicinebusinessTomography X-Ray ComputedBiomarkers030215 immunology
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Skeletal alterations, developmental delay and new mutations in juvenile-onset Pompe disease.

2018

Abstract Pompe disease is an autosomal recessive disorder caused by a deficiency of acid α-glucosidase. In addition to the severe infantile form with cardiac involvement, late-onset variants can affect older children, adolescents (aged >1 year old) or adults. Patients with juvenile (a subgroup of late-onset type) Pompe disease typically do not have cardiac alterations e.g. hypertrophic cardiomyopathy, and the diagnosis is often difficult because it can clinically resemble myriad other neuromuscular disorders. A high level of clinical suspicion is necessary for a timely and accurate diagnosis. We describe 3 interesting cases of patients with juvenile-onset Pompe disease who presented some un…

0301 basic medicineMalePediatricsmedicine.medical_specialtyAdolescentDevelopmental DisabilitiesDisease03 medical and health sciences0302 clinical medicinemedicineJuvenileHumansMuscle SkeletalGenetics (clinical)business.industryGlycogen Storage Disease Type IIGenetic variantsalpha-Glucosidases030104 developmental biologyJuvenile onsetNeurologyPediatrics Perinatology and Child HealthMutationNeurology (clinical)Glucan 14-alpha-Glucosidasebusiness030217 neurology & neurosurgeryNeuromuscular disorders : NMD
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Does education protect against depression? Evidence from the Young Finns Study using Mendelian randomization

2018

Using participants (N = 1733) drawn from the nationally representative longitudinal Young Finns Study (YFS) we estimate the effect of education on depressive symptoms. In 2007, when the participants were between 30 and 45 years old, they reported their depressive symptoms using a revised version of Beck's Depression Inventory. Education was measured using register information on the highest completed level of education in 2007, which was converted to years of education. To identify a causal relationship between education and depressive symptoms we use an instrumental variables approach (Mendelian randomization, MR) with a genetic risk score as an instrument for years of education. The genet…

0301 basic medicineMaleSYMPTOMSEpidemiologyLOCIGenome-wide association studyVARIANTS0302 clinical medicinekoulutustaustaRisk FactorsMedicine030212 general & internal medicineta515Depression (differential diagnoses)FinlandRISKeducationDepressionInstrumental variableta3142Middle Aged3142 Public health care science environmental and occupational healthOrdinary least squaresdepressionEducational StatusFemaleHEALTHAdultmasennusMODELS03 medical and health scienceskoulutustasoLinear regressionMendelian randomizationMendelian randomizationHumansGENOME-WIDE ASSOCIATIONEstimationta511instrumental variablesbusiness.industryPublic Health Environmental and Occupational HealthsosiaaliepidemiologiaMendelian Randomization AnalysisConfidence interval030104 developmental biology3121 General medicine internal medicine and other clinical medicinebusinessDemographyGenome-Wide Association Study
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Meta-analysis of genome-wide association studies discovers multiple loci for chronic lymphocytic leukemia

2016

Chronic lymphocytic leukemia (CLL) is a common lymphoid malignancy with strong heritability. To further understand the genetic susceptibility for CLL and identify common loci associated with risk, we conducted a meta-analysis of four genome-wide association studies (GWAS) composed of 3,100 cases and 7,667 controls with follow-up replication in 1,958 cases and 5,530 controls. Here we report three new loci at 3p24.1 (rs9880772, EOMES, P=2.55 × 10−11), 6p25.2 (rs73718779, SERPINB6, P=1.97 × 10−8) and 3q28 (rs9815073, LPP, P=3.62 × 10−8), as well as a new independent SNP at the known 2q13 locus (rs9308731, BCL2L11, P=1.00 × 10−11) in the combined analysis. We find suggestive evidence (P<5 × 10−…

0301 basic medicineMedicin och hälsovetenskapChronic lymphocytic leukemiaGeneral Physics and AstronomyGenome-wide association studyVARIANTSMedical and Health SciencesMalalties hereditàries[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyChronicGeneticsRISKLeukemiaMultidisciplinaryBANK1VDP::Medisinske Fag: 700::Helsefag: 800::Samfunnsmedisin sosialmedisin: 801Bcl-2-Like Protein 11QAdaptor Proteins[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologySingle NucleotideLymphocytic3. Good healthPRIORITIZATIONMultidisciplinary SciencesLeukemiamedicine.anatomical_structureScience & Technology - Other TopicsTRANSCRIPTION FACTOR EOMESODERMINGenetic disordersEXPRESSIONSUSCEPTIBILITY LOCIScienceEuropean Continental Ancestry GroupFAS GENE-MUTATIONSLocus (genetics)BiologyPolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyCLASSIFICATIONWhite PeopleArticle03 medical and health sciencesProto-Oncogene ProteinsMD MultidisciplinarymedicineGenetic predispositionSNPHumansLeucèmia limfocítica crònicaGenetic Predisposition to DiseasePolymorphismB cellSerpinsGenetic associationAdaptor Proteins Signal TransducingScience & TechnologySignal TransducingB-CellMembrane ProteinsGeneral Chemistrymedicine.diseaseLeukemia Lymphocytic Chronic B-Cell030104 developmental biologyChronic lymphocytic leukemiaVDP::Medical disciplines: 700::Health sciences: 800::Community medicine Social medicine: 801Apoptosis Regulatory ProteinsT-Box Domain ProteinsFOLLICULAR LYMPHOMAGenome-Wide Association Study
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