Search results for "Sequencing"

showing 10 items of 1087 documents

Single-cell analysis of the ventricular-subventricular zone reveals signatures of dorsal and ventral adult neurogenesis

2021

The ventricular-subventricular zone (V-SVZ), on the walls of the lateral ventricles, harbors the largest neurogenic niche in the adult mouse brain. Previous work has shown that neural stem/progenitor cells (NSPCs) in different locations within the V-SVZ produce different subtypes of new neurons for the olfactory bulb. The molecular signatures that underlie this regional heterogeneity remain largely unknown. Here, we present a single-cell RNA-sequencing dataset of the adult mouse V-SVZ revealing two populations of NSPCs that reside in largely non-overlapping domains in either the dorsal or ventral V-SVZ. These regional differences in gene expression were further validated using a single-nucl…

MaleNervous systemMouseTransgenicneuroscienceMiceNeural Stem CellsLateral VentriclesBiology (General)education.field_of_studyGeneral NeuroscienceNeurogenesisQRGeneral MedicineStem Cells and Regenerative Medicineadult neurogenesismedicine.anatomical_structureolfactory bulbNeurologicalMedicineStem Cell Research - Nonembryonic - Non-HumanFemaleSingle-Cell AnalysisStem cellMicrodissectionneuroblastResearch ArticleQH301-705.51.1 Normal biological development and functioningNeurogenesisSciencePopulationregenerative medicineSubventricular zoneMice TransgenicBiologysingle-cell sequencingGeneral Biochemistry Genetics and Molecular BiologyNeuroblaststem cellsUnderpinning researchGeneticsmedicineAnimalseducationmouseGeneral Immunology and MicrobiologyNeurosciencesStem Cell ResearchOlfactory bulbstem cellnervous systemBiochemistry and Cell BiologyNeuronTranscriptomeNeuroscienceNeuroscienceregional differenceseLife
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Next-generation-sequencing-based identification of familial hypercholesterolemia-related mutations in subjects with increased LDL–C levels in a latvi…

2015

Background Familial hypercholesterolemia (FH) is one of the commonest monogenic disorders, predominantly inherited as an autosomal dominant trait. When untreated, it results in early coronary heart disease. The vast majority of FH remains undiagnosed in Latvia. The identification and early treatment of affected individuals remain a challenge worldwide. Most cases of FH are caused by mutations in one of four genes, APOB, LDLR, PCSK9, or LDLRAP1. The spectrum of disease-causing variants is very diverse and the variation detection panels usually used in its diagnosis cover only a minority of the disease-causing gene variants. However, DNA-based tests may provide an FH diagnosis for FH patients…

MaleNonsynonymous substitutionApolipoprotein BCoronary Artery DiseaseFamilial hypercholesterolemiaDiseaseCohort StudiesPCSK9Genetics(clinical)Family historyGenetics (clinical)Aged 80 and overGeneticseducation.field_of_studybiologySerine EndopeptidasesHigh-Throughput Nucleotide SequencingAutosomal dominant traitMiddle AgedLDLRAP1Apolipoprotein B-100Femalelipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9APOBResearch ArticleAdultPopulationPolymorphism Single NucleotideLDLHyperlipoproteinemia Type IIYoung AdultGeneticsmedicineHumanseducationAdaptor Proteins Signal TransducingAgedDiagnostic toolsPCSK9Cholesterol LDLmedicine.diseaseLatviaGenetics PopulationLDLRReceptors LDLMutationNext-generation sequencingbiology.proteinBMC Medical Genetics
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Biological and clinical significance of dysplastic hematopoiesis in patients with newly diagnosed multiple myeloma

2020

On behalf of the PETHEMA/GEM Cooperative Group.

MaleOncologyPhysics::Instrumentation and Detectorsmedicine.medical_treatmentKaplan-Meier EstimateHematopoietic stem cell transplantationBiochemistryhemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsTumor MicroenvironmentProspective StudiesComputer Science::Operating SystemsIn Situ Hybridization FluorescenceMultiple myelomaRandomized Controlled Trials as TopicComputer Science::Cryptography and SecurityHazard ratioHematopoietic Stem Cell TransplantationHigh-Throughput Nucleotide SequencingHematologyMiddle AgedFlow CytometryPrognosisCombined Modality TherapyProgression-Free Survivalmedicine.anatomical_structureFemaleClonal HematopoiesisMultiple Myelomamedicine.medical_specialtyImmunologyTransplantation AutologousInternal medicinemedicineHumansClinical significanceProgression-free survivalComputer Science::Distributed Parallel and Cluster ComputingAgedAntineoplastic Combined Chemotherapy Protocolbusiness.industryCell Biologymedicine.diseaseTransplantationClinical Trials Phase III as TopicMyelodysplastic SyndromesMutationBone marrowbusinessMonoclonal gammopathy of undetermined significance
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Rare variants in the genetic background modulate cognitive and developmental phenotypes in individuals carrying disease-associated variants

2019

Purpose: To assess the contribution of rare variants in the genetic background toward variability of neurodevelopmental phenotypes in individuals with rare copy-number variants (CNVs) and gene-disruptive variants. Methods: We analyzed quantitative clinical information, exome sequencing, and microarray data from 757 probands and 233 parents and siblings who carry disease-associated variants. Results: The number of rare likely deleterious variants in functionally intolerant genes (“other hits”) correlated with expression of neurodevelopmental phenotypes in probands with 16p12.1 deletion (n=23, p=0.004) and in autism probands carrying gene-disruptive variants (n=184, p=0.03) compared with thei…

MaleParents0301 basic medicineProbandNeuronalGenetic Carrier Screening16p11.2 deletion030105 genetics & heredityCognitionFamily historyNeural Cell Adhesion MoleculesGenetics (clinical)Exome sequencingSequence DeletionGeneticsGenetic Carrier ScreeningPhenotypePenetrancePedigreePhenotypeAutistic Disorder/genetics; Autistic Disorder/physiopathology; Cell Adhesion Molecules Neuronal/genetics; Chromosomes Human Pair 16/genetics; Cognition/physiology; DNA Copy Number Variations/genetics; Female; Gene Expression Regulation/genetics; Genetic Background; Genetic Carrier Screening; Humans; Male; Methyltransferases/genetics; Nerve Tissue Proteins/genetics; Parents; Pedigree; Phenotype; Proteins/genetics; Sequence Deletion/genetics; Siblings; 16p11.2 deletion; CNV; autism; modifier; phenotypic variabilityFemaleGenetic BackgroundHumanDNA Copy Number VariationsCell Adhesion Molecules NeuronalCNVautismNerve Tissue ProteinsBiologyChromosomesArticle03 medical and health sciencesmental disordersmedicineHumansAutistic DisorderBiologyGenemodifierPair 16SiblingsCalcium-Binding ProteinsProteinsMethyltransferasesmedicine.disease16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Genetics (clinical)Cytoskeletal Proteins030104 developmental biologyGene Expression Regulation[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutismphenotypic variabilityHuman medicine16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Autistic Disorder; Cell Adhesion Molecules Neuronal; Chromosomes Human Pair 16; Cognition; DNA Copy Number Variations; Female; Gene Expression Regulation; Genetic Background; Humans; Male; Methyltransferases; Nerve Tissue Proteins; Parents; Pedigree; Phenotype; Proteins; Sequence Deletion; Siblings; Genetic Carrier ScreeningCell Adhesion MoleculesChromosomes Human Pair 16Transcription FactorsGenetics in Medicine
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Delineation of the 3p14.1p13 microdeletion associated with syndromic distal limb contractures

2014

International audience; Distal limb contractures (DLC) represent a heterogeneous clinical and genetic condition. Overall, 20–25% of the DLC are caused by mutations in genes encoding the muscle contractile apparatus. Large interstitial deletions of the 3p have already been diagnosed by standard chromosomal analysis, but not associated with a specific phenotype. We report on four patients with syndromic DLC presenting with a de novo 3p14.1p13 micro-deletion. The clinical features associated multiple contractures, feeding problems, developmental delay, and intellectual disability. Facial dysmorphism was constant with low-set posteriorly rotated ears and blepharophimosis. Review of previously r…

MalePathologymedicine.medical_specialtyContracture[SDV]Life Sciences [q-bio]Locus (genetics)FOXP1BiologyMicedistal limb contracturessymbols.namesakeExonEIF4E3Intellectual disabilityGeneticsmedicineAnimalsHumans[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]3p141p13 microdeletionGenetics (clinical)ArthrogryposisChromosome AberrationsMice KnockoutSanger sequencingGeneticsComparative Genomic Hybridization[ SDV ] Life Sciences [q-bio]ExtremitiesForkhead Transcription FactorsSyndromeFOXP1Microdeletion syndromemedicine.diseaseBlepharophimosisPhenotypeRepressor Proteins[SDV] Life Sciences [q-bio]array-CGH[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]symbolsFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Chromosomes Human Pair 3FranceCarrier Proteinsintronic regulatory sequenceAmerican Journal of Medical Genetics Part A
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Targeted next-generation sequencing of deafness genes in hearing-impaired individuals uncovers informative mutations

2014

Purpose: Targeted next-generation sequencing provides a remarkable opportunity to identify variants in known disease genes, particularly in extremely heterogeneous disorders such as nonsyndromic hearing loss. The present study attempts to shed light on the complexity of hearing impairment. Methods: Using one of two next-generation sequencing panels containing either 80 or 129 deafness genes, we screened 30 individuals with nonsyndromic hearing loss (from 23 unrelated families) and analyzed 9 normal-hearing controls. Results: Overall, we found an average of 3.7 variants (in 80 genes) with deleterious prediction outcome, including a number of novel variants, in individuals with nonsyndromic h…

MaleProbandUsher syndromeGene DosageDeafnessBioinformaticsmedicine.disease_causesensorineural hearing lossConnexinsCohort Studiestargeted next-generation sequencingOriginal Research Articlemutational loadChildGenetics (clinical)Oligonucleotide Array Sequence AnalysisGeneticsMutationmedicine.diagnostic_testHomozygoteHigh-Throughput Nucleotide SequencingPedigreeConnexin 26Treatment OutcomeChild PreschoolFemalemedicine.symptomAdultAdolescentSequence analysisHearing lossdeafness gene panelMolecular Sequence DataBiologynonsyndromic hearing lossDNA sequencingYoung AdultAudiometryGenetic variationotorhinolaryngologic diseasesmedicineHumansGenetic Predisposition to DiseaseFamily HealthBase SequenceGenetic VariationInfantDNASequence Analysis DNAmedicine.diseaseMutationAudiometryGene DeletionGenetics in Medicine
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Identification of novel, clonally stable, somatic mutations targeting transcription factors PAX5 and NKX2-3, the epigenetic regulator LRIF1, and BRAF…

2021

Diagnosis of B-cell chronic lymphocytic leukemia (B-CLL) is usually straightforward, involving clinical, immunophenotypic (Matutes score), and (immuno)genetic analyses (to refine patient prognosis for treatment). CLL cases with atypical presentation (e.g., Matutes ≤ 3) are also encountered, and for these diseases, biology and prognostic impact are less clear. Here we report the genomic characterization of a case of atypical B-CLL in a 70-yr-old male patient; B-CLL cells showed a Matutes score of 3, chromosomal translocation t(14;18)(q32;q21) (BCL2/IGH), mutated IGHV, deletion 17p, and mutations in BCL2, NOTCH1 (subclonal), and TP53 (subclonal). Quite strikingly, a novel PAX5 mutation that w…

MaleProto-Oncogene Proteins B-rafChronic lymphocytic leukemiaCell Cycle ProteinsBiologymedicine.disease_causeSomatic evolution in cancerTranslocation GeneticEpigenesis Genetichematological neoplasmClonal Evolutionimmune system diseaseshemic and lymphatic diseasesExome SequencingmedicineHumansEpigeneticsReceptor Notch1neoplasmsLoss functionExome sequencingAgedHomeodomain ProteinsMutationPAX5 Transcription FactorGeneral Medicinemedicine.diseasePrognosisLeukemia Lymphocytic Chronic B-CellProto-Oncogene Proteins c-bcl-2MutationCancer researchPAX5Tumor Suppressor Protein p53IGHV@Rapid Cancer CommunicationTranscription FactorsCold Spring Harbor Molecular Case Studies
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Epigenetic Control of the foxp3 Locus in Regulatory T Cells

2007

Compelling evidence suggests that the transcription factor Foxp3 acts as a master switch governing the development and function of CD4+ regulatory T cells (Tregs). However, whether transcriptional control of Foxp3 expression itself contributes to the development of a stable Treg lineage has thus far not been investigated. We here identified an evolutionarily conserved region within the foxp3 locus upstream of exon-1 possessing transcriptional activity. Bisulphite sequencing and chromatin immunoprecipitation revealed complete demethylation of CpG motifs as well as histone modifications within the conserved region in ex vivo isolated Foxp3+CD25+CD4+ Tregs, but not in naïve CD25−CD4+ T cells. …

MaleQH301-705.5Bisulfite sequencingImmunologyMolecular Sequence Datachemical and pharmacologic phenomenaCell SeparationThymus GlandBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticMiceTranscriptional regulationAnimalsEpigeneticsBiology (General)Regulation of gene expressionMice Inbred BALB CGeneral Immunology and MicrobiologyBase SequenceGeneral NeuroscienceInterleukin-2 Receptor alpha SubunitFOXP3Homo (human)hemic and immune systemsForkhead Transcription FactorsDNA MethylationFlow CytometryMolecular biologyMus (mouse)Cell biologyIn VitroDNA demethylationGene Expression RegulationDNA methylationCpG IslandsGeneral Agricultural and Biological SciencesChromatin immunoprecipitationResearch ArticlePLoS Biology
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Intestinal malrotation in a female newborn affected by Osteopathia Striata with Cranial Sclerosis due to a de novo heterozygous nonsense mutation of …

2022

Abstract Background Osteopathia Striata with Cranial Sclerosis (OS-CS), also known as Horan-Beighton Syndrome, is a rare genetic disease; about 90 cases have been reported to date. It is associated with mutations (heterozygous for female subjects and hemizygous for males) of the AMER1 gene, located at Xq11.2, and shows an X-linked pattern of transmission. Typical clinical manifestations include macrocephaly, characteristic facial features (frontal bossing, epicanthal folds, hypertelorism, depressed nasal bridge, orofacial cleft, prominent jaw), hearing loss and developmental delay. Males usually present a more severe phenotype than females and rarely survive. Diagnostic suspicion is based o…

MaleSclerosisCase report Next generation sequencing OS-CS Skeletal dysplasia X-inactivationCleft LipTumor Suppressor ProteinsInfant NewbornGeneral MedicineMegalencephalyCleft PalateCodon NonsenseHumansFemaleBone DiseasesAdaptor Proteins Signal Transducing
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Concordance of assays designed for the quantification of JAK2V617F: a multicenter study

2008

Background Many different techniques have been designed for the quantification of JAK2 V617F allelic burden, sometimes producing discrepant results. Design and Methods JAK2 V617F quantification techniques were compared among 16 centers using 11 assays based on quantitative polymerase chain reaction (with mutation-specific primers or probes, or fluorescent resonance energy transfer/melting curve analysis), allele-specific polymerase chain reaction, conventional sequencing or pyrosequencing. Results A first series of blinded samples (granulocyte DNA, n=29) was analyzed. Seven assays (12 centers) reported values inside the mean±2SD; the mean coefficient of variation was 31%. Sequencing techniq…

MaleSerial dilutionPhenylalanineCoefficient of variationBiologyMelting curve analysislaw.inventionlawhemic and lymphatic diseasesTaqManHumansAllelesPolymerase chain reactionValineOriginal ArticlesHematologyJanus Kinase 2Molecular biologyPedigreePhenotypeReal-time polymerase chain reactionMutationPyrosequencingFemalePrimer (molecular biology)Thrombocythemia EssentialHaematologica
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