Search results for "HP"

showing 10 items of 1505 documents

Aging and serum exomiR content in women-effects of estrogenic hormone replacement therapy.

2017

AbstractExosomes participate in intercellular messaging by transporting bioactive lipid-, protein- and RNA-molecules and -complexes. The contents of the exosomes reflect the physiological status of an individual making exosomes promising targets for biomarker analyses. In the present study we extracted exosome microRNAs (exomiRs) from serum samples of premenopausal women (n = 8) and monozygotic postmenopausal twins (n = 10 female pairs), discordant for the use of estrogenic hormone replacement therapy (HRT), in order to see whether the age or/and the use of HRT associates with exomiR content. A total of 241 exomiRs were detected by next generation sequencing, 10 showing age, 14 HRT and 10 a…

0301 basic medicineMICRORNASTranscriptomeMedicineGene Regulatory NetworksMultidisciplinaryEstradiolmicroRNAEstrogen Replacement TherapyEndocrine system and metabolic diseasesHigh-Throughput Nucleotide Sequencingta3141Middle AgedMenopausePostmenopauseDISCORDANTPOSTMENOPAUSAL WOMENTransgender hormone therapymiRNAsBiomarker (medicine)SKELETAL-MUSCLEFemaleAdultEXPRESSIONmedicine.medical_specialtyMENOPAUSEBODY-COMPOSITIONexosomesta3111ExosomeArticleestrogenic hormone replacement therapy03 medical and health sciencesBreast cancerInternal medicineHumansBREAST-CANCERbusiness.industryta1184Gene Expression ProfilingReproducibility of Resultsbiomarkersmedicine.diseaseGene expression profilingMONOZYGOTIC TWIN PAIRS030104 developmental biologyEndocrinologyPremenopauseCELLSNext-generation sequencing3111 Biomedicinemikro-RNAbusinessTranscriptomeHormone
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Assessment of Targeted Next-Generation Sequencing as a Tool for the Diagnosis of Charcot-Marie-Tooth Disease and Hereditary Motor Neuropathy

2016

Charcot-Marie-Tooth disease is characterized by broad genetic heterogeneity with >50 known disease-associated genes. Mutations in some of these genes can cause a pure motor form of hereditary motor neuropathy, the genetics of which are poorly characterized. We designed a panel comprising 56 genes associated with Charcot-Marie-Tooth disease/hereditary motor neuropathy. We validated this diagnostic tool by first testing 11 patients with pathological mutations. A cohort of 33 affected subjects was selected for this study. The DNAJB2 c.352+1G>A mutation was detected in two cases; novel changes and/or variants with low frequency (50 known disease-associated genes. Mutations in some of these gene…

0301 basic medicineMaleDiseaseBioinformaticsDNA sequencingPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineCharcot-Marie-Tooth DiseaseMedicineHumansGeneGeneticsbusiness.industryGenetic heterogeneityHaplotypeCase-control studyHigh-Throughput Nucleotide SequencingReproducibility of ResultsHSP40 Heat-Shock Proteins030104 developmental biologyHaplotypesCase-Control StudiesMutation (genetic algorithm)MutationMolecular MedicineFemalebusinessHereditary Sensory and Motor Neuropathy030217 neurology & neurosurgeryFounder effectMolecular Chaperones
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Dominant variants in the splicing factor PUF60 cause a recognizable syndrome with intellectual disability, heart defects and short stature

2016

Item does not contain fulltext Verheij syndrome, also called 8q24.3 microdeletion syndrome, is a rare condition characterized by ante- and postnatal growth retardation, microcephaly, vertebral anomalies, joint laxity/dislocation, developmental delay (DD), cardiac and renal defects and dysmorphic features. Recently, PUF60 (Poly-U Binding Splicing Factor 60 kDa), which encodes a component of the spliceosome, has been discussed as the best candidate gene for the Verheij syndrome phenotype, regarding the cardiac and short stature phenotype. To date, only one patient has been reported with a de novo variant in PUF60 that probably affects function (c.505C>T leading to p.(His169Tyr)) associated wi…

0301 basic medicineMaleMESH: Heart Defects Congenital / physiopathologyMicrocephalyPathologyMESH: Heart Defects Congenital / geneticsMESH: Exome / genetics030105 genetics & heredityMESH: RNA Splicing / geneticsMicrophthalmia[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesMESH: ChildExomeMESH: RNA Splicing Factors / geneticsChildFrameshift MutationMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingColobomaMESH: Frameshift MutationHigh-Throughput Nucleotide SequencingMicrodeletion syndromeMicrocephaly Verheij syndrome PUF60ChemistryPhenotypeChild PreschoolDISEASESMicrocephalyMedical geneticsFemaleRNA Splicing Factorsmedicine.symptomChromosome DeletionChromosomes Human Pair 8MESH: Dwarfism / genetics*Heart Defects Congenitalmedicine.medical_specialtyGENESAdolescentRNA SplicingMESH: Chromosome DeletionDwarfismBiologyMESH: PhenotypeShort statureArticlePUF6003 medical and health sciencesInternal medicineIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansCraniofacialBiologyMESH: AdolescentNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]MESH: HumansMESH: Child Preschoolmedicine.diseaseMESH: Repressor Proteins / geneticsMESH: MaleRepressor Proteins030104 developmental biologyEndocrinologyMESH: Chromosomes Human Pair 8 / geneticsMESH: Dwarfism / physiopathologyMESH: Intellectual Disability / physiopathologyHuman medicineMESH: Intellectual Disability / geneticsVerheij syndromeMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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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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High Throughput Sequencing Identifies Misregulated Genes in the Drosophila Polypyrimidine Tract-Binding Protein (hephaestus) Mutant Defective in Sper…

2015

The Drosophila polypyrimidine tract-binding protein (dmPTB or hephaestus) plays an important role during spermatogenesis. The heph2 mutation in this gene results in a specific defect in spermatogenesis, causing aberrant spermatid individualization and male sterility. However, the array of molecular defects in the mutant remains uncharacterized. Using an unbiased high throughput sequencing approach, we have identified transcripts that are misregulated in this mutant. Aberrant transcripts show altered expression levels, exon skipping, and alternative 5' ends. We independently verified these findings by reverse-transcription and polymerase chain reaction (RT-PCR) analysis. Our analysis shows m…

0301 basic medicineMalePhysiologyMutantGene Expressionlcsh:MedicineArtificial Gene Amplification and ExtensionPolymerase Chain ReactionBiochemistryConserved sequence0302 clinical medicineSequencing techniquesReproductive PhysiologyAnimal CellsInvertebrate GenomicsMedicine and Health SciencesDrosophila ProteinsProtein IsoformsCell Cycle and Cell Divisionlcsh:ScienceConserved SequencePhylogenyGeneticsRegulation of gene expressionMultidisciplinarybiologyChromosome BiologyDrosophila MelanogasterMessenger RNAHigh-Throughput Nucleotide SequencingRNA sequencingAnimal ModelsGenomicsSpermatidsInsectsNucleic acidsMeiosisCell ProcessesDrosophilaDrosophila melanogasterTranscription Initiation SiteCellular TypesDrosophila ProteinPolypyrimidine Tract-Binding ProteinResearch ArticleArthropodaMolecular Sequence DataReal-Time Polymerase Chain ReactionResearch and Analysis Methods03 medical and health sciencesModel OrganismsGeneticsAnimalsPolypyrimidine tract-binding proteinRNA MessengerSpermatogenesisMolecular Biology TechniquesMolecular BiologyBinding SitesBase SequenceGene Expression Profilinglcsh:ROrganismsBiology and Life SciencesCell BiologyReverse Transcriptase-Polymerase Chain Reactionbiology.organism_classificationInvertebratesExon skippingSpermGene expression profiling030104 developmental biologyGene OntologyGerm CellsGene Expression RegulationAnimal GenomicsMutationbiology.proteinRNAlcsh:QTranscriptome030217 neurology & neurosurgeryPLoS ONE
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Detection of Missing Proteins Using the PRIDE Database as a Source of Mass Spectrometry Evidence

2016

The current catalogue of the human proteome is not yet complete, as experimental proteomics evidence is still elusive for a group of proteins known as the missing proteins. The Human Proteome Project (HPP) has been successfully using technology and bioinformatic resources to improve the characterization of such challenging proteins. In this manuscript, we propose a pipeline starting with the mining of the PRIDE database to select a group of data sets potentially enriched in missing proteins that are subsequently analyzed for protein identification with a method based on the statistical analysis of proteotypic peptides. Spermatozoa and the HEK293 cell line were found to be a promising source…

0301 basic medicineMaleProteomicsFrontal cortexFuture studiesProteomePlacentaBiologyMass spectrometrycomputer.software_genreTandem mass spectrometryProteomicsBiochemistryArticleRetina03 medical and health sciencesPregnancyTandem Mass SpectrometryMS/MS proteomicsHuman proteome projectHumansDatabases ProteinAortaPRIDE databaseDatabaseC-HPPComputational BiologyGeneral ChemistrySpermatozoaFrontal Lobe030104 developmental biologyHEK293 CellsProteomeProtein identificationFemalemissing proteinscomputerJournal of Proteome Research
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DRH1 - a novel blood-based HPV tumour marker.

2020

Abstract Background To date, no studies have successfully shown that a highly specific, blood-based tumour marker to detect clinically relevant HPV-induced disease could be used for screening, monitoring therapy response or early detection of recurrence. This study aims to assess the clinical performance of a newly developed HPV16-L1 DRH1 epitope-specific serological assay. Methods In a multi-centre study sera of 1486 patients (301 Head and Neck Squamous Cell Carcinoma (HNSCC) patients, 12 HIV+ anal cancer patients, 80 HIV-positive patients, 29 Gardasil-9-vaccinees, 1064 healthy controls) were tested for human HPV16-L1 DRH1 antibodies. Analytical specificity was determined using WHO referen…

0301 basic medicineMaleResearch paperlcsh:MedicineHIV InfectionsDiseaseGastroenterologyHNSCC0302 clinical medicineNeoplasmsTumour markerMedicineProspective StudiesAged 80 and overlcsh:R5-920Human papillomavirus 16medicine.diagnostic_testbiologyGeneral MedicineMiddle AgedAnus NeoplasmsVaccinationHead and Neck Neoplasms030220 oncology & carcinogenesisArea Under CurveCarcinoma Squamous CellScreeningBiomarker (medicine)FemaleAntibodylcsh:Medicine (General)Blood testAdultHPV16medicine.medical_specialtyEarly detectionSensitivity and SpecificityGeneral Biochemistry Genetics and Molecular BiologyAntibodies03 medical and health sciencesInternal medicineBiomarkers TumorBlood testAnal cancerHumansPapillomavirus VaccinesAgedbusiness.industrylcsh:RPapillomavirus InfectionsOncogene Proteins Viralmedicine.diseaseHead and neck squamous-cell carcinoma030104 developmental biologyCross-Sectional StudiesCase-Control Studiesbiology.proteinCapsid ProteinsbusinessCarrier ProteinsEBioMedicine
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Mutations in SKI in Shprintzen-Goldberg syndrome lead to attenuated TGF-β responses through SKI stabilization.

2020

ABSTRACTShprintzen-Goldberg syndrome (SGS) is a multisystemic connective tissue disorder, with considerable clinical overlap with Marfan and Loeys-Dietz syndromes. These syndromes have commonly been associated with enhanced TGF-β signaling. In SGS patients, heterozygous point mutations have been mapped to the transcriptional corepressor SKI, which is a negative regulator of TGF-β signaling that is rapidly degraded upon ligand stimulation. The molecular consequences of these mutations, however, are not understood. Here we use a combination of structural biology, genome editing and biochemistry to show that SGS mutations in SKI abolish its binding to phosphorylated SMAD2 and SMAD3. This resul…

0301 basic medicineMaleSMADmedicine.disease_causeMarfan SyndromeActivin0302 clinical medicineGenome editingTransforming Growth Factor betaGene expressionBiology (General)MutationShprintzen-Goldberg syndromeGeneral NeuroscienceQRShprintzen–Goldberg syndromeGeneral MedicineLigand (biochemistry)Chromosomes and Gene ExpressionCell biologyDNA-Binding ProteinsMedicinePhosphorylationFemaleSignal TransductionResearch ArticleHumanTGF-βQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCraniosynostosesstomatognathic systemBiochemistry and Chemical BiologyProto-Oncogene ProteinsmedicineHumansGeneral Immunology and MicrobiologyPoint mutationmedicine.diseaseSKIArachnodactyly030104 developmental biologyStructural biologyMutation030217 neurology & neurosurgerySMADTransforming growth factoreLife
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Genetic epidemiology of autosomal recessive hypercholesterolemia in Sicily: Identification by next-generation sequencing of a new kindred.

2017

Background Autosomal recessive hypercholesterolemia (ARH) is a rare inherited lipid disorder. In Sardinia, differently from other world regions, the mutated allele frequency is high. It is caused by mutations in the low-density lipoprotein receptor adaptor protein 1 gene. Fourteen different mutations have been reported so far; in Sardinia, 2 alleles (ARH1 and ARH2) explain most of the cases. Four ARH patients, all carriers of the ARH1 mutation, have been identified in mainland Italy and 2 in Sicily. Objective The objectives of the study were to improve the molecular diagnosis of familial hypercholesterolemia (FH) and to estimate the frequency of the ARH1 allele in 2 free-living Sicilian pop…

0301 basic medicineMaleSettore MED/09 - Medicina InternaEndocrinology Diabetes and MetabolismFamilial hypercholesterolemia030204 cardiovascular system & hematology0302 clinical medicineChildN-Glycosyl HydrolasesSicilyGeneticsAged 80 and overeducation.field_of_studyNutrition and DieteticsAllele frequencyHomozygoteHigh-Throughput Nucleotide SequencingAutosomal recessive hypercholesterolemiaMiddle AgedAutosomal Recessive HypercholesterolemiaSettore MED/26 - NeurologiaFemaleCardiology and Cardiovascular MedicineAdultAdolescentGenotypePopulationHypercholesterolemiaBiologyDNA sequencing03 medical and health sciencesYoung AdultARH1Internal MedicinemedicineHumansAlleleeducationGenotypingAllele frequencyAllelesAdaptor Proteins Signal TransducingAgedHeterozygous carrierSequence Analysis DNAmedicine.diseaseNGS-based gene panel030104 developmental biologyGenetic epidemiologyReceptors LDLJournal of clinical lipidology
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Genetic justification of severe COVID-19 using a rigorous algorithm

2021

Recent studies suggest excessive complement activation in severe coronavirus disease-19 (COVID-19). The latter shares common characteristics with complement-mediated thrombotic microangiopathy (TMA). We hypothesized that genetic susceptibility would be evident in patients with severe COVID-19 (similar to TMA) and associated with disease severity. We analyzed genetic and clinical data from 97 patients hospitalized for COVID-19. Through targeted next-generation-sequencing we found an ADAMTS13 variant in 49 patients, along with two risk factor variants (C3, 21 patients; CFH,34 patients). 31 (32%) patients had a combination of these, which was independently associated with ICU hospitalization (…

0301 basic medicineMaleThrombomodulinSeverity of Illness Index0302 clinical medicineRisk FactorsImmunology and AllergyMedicineComplement ActivationRigorous algorithmmedicine.diagnostic_testHigh-Throughput Nucleotide SequencingComplement C3EculizumabEculizumabMiddle AgedHospitalizationSettore ICAR/09 - Tecnica Delle CostruzioniIntensive Care UnitsFactor HComplement Factor HFemaleAlgorithmsmedicine.drugmedicine.medical_specialtyThrombotic microangiopathyCritical CareImmunologyComplementADAMTS13 Protein03 medical and health sciencesInternal medicineFull Length ArticleSeverity of illnessGenetic predispositionGenetic susceptibilityHumansGenetic Predisposition to DiseaseGenetic TestingRisk factorGenetic testingAgedbusiness.industryThrombotic MicroangiopathiesCOVID-19medicine.diseaseComplement system030104 developmental biologySARS-CoV2business030215 immunologyClinical Immunology (Orlando, Fla.)
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