Search results for "loss function"

showing 10 items of 46 documents

How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights

2021

Osteoarthritis (OA) is a degenerative bone disease that involved micro and macro-environment of joints. To date, there are no radical curative treatments for OA and novel therapies are mandatory. Recent evidence suggests the role of miRNAs in OA progression. In our previous studies, we demonstrated the role of miR-31-5p and miR-33a families in different bone regeneration signaling. Here, we investigated the role of miR-31-5p and miR-33a-5p in OA progression. A different expression of miR-31-5p and miR-33a-5p into osteoblasts and chondrocytes isolated from joint tissues of OA patients classified in based on different Kellgren and Lawrence (KL) grading was highlighted

Male0301 basic medicineBone diseasechondrocytesOsteoarthritisCX43lcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5Cells CulturedSpectroscopymicroRNAosteoblastsGeneral MedicineMiddle AgedPrognosisComputer Science ApplicationsmicroRNAsmir-31030220 oncology & carcinogenesischondrocyteosteoblastFemalemedicine.symptomSignal TransductionAdultSp1 Transcription FactorInflammationBiologyArticleCatalysisInorganic Chemistry03 medical and health sciencesmicroRNAmedicineHumansPhysical and Theoretical ChemistryBone regenerationMolecular BiologyGeneLoss functionAgedOrganic Chemistrymedicine.diseaseSP1osteoarthritis030104 developmental biologyGene Expression Regulationlcsh:Biology (General)lcsh:QD1-999Connexin 43Cancer researchFollow-Up StudiesInternational Journal of Molecular Sciences
researchProduct

Heterozygous HMGB1 loss-of-function variants are associated with developmental delay and microcephaly

2021

International audience; 13q12.3 microdeletion syndrome is a rare cause of syndromic intellectual disability. Identification and genetic characterization of patients with 13q12.3 microdeletion syndrome continues to expand the phenotypic spectrum associated with it. Previous studies identified four genes within the approximately 300 Kb minimal critical region including two candidate protein coding genes: KATNAL1 and HMGB1. To date, no patients carrying a sequence-level variant or a single gene deletion in HMGB1 or KATNAL1 have been described. Here we report six patients with loss-of-function variants involving HMGB1 and who had phenotypic features similar to the previously described 13q12.3 m…

Male0301 basic medicineHeterozygoteMicrocephalyAdolescentDNA Copy Number VariationsLanguage delay[SDV]Life Sciences [q-bio]KaryotypeInheritance Patternschemical and pharmacologic phenomena030105 genetics & heredityBiologydysmorphic featuresloss of function mutation03 medical and health sciencesExome SequencingIntellectual disabilityGeneticsmedicineHumansGenetic Predisposition to DiseaseHMGB1 ProteinChildGeneGenetic Association StudiesIn Situ Hybridization FluorescenceGenetics (clinical)Loss functionGeneticsHMGB1FaciesExonsdevelopmental disabilitiesMicrodeletion syndromemedicine.diseasePhenotypePhenotype030104 developmental biologyChild PreschoolMicrocephalyFemaleHaploinsufficiency
researchProduct

Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

2018

© 2018 Elsevier Inc.

MaleAls geneGenome-wide association studyFAMILIAL ALSALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS0302 clinical medicine80 and overPsychologyGWASKIF5AAetiologycargoAged 80 and over0303 health sciencesFrench ALS ConsortiumKinesinKINESIN HEAVY-CHAINCognitive Sciencesaxonal transportHumanHereditary spastic paraplegiaNeuroscience(all)Single-nucleotide polymorphismTARGETED DISRUPTIONArticle03 medical and health sciencesGeneticsHumansAmino Acid SequenceLoss functionAgedHEXANUCLEOTIDE REPEATNeuroscience (all)MUTATIONSAmyotrophic Lateral Sclerosis3112 Neurosciences1702 Cognitive Sciencemedicine.diseaseITALSGEN ConsortiumAnswer ALS Foundation030104 developmental biologyALS Sequencing ConsortiumHuman medicine1109 Neurosciences030217 neurology & neurosurgery0301 basic medicineALS; GWAS; KIF5A; WES; WGS; axonal transport; cargo[SDV]Life Sciences [q-bio]KinesinsNeurodegenerativeGenetic analysisGenomeAMYOTROPHIC-LATERAL-SCLEROSIS3124 Neurology and psychiatryCohort StudiesPathogenesisLoss of Function MutationMissense mutation2.1 Biological and endogenous factorsAmyotrophic lateral sclerosisNYGC ALS ConsortiumGeneticsGeneral NeuroscienceALS axonal transport cargo GWAS KIF5A WES WGSMiddle AgedPhenotypeSettore MED/26 - NEUROLOGIANeurologicalProject MinE ALS Sequencing ConsortiumKinesinWESFemaleAdultBiologyGENOTYPE IMPUTATIONALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Adult; Aged; Aged 80 and over; Amino Acid Sequence; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Genome-Wide Association Study; Humans; Kinesin; Loss of Function Mutation; Male; Middle Aged; Young AdultNOYoung AdultRare DiseasesmedicineSLAGEN ConsortiumGene030304 developmental biologyClinical Research in ALS and Related Disorders for Therapeutic Development (CReATe) ConsortiumNeurology & NeurosurgeryHuman GenomeNeurosciencesAXONAL-TRANSPORTBrain DisordersALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS;Family memberDNA-DAMAGEMOTOR-NEURONS3111 BiomedicineCohort StudieALSGenomic Translation for ALS Care (GTAC) ConsortiumWGSAmyotrophic Lateral SclerosiGenome-Wide Association StudyALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Neuroscience (all)
researchProduct

De novo loss-of-function KCNMA1 variants are associated with a new multiple malformation syndrome and a broad spectrum of developmental and neurologi…

2019

Abstract KCNMA1 encodes the large-conductance Ca2+- and voltage-activated K+ (BK) potassium channel α-subunit, and pathogenic gain-of-function variants in this gene have been associated with a dominant form of generalized epilepsy and paroxysmal dyskinesia. Here, we genetically and functionally characterize eight novel loss-of-function (LoF) variants of KCNMA1. Genome or exome sequencing and the participation in the international Matchmaker Exchange effort allowed for the identification of novel KCNMA1 variants. Patch clamping was used to assess functionality of mutant BK channels. The KCNMA1 variants p.(Ser351Tyr), p.(Gly356Arg), p.(Gly375Arg), p.(Asn449fs) and p.(Ile663Val) abolished the …

MaleAtaxiaGenotypeDevelopmental DisabilitiesMutation MissenseBiology03 medical and health sciences0302 clinical medicineNeurodevelopmental disorderProtein DomainsLoss of Function MutationGeneticsmedicineHumansMissense mutationAbnormalities MultipleGenetic Predisposition to DiseaseProtein Interaction Domains and MotifsAlleleLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMolecular BiologyAllelesGenetic Association StudiesGenetics (clinical)Loss functionExome sequencing030304 developmental biologyGenetics0303 health sciencesInfant NewbornGeneral MedicineParoxysmal dyskinesiamedicine.diseaseElectrophysiological PhenomenaPedigreePhenotypeAmino Acid SubstitutionSpeech delayFemaleGeneral Articlemedicine.symptom030217 neurology & neurosurgeryHuman Molecular Genetics
researchProduct

Loss-of-function maternal-effect mutations of PADI6 are associated with familial and sporadic Beckwith-Wiedemann syndrome with multi-locus imprinting…

2020

Abstract Background PADI6 is a component of the subcortical maternal complex, a group of proteins that is abundantly expressed in the oocyte cytoplasm, but is required for the correct development of early embryo. Maternal-effect variants of the subcortical maternal complex proteins are associated with heterogeneous diseases, including female infertility, hydatidiform mole, and imprinting disorders with multi-locus imprinting disturbance. While the involvement of PADI6 in infertility is well demonstrated, its role in imprinting disorders is less well established. Results We have identified by whole-exome sequencing analysis four cases of Beckwith-Wiedemann syndrome with multi-locus imprintin…

MaleBeckwith-Wiedemann SyndromeGenomic imprintingMulti-locus imprinting disturbanceBeckwith–Wiedemann syndromeWhole Exome SequencingProtein-Arginine Deiminase Type 60302 clinical medicinePregnancyImprinting (psychology)ChildGenetics (clinical)Genetics0303 health sciencesDNA methylationPADI6Beckwith-Wiedemann syndrome; DNA methylation; Genomic imprinting; Infertility; Maternal-effect variants; Multi-locus imprinting disturbance; PADI6; Subcortical maternal complex; Adolescent; Adult; Beckwith-Wiedemann Syndrome; Child Preschool; DNA Methylation; Female; Genomic Imprinting; Heterozygote; Humans; Hydatidiform Mole; Infant; Infertility Female; Male; Maternal Inheritance; Mutation; Oocytes; Pedigree; Phenotype; Pregnancy; Protein-Arginine Deiminase Type 6; Siblings; Whole Exome SequencingFemale infertilityMaternal effectHydatidiform MolePedigreePhenotypeChild Preschool030220 oncology & carcinogenesisDNA methylationFemaleMaternal InheritanceInfertility FemaleAdultHeterozygoteAdolescentSubcortical maternal complexBiology03 medical and health sciencesExome SequencingGeneticsmedicineHumansMaternal-effect variantsPreschoolMolecular BiologyLoss function030304 developmental biologyMaternal-effect variantResearchSiblingsInfantmedicine.diseaseHuman geneticsInfertilityMutationOocytesGenomic imprintingDevelopmental BiologyClinical Epigenetics
researchProduct

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
researchProduct

Loss‐of‐function variants in ARHGEF9 are associated with an X‐linked intellectual disability dominant disorder

2021

ARHGEF9 defects lead to an X-linked intellectual disability disorder related to inhibitory synaptic dysfunction. This condition is more frequent in males, with a few affected females reported. Up to now, sequence variants and gross deletions have been identified in males, while only chromosomal aberrations have been reported in affected females who showed a skewed pattern of X-chromosome inactivation (XCI), suggesting an X-linked recessive (XLR) disorder. We report three novel loss-of-function (LoF) variants in ARHGEF9: A de novo synonymous variant affecting splicing (NM_015185.2: c.1056G>A, p.(Lys352=)) in one female; a nonsense variant in another female (c.865C>T, p.(Arg289*)), that is, a…

MaleX-linked intellectual disabilitymedia_common.quotation_subjectNonsenseMutation MissenseBiology03 medical and health sciencesGenes X-LinkedX Chromosome InactivationIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansMissense mutationGenetics (clinical)Loss function030304 developmental biologymedia_commonGenetics0303 health sciences030305 genetics & hereditymedicine.diseaseCodon NonsenseRNA splicingFemaleRho Guanine Nucleotide Exchange FactorsHuman Mutation
researchProduct

PCSK9 rs11591147 R46L loss-of-function variant protects against liver damage in individuals with NAFLD

2020

Background and Aims: The proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a key role in cholesterol homeostasis, and its inhibition represents an effective therapy to lower low-density lipoprotein cholesterol (LDL-C) levels. In this study, we examined the impact of the PCSK9 rs11591147 loss-of-function (LOF) variant on liver damage in a multicenter collection of patients at risk of nonalcoholic steatohepatitis (NASH), in clinical samples and experimental models. Methods: We considered 1874 consecutive individuals at risk of NASH as determined by histology. The SNP rs11591147, encoding for the p.R46L variant of PCSK9, was genotyped by TaqMan assays. We also evaluated 1) PCSK9 mRNA…

Malemedicine.medical_specialtyProprotein Convertase 9.GastroenterologyPCSK903 medical and health sciencesMice0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseSettore BIO/13 - Biologia ApplicataInternal medicineNonalcoholic fatty liver diseaseMedicineSNPAnimalsHumansFIBROSISLoss functionSettore MED/12 - GastroenterologiaHepatologybusiness.industryAnimalPCSK9ConfoundingNASHCholesterol LDLProprotein convertasemedicine.diseaseLiver030220 oncology & carcinogenesisKexin030211 gastroenterology & hepatologyProprotein Convertase 9businessHuman
researchProduct

Drosophila DJ-1 mutants are sensitive to oxidative stress and show reduced lifespan and motor deficits.

2007

Parkinson's disease (PD) is a progressive movement disorder caused by the selective and massive loss of dopaminergic neurons (DA) in the substantia nigra pars compacta (SNc). DJ-1 loss-of-function mutations are involved in inherited early-onset PD forms and result in dysfunction of the oxidative stress response. In mice models, DJ-1 loss provokes sensitivity to oxidative insults but does not produce neurodegeneration. Similar results have been found when analyzing Drosophila mutants for the DJ-1 orthologous genes, DJ-1alpha and DJ-1beta. Here, we report the analysis of two new mutations for the Drosophila DJ-1 genes. Both ubiquitous induction of DJ-1alpha knockdown by RNAi and loss of funct…

Parkinson's diseaseDopamineProtein Deglycase DJ-1Substantia nigraNerve Tissue ProteinsBiologyMotor Activitymedicine.disease_causeLife ExpectancyGeneticsmedicineAnimalsDrosophila ProteinsLoss functionNeuronsGene knockdownPars compactaNeurodegenerationAge FactorsGeneral MedicineAnatomymedicine.diseaseCell biologyOxidative Stressmedicine.anatomical_structureMutationRNA InterferenceNeuronOxidative stressGene
researchProduct

Should we use gait speed in COPD, FEV 1 in frailty and dyspnoea in both?

2016

Frailty is a progressive physiological decline in multiple organ systems marked by loss of function, loss of physiological reserve and increased vulnerability to disease [1]. Biological (inflammation and loss of hormones), clinical ( e.g. sarcopenia and osteoporosis) and social factors are involved in frailty onset, evolution and prognosis [2, 3]. Links between frailty, dyspnoea and chronic respiratory diseases represent a novel and practical approach

Pulmonary and Respiratory Medicinemedicine.medical_specialty[SDV]Life Sciences [q-bio]OsteoporosisDiseaseIdoso FragilizadoDispneia03 medical and health sciencesPulmonary Disease Chronic Obstructive0302 clinical medicineInternal medicineForced Expiratory VolumemedicineHumans030212 general & internal medicineLoss functionOrgan systemComputingMilieux_MISCELLANEOUSAgedAged 80 and overCOPDFrailtybusiness.industrymedicine.disease3. Good healthGait speedWalking SpeedPreferred walking speedDyspnea030228 respiratory systemSarcopeniaPhysical therapyCardiologyDoença Pulmonar Obstrutiva CrónicaVolume Expiratório ForçadoAged; Aged 80 and over; Dyspnea; Forced Expiratory Volume; Frailty; Humans; Pulmonary Disease Chronic Obstructive; Walking Speed; Pulmonary and Respiratory MedicinebusinessHuman
researchProduct