Search results for "Predisposition"

showing 10 items of 771 documents

Widening of the genetic and clinical spectrum of Lamb-Shaffer syndrome, a neurodevelopmental disorder due to SOX5 haploinsufficiency

2020

International audience; PURPOSE: Lamb-Shaffer syndrome (LAMSHF) is a neurodevelopmental disorder described in just over two dozen patients with heterozygous genetic alterations involving SOX5, a gene encoding a transcription factor regulating cell fate and differentiation in neurogenesis and other discrete developmental processes. The genetic alterations described so far are mainly microdeletions. The present study was aimed at increasing our understanding of LAMSHF, its clinical and genetic spectrum, and the pathophysiological mechanisms involved.METHODS: Clinical and genetic data were collected through GeneMatcher and clinical or genetic networks for 41 novel patients harboring various ty…

MaleMedizinHaploinsufficiencyL-SOX5VARIANTS0302 clinical medicineNeurodevelopmental disorderIntellectual disabilityMissense mutation2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)GeneticsPediatricGenetics & Heredity0303 health sciencesPedigreeFAMILYDNA-Binding Proteinsdevelopmental delayTRANSCRIPTION FACTORSPhenotypeintellectual disabilityChild Preschoolmissense variantsFemalemissense variants.HaploinsufficiencySOXD Transcription FactorsAdultEXPRESSIONAdolescentIntellectual and Developmental Disabilities (IDD)Clinical SciencesMutation MissenseautismCell fate determinationBiologyLONG FORMSEQUENCEArticle03 medical and health sciencesYoung AdultRare DiseasesClinical ResearchCARTILAGEIntellectual DisabilitymedicineGeneticsAnimalsHumansLanguage Development DisordersGenetic Predisposition to DiseasePreschoolTranscription factorGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMUTATIONSHuman GenomeInfantmedicine.diseaseBrain DisordersNeurodevelopmental DisordersDeciphering Developmental Disorder StudyMutationAutismepilepsyMissense030217 neurology & neurosurgeryGENERATIONGenetics in Medicine
researchProduct

Age-Dependent Association of Human Mannose-Binding Lectin Mutations With Susceptibility to Invasive Meningococcal Disease in Childhood

2007

Mannose-binding lectin (MBL) is an important factor of the innate immune system, and MBL-initiated complement activation is an important early defense mechanism against various bacterial infections, including invasive meningococcal disease.In a pediatric cohort (ages 2-215 months) with invasive meningococcal disease, we investigated the overall and age-stratified frequency of 3 MBL exon 1 variations (C154T, G161A, G170A), previously shown to result in markedly decreased MBL plasma concentrations, by allele specific fluorescent hybridization probe real-time PCR assays and direct sequencing. Healthy age-matched volunteers with the same ethnic background and no history of meningococcal disease…

MaleMicrobiology (medical)AgingAdolescentMannosechemical and pharmacologic phenomenaMeningococcal diseasemedicine.disease_causeMannose-Binding Lectinchemistry.chemical_compoundPrevalencemedicineHumansGenetic Predisposition to DiseaseChildMannan-binding lectinMutationInnate immune systembiologybusiness.industryInfantLectinbacterial infections and mycosesmedicine.diseaseComplement systemMeningococcal InfectionsInfectious DiseaseschemistryChild PreschoolMutationPediatrics Perinatology and Child HealthImmunologyCohortbiology.proteinFemalebusinessPediatric Infectious Disease Journal
researchProduct

The oral-facial-digital syndrome gene C2CD3 encodes a positive regulator of centriole elongation

2014

Centrioles are microtubule-based, barrel-shaped structures that initiate the assembly of centrosomes and cilia(1,2). How centriole length is precisely set remains elusive. The microcephaly protein CPAP (also known as MCPH6) promotes procentriole growth(3-5), whereas the oral-facial-digital (OFD) syndrome protein OFD1 represses centriole elongation(6,7). Here we uncover a new subtype of OFD with severe microcephaly and cerebral malformations and identify distinct mutations in two affected families in the evolutionarily conserved C2CD3 gene. Concordant with the clinical overlap, C2CD3 colocalizes with OFD1 at the distal end of centrioles, and C2CD3 physically associates with OFD1. However, wh…

MaleMicrocephalyCentrioleMicrotubule-associated proteinsportsBiologyCiliopathiesCentriole elongationArticleCell LineProcentrioleGeneticsmedicineHumansGenetic Predisposition to DiseaseCentriolesGeneticsCiliumProteinsOrofaciodigital Syndromesmedicine.diseasesports.leagueHEK293 CellsCentrosomeChild PreschoolMicrocephalyMicrotubule-Associated Proteins
researchProduct

EPHA7 haploinsufficiency is associated with a neurodevelopmental disorder

2021

International audience; Ephrin receptor and their ligands, the ephrins, are widely expressed in the developing brain. They are implicated in several developmental processes that are crucial for brain development. Deletions in genes encoding for members of the Eph/ephrin receptor family were reported in several neurodevelopmental disorders. The ephrin receptor A7 gene (EPHA7) encodes a member of ephrin receptor subfamily of the protein-tyrosine kinase family. EPHA7 plays a role in corticogenesis processes, determines brain size and shape, and is involved in development of the central nervous system. One patient only was reported so far with a de novo deletion encompassing EPHA7 in 6q16.1. We…

MaleMicrocephaly[SDV]Life Sciences [q-bio]6q161 microdeletionInheritance PatternsEPHA7HaploinsufficiencyBiologyspeech and language developmentNeurodevelopmental disorderExome SequencingGeneticsmedicineEphrinHumansGenetic Predisposition to DiseasemicrocephalyGenetics (clinical)Genetic Association StudiesIn Situ Hybridization FluorescenceGeneticsComparative Genomic Hybridization6q16.1 microdeletionErythropoietin-producing hepatocellular (Eph) receptorReceptor EphA7medicine.diseasePenetrancePhenotypeneurodevelopmental disorderPedigree[SDV] Life Sciences [q-bio]PhenotypeNeurodevelopmental Disordersintellectual disabilityEPHA7MutationChromosomes Human Pair 6FemaleHaploinsufficiencyClinical Genetics
researchProduct

Aberrant methylation within RUNX3 CpG island associated with the nuclear and mitochondrial microsatellite instability in sporadic gastric cancers. Re…

2007

Background: Gastric cancer (GC) development is a multistep process, during which numerous alterations accumulate in nuclear and mitochondrial DNA. A deficiency of repair machinery brings about an accumulation of errors introduced within simple repetitive microsatellite sequences during replication of DNA. Aberrant methylation is related to microsatellite instability (MSI) by the silencing of the hMLH1 gene. The aim of this study is to investigate a possible relationship between the RUNX3 promoter methylation, nuclear microsatellite instability (nMSI) and mitochondrial microsatellite instability (mtMSI), in order to clarify its biological role in GC. Patients and methods: nMSI and mtMSI were…

MaleMitochondrial DNAGC Rich SequenceBiologyDNA Mitochondriallaw.inventionlawStomach NeoplasmsmedicineHumansGenetic Predisposition to DiseaseProspective StudiesPolymerase chain reactionAgedCell NucleusCancerMicrosatellite instabilityHematologyMethylationDNA MethylationMiddle Agedmedicine.diseaseMolecular biologydigestive system diseasesCore Binding Factor Alpha 3 SubunitOncologyCpG siteMicrosatelliteCpG IslandsFemaleMicrosatellite InstabilityMicrosatellite Repeats
researchProduct

Hereditary common cancers: molecular and clinical genetics.

2001

This review focuses on the functional role and structural features of the genes involved in common hereditary cancers. Most of these tumors are sporadic and the genetic alterations responsible for their genesis take place over several cell generations; nevertheless, 5 to 10% of the human tumors are hereditary, with a rapid development. Cancer susceptibility genes have been classified as "gatekeepers" (e.g. RB1, ki-ras) and "caretakers" (e.g. hMLH1 and hMSH2, BRCA1). The first step in identifying individuals at high risk of developing a specific inherited form of cancer, and who should therefore undergo genetic tests, is the detailed construction of family history (an accurate cancer family …

MaleModels GeneticSettore MED/06 - Oncologia MedicaBRCA geneRisk AssessmentHereditary cancerPedigreeAPC geneNeoplasmsBiomarkers TumorAnimalsHumansFemaleGenes Tumor SuppressorGenetic Predisposition to DiseaseMMR genesAnticancer research
researchProduct

Phenotypic and biochemical analysis of an international cohort of individuals with variants in NAA10 and NAA15.

2019

Abstract N-alpha-acetylation is one of the most common co-translational protein modifications in humans and is essential for normal cell function. NAA10 encodes for the enzyme NAA10, which is the catalytic subunit in the N-terminal acetyltransferase A (NatA) complex. The auxiliary and regulatory subunits of the NatA complex are NAA15 and Huntington-interacting protein (HYPK), respectively. Through a genotype-first approach with exome sequencing, we identified and phenotypically characterized 30 individuals from 30 unrelated families with 17 different de novo or inherited, dominantly acting missense variants in NAA10 or NAA15. Clinical features of affected individuals include variable levels…

MaleModels Molecular0301 basic medicineProtein ConformationMicrophthalmia0302 clinical medicineEnzyme StabilityMissense mutationN-Terminal Acetyltransferase EChildN-Terminal Acetyltransferase AExome sequencingGenetics (clinical)GeneticsbiologyGeneral MedicinePhenotypeRecombinant ProteinsChemistryPhenotypeChild PreschoolHMG-CoA reductaseCohortFemaleGeneral ArticleCorrigendumAdultNatA complexmedicine.medical_specialtyAdolescentGenotypeFrameshift mutationStructure-Activity RelationshipYoung Adult03 medical and health sciencesMolecular geneticsGeneticsmedicineHumansGenetic Predisposition to DiseaseGenetic TestingAlleleBiologyMolecular BiologyAllelesGenetic Association StudiesComputational BiologyFaciesGenetic VariationInfantmedicine.diseaseEnzyme ActivationLenz microphthalmia syndrome030104 developmental biologyGenetic LociMutationbiology.proteinHuman medicineBiomarkers030217 neurology & neurosurgeryNAA15Human molecular genetics
researchProduct

Common variants in the HLA-DQ region confer susceptibility to idiopathic achalasia

2014

Idiopathic achalasia is characterized by a failure of the lower esophageal sphincter to relax due to a loss of neurons in the myenteric plexus(1,2). This ultimately leads to massive dilatation and an irreversibly impaired megaesophagus. We performed a genetic association study in 1,068 achalasia cases and 4,242 controls and fine-mapped a strong MHC association signal by imputing classical HLA haplotypes and amino acid polymorphisms. An eight-residue insertion at position 227-234 in the cytoplasmic tail of HLA-DQ beta 1 (encoded by HLA-DQB1*05:03 and HLA-DQB1*06:01) confers the strongest risk for achalasia (P = 1.73 x 10(-19)). In addition, two amino acid substitutions in the. extracellular …

MaleModels MolecularAchalasiaImmunogeneticsBiologyMajor histocompatibility complexPolymorphism Single Nucleotidedigestive systemHLA-DQ alpha-ChainsHLA-DQ AntigensHLA-DQotorhinolaryngologic diseasesGeneticsmedicineHLA-DQ beta-ChainsHumansGenetic Predisposition to DiseaseEsophagusAllelesGenetic Association StudiesGenetic associationGeneticsAchalasiaMotility disorderASSOCIATIONmedicine.diseasedigestive system diseasesEsophageal AchalasiaINSIGHTSLogistic Modelsmedicine.anatomical_structureAmino Acid SubstitutionHaplotypesCase-Control StudiesImmunologybiology.proteinFemaleIdiopathic achalasiageneticMHCNature Genetics
researchProduct

20 ans après: a second mutation in MAOA identified by targeted high-throughput sequencing in a family with altered behavior and cognition

2013

Intellectual disability (ID) is characterized by an extraordinary genetic heterogeneity, with >250 genes that have been implicated in monogenic forms of ID. Because this complexity precluded systematic testing for mutations and because clinical features are often non-specific, for some of these genes only few cases or families have been unambiguously documented. It is the case of the X-linked gene encoding monoamine oxidase A (MAOA), for which only one nonsense mutation has been identified in Brunner syndrome, characterized in a single family by mild non-dysmorphic ID and impulsive, violent and aggressive behaviors. We have performed targeted high-throughput sequencing of 220 genes, includi…

MaleModels MolecularBrunner syndromeNonsense mutationMutation MissenseArticleIntellectual DisabilityGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseAmino Acid SequenceMonoamine OxidaseGenetics (clinical)GeneticsFamily HealthbiologyBase SequenceGenetic heterogeneityPoint mutationHigh-Throughput Nucleotide Sequencingmedicine.diseasePedigreeProtein Structure TertiaryAutism spectrum disorderAttention Deficit and Disruptive Behavior DisordersChild Development Disorders Pervasivebiology.proteinAutismFemaleMonoamine oxidase A
researchProduct

Haploinsufficiency of the NOTCH1 receptor as a cause of Adams-Oliver syndrome with variable cardiac anomalies

2015

Background— Adams–Oliver syndrome (AOS) is a rare disorder characterized by congenital limb defects and scalp cutis aplasia. In a proportion of cases, notable cardiac involvement is also apparent. Despite recent advances in the understanding of the genetic basis of AOS, for the majority of affected subjects, the underlying molecular defect remains unresolved. This study aimed to identify novel genetic determinants of AOS. Methods and Results— Whole-exome sequencing was performed for 12 probands, each with a clinical diagnosis of AOS. Analyses led to the identification of novel heterozygous truncating NOTCH1 mutations (c.1649dupA and c.6049_6050delTC) in 2 kindreds in which AOS was segregat…

MaleModels MolecularProbandreceptorGene ExpressionHaploinsufficiencyNOTCH1Ectodermal DysplasiaMissense mutationExomeReceptor Notch1ChildExomeGenetics (clinical)GeneticsReverse Transcriptase Polymerase Chain ReactionAutosomal dominant traitMiddle AgedPedigreeembryonic structuresheart defectscardiovascular systemFemaleCardiology and Cardiovascular MedicineHaploinsufficiencySignal TransductionAdultHeart Defects CongenitalAdolescentLimb Deformities CongenitalNotch signaling pathwayBiologyArticleYoung AdultAdams-Oliver syndromeGeneticsmedicineHumansGenetic Predisposition to DiseaseGeneFamily HealthBase SequencecongenitalAdams-Oliver syndrome; genetics; haploinsufficiency; heart defects; congenital; receptor; NOTCH1; Cardiology and Cardiovascular Medicine; Genetics (clinical); GeneticsSequence Analysis DNAmedicine.diseaseProtein Structure TertiaryScalp DermatosesHuman medicineAdams–Oliver syndromeCirculation. Cardiovascular genetics
researchProduct