Search results for "Haploinsufficiency"

showing 10 items of 54 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
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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
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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
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Proteomic signature of the Dravet syndrome in the genetic Scn1a-A1783V mouse model.

2021

Abstract Background Dravet syndrome is a rare, severe pediatric epileptic encephalopathy associated with intellectual and motor disabilities. Proteomic profiling in a mouse model of Dravet syndrome can provide information about the molecular consequences of the genetic deficiency and about pathophysiological mechanisms developing during the disease course. Methods A knock-in mouse model of Dravet syndrome with Scn1a haploinsufficiency was used for whole proteome, seizure, and behavioral analysis. Hippocampal tissue was dissected from two- (prior to epilepsy manifestation) and four- (following epilepsy manifestation) week-old male mice and analyzed using LC-MS/MS with label-free quantificati…

MaleProteomics0301 basic medicineProteomeHippocampusEpilepsies MyoclonicHaploinsufficiencyScn1aHippocampusSynaptic TransmissionElevated Plus Maze TestEpilepsyMice0302 clinical medicineTandem Mass Spectrometry11-beta-Hydroxysteroid Dehydrogenase Type 1Genetic epilepsyCarbon-Nitrogen LigasesGene Knock-In TechniquesGliosisNeuronal PlasticityBehavior AnimalEpileptic encephalopathyImmunohistochemistryAstrogliosisNeurologyProteomeDisease ProgressionFemaleHaploinsufficiencySignal TransductionRC321-571Dopamine and cAMP-Regulated Phosphoprotein 32Neovascularization PhysiologicNeurosciences. Biological psychiatry. NeuropsychiatryBiologyNitric Oxide03 medical and health sciencesDravet syndromemedicineAnimalsHyperthermiaSocial Behaviorras-GRF1Proteomic Profilingmedicine.diseaseVascular Endothelial Growth Factor Receptor-2NAV1.1 Voltage-Gated Sodium ChannelDisease Models Animal030104 developmental biologyRotarod Performance TestSynaptic plasticityEpileptic Encephalopathy ; Genetic Epilepsy ; Mice ; Proteome ; Scn1aCalcium-Calmodulin-Dependent Protein Kinase Type 2Open Field TestNeuroscience030217 neurology & neurosurgeryChromatography Liquid
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Mandibular-pelvic-patellar syndrome (mpp) is a novel pitx1-related disorder due to alteration of pitx1 transactivation ability

2020

International audience; PITX1 is a homeobox transcription factor essential for hindlimb morphogenesis. Two PITX1-related human disorders have been reported to date: PITX1 ectopic expression causes Liebenberg syndrome, characterized by malformation of upper limbs showing a "lower limb" appearance; PITX1 deletions or missense variation cause a syndromic picture including clubfoot, tibial hemimelia, and preaxial polydactyly. We report two novel PITX1 missense variants, altering PITX1 transactivation ability, in three individuals from two unrelated families showing a distinct recognizable autosomal dominant syndrome, including first branchial arch, pelvic, patellar, and male genital abnormaliti…

MaleTranscriptional ActivationPathologymedicine.medical_specialtyHindlimb morphogenesis[SDV]Life Sciences [q-bio]Mutation MissensepelvisBiologyPierre-Robin03 medical and health sciencesTransactivationGeneticsmedicineMissense mutationAnimalsHumansPaired Box Transcription FactorsChildPITX1Genetics (clinical)030304 developmental biologyMice Knockoutcleft palate0303 health sciencesBone Diseases Developmental030305 genetics & heredityPreaxial polydactylyInfant NewbornLiebenberg syndromemedicine.disease3. Good healthgenitalpatella[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolHomeoboxEctopic expressionHaploinsufficiency
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2p15-p16.1 microdeletions encompassing and proximal to BCL11A are associated with elevated HbF in addition to neurologic impairment.

2015

Elevated fetal hemoglobin (HbF) ameliorates the clinical severity of hemoglobinopathies such as β-thalassemia and sickle cell anemia. Currently, the only curative approach for individuals under chronic transfusion/chelation support therapy is allogeneic stem cell transplantation. However, recent analyses of heritable variations in HbF levels have provided a new therapeutic target for HbF reactivation: the transcriptional repressor BCL11A. Erythroid-specific BCL11A abrogation is now actively being sought as a therapeutic avenue, but the specific impact of such disruption in humans remains to be determined. Although single nucleotide polymorphisms in BCL11A erythroid regulatory elements have …

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAdolescentImmunologyBiologyBiochemistrySettore MED/38 - Pediatria Generale E SpecialisticaRed Cells Iron and ErythropoiesisInternal medicinehemic and lymphatic diseasesFetal hemoglobinmedicineGene silencingHumansChildNervous System DiseaseFetal HemoglobinNuclear ProteinHematologyNuclear ProteinsCell BiologyHematologymedicine.diseasePhenotypeSickle cell anemiaUp-RegulationTransplantationRepressor ProteinsSettore MED/03 - Genetica MedicaChromosomes Human Pair 22p15-p16.1 microdeletions BCL11A HbF neurologicImmunologyFemaleStem cellChromosome DeletionNervous System DiseasesCarrier ProteinHaploinsufficiencyCarrier ProteinsHumanBlood
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Haploinsufficiency of ATP1A2 encoding the Na+/K+ pump alpha2 subunit associated with familial hemiplegic migraine type 2.

2003

Headache attacks and autonomic dysfunctions characterize migraine, a very common, disabling disorder with a prevalence of 12% in the general population of Western countries(1,2). About 20% of individuals affected with migraine experience aura, a visual or sensory-motor neurological dysfunction that usually precedes or accompanies the headache(3). Although the mode of transmission is controversial(4), population-based and twin studies have implicated genetic factors, especially in migraine with aura(5,6). Familial hemiplegic migraine is a hereditary form of migraine characterized by aura and some hemiparesis. Here we show that mutations in the gene ATP1A2 that encodes the alpha2 subunit of t…

Malemedicine.medical_specialtyAuraCell SurvivalPopulationMigraine with AuraMolecular Sequence DataDrug ResistanceBiologyHaploidyTransfectionATP1A2Internal medicineATP1A3Chlorocebus aethiopsGeneticsmedicineAnimalsHumansEnzyme InhibitorseducationOuabainFamilial hemiplegic migraineChromatography High Pressure LiquidGeneticseducation.field_of_studyBase Sequencemedicine.diseaseMigraine with auraPeptide FragmentsPedigreeEndocrinologyMigraineChromosomes Human Pair 1Case-Control StudiesCOS CellsMutationMutagenesis Site-DirectedFemaleCalcium Channelsmedicine.symptomSodium-Potassium-Exchanging ATPaseHaploinsufficiencyHeLa CellsNature genetics
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Haploinsufficiency of 16.4 Mb from chromosome 22pter-q11.21 in a girl with unilateral conductive hearing loss.

2009

We present the postnatal diagnosis of a de novo der(18)t(18;22)(p11.32;q11.21)pat, resulting in an unbalanced 45,XX,der (18)t(18;22) karyotype in a girl with conductive hearing loss on the left and ptosis of the right upper eye-lid. Unilateral ptosis was also observed in the patient’s 2 years and 8 months younger sister, who grows noticeably faster and appears to be a much quicker learner. After speech therapy the patient was eventually placed in normal school. The haploinsufficient 16.4-Mb region on chromosome 22pter→q11.21 contains 10 genes as well as many predicted genes, pseudogenes, and retrotransposed sequences with unknown functions. This observation may prove useful for prenatal dia…

Pathologymedicine.medical_specialtymedia_common.quotation_subjectChromosomes Human Pair 22BiologyHearing Loss UnilateralGeneticsmedicineHumansSpeechGirlMolecular BiologyGenetics (clinical)media_commonGeneticsInfant NewbornChromosomeKaryotypemedicine.diseaseConductive hearing lossHaplotypesKaryotypingFemaleUnilateral conductive hearing lossHaploinsufficiencyChromosomes Human Pair 18Chromosome 22Cytogenetic and genome research
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HSP70, the Key to Account for Erythroid Tropism of Diamond-Blackfan Anemia?

2015

Abstract Diamond-Blackfan anemia (DBA) was the first ribosomopathy identified and is characterized by a moderate to severe, usually macrocytic aregenerative anemia associated with congenital malformations in 50% of the DBA cases. This congenital rare erythroblastopenia is due to a blockade in erythroid differentiation between the BFU-e and CFU-e stages. The link between a haploinsufficiency in a ribosomal protein (RP) gene that now encompass 15 different RP genes and the erythroid defect is still to be fully defined. Recently, mutations in TSR2 and GATA1 genes have been identified in a few DBA families. The GATA1 gene encodes for the major transcription factor critical for erythropoiesis an…

Programmed cell deathGene knockdownRibosomopathyImmunologyGATA1Cell BiologyHematologyGene mutationBiologymedicine.diseaseBiochemistryhemic and lymphatic diseasesmedicineCancer researchErythropoiesisDiamond–Blackfan anemiaHaploinsufficiencyBlood
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GH successful treatment in a female with a de novo 46,XX,add(X)(p36),t(X;Y)(p36.3;p11.2), growth impairment and SHOX-haploinsufficiency

2019

Abstract Children with chromosome translocations, concerning X chromosome, have a genetic pattern different from Turner syndrome; however, when a translocation involves the of part of X chromosome including short stature homeobox-containing Sex-determining Region Y gene, growth may be severely compromised. We describe the clinical case of a 2.2-year-old-female, arrived at our paediatric unit for a decrease of height velocity. The karyotype was 46,XX,add(X)(p36.3). Array comparative genomic hybridization showed a fragment of Y chromosome, extended from 8.803.981 (Yp11.2) to 28.767.604 (Yq11.23). The final karyotype was 46,XX,add(X)(p36),t(X;Y)(p36.3;p11.2). Fluorescence in situ Hybridization…

Pseudoautosomal regionChromosomal translocationY chromosomeShort statureChromosome translocation03 medical and health sciences0302 clinical medicine030225 pediatricsTurner syndromemedicineTreatment adherence030212 general & internal medicineLetter to the EditorGrowth hormoneX chromosomemedicine.diagnostic_testbusiness.industrylcsh:RJ1-570lcsh:PediatricsKaryotypemedicine.diseaseMolecular biologySHOX haploinsufficiencymedicine.symptombusinessFluorescence in situ hybridization
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