Search results for " loss of function"

showing 6 items of 6 documents

Functional analysis of TLK2 variants and their proximal interactomes implicates impaired kinase activity and chromatin maintenance defects in their p…

2020

IntroductionThe Tousled-like kinases 1 and 2 (TLK1 and TLK2) are involved in many fundamental processes, including DNA replication, cell cycle checkpoint recovery and chromatin remodelling. Mutations in TLK2 were recently associated with ‘Mental Retardation Autosomal Dominant 57’ (MRD57, MIM# 618050), a neurodevelopmental disorder characterised by a highly variable phenotype, including mild-to-moderate intellectual disability, behavioural abnormalities, facial dysmorphisms, microcephaly, epilepsy and skeletal anomalies.MethodsWe re-evaluate whole exome sequencing and array-CGH data from a large cohort of patients affected by neurodevelopmental disorders. Using spatial proteomics (BioID) and…

0301 basic medicineNeurobiologia del desenvolupamentMicrocephalymissenseMolecular biologyBiologymedicine.disease_causemedicalloss of function mutation03 medical and health sciencesmutation.0302 clinical medicineNeurodevelopmental disordermedicineChromatin maintenanceMissense mutationmolecular biologygeneticsDevelopmental neurobiologyKinase activitygenetic research; genetics; loss of function mutation; medical; missense; molecular biology; mutationGenetics (clinical)Exome sequencingBiologia molecularGeneticsMutationgenetic researchmedicine.diseaseChromatin030104 developmental biologymutationgenetic030217 neurology & neurosurgery
researchProduct

A Novel Loss of Function Mutation of PCSK9 Gene in White Subjects With Low-Plasma Low-Density Lipoprotein Cholesterol

2007

Objectives— The PCSK9 gene, encoding a pro-protein convertase involved in posttranslational degradation of low-density lipoprotein receptor, has emerged as a key regulator of plasma low-density lipoprotein cholesterol. In African-Americans two nonsense mutations resulting in loss of function of PCSK9 are associated with a 30% to 40% reduction of plasma low-density lipoprotein cholesterol. The aim of this study was to assess whether loss of function mutations of PCSK9 were a cause of familial hypobetalipoproteinemia and a determinant of low-plasma low-density lipoprotein cholesterol in whites. Methods and Results— We sequenced PCSK9 gene in 18 familial hypobetalipoproteinemia subjects and i…

AdultMalemedicine.medical_specialtyNonsense mutationBiologymedicine.disease_causePolymorphism Single NucleotideRisk AssessmentSensitivity and SpecificityStatistics NonparametricWhite Peopleloss of function mutationHypobetalipoproteinemiaschemistry.chemical_compoundPCSK9 GeneGene FrequencyInternal medicinemedicineHumansGenetic Predisposition to DiseaseMutationhypocholesterolemiaCholesterolIncidencePCSK9Serine EndopeptidasesCholesterol LDLmedicine.diseaseHypocholesterolemiaEndocrinologyfamilial hypobetalipoproteinemiachemistryCodon NonsensePCSK9 geneCase-Control Studiesfamilial hypobetalipoproteinemia hypocholesterolemia loss of function mutation PCSK9 genefamilial hypobetalipoproteinemia; hypocholesterolemia; loss of function mutation; PCSK9 gene.FemaleProprotein ConvertasesHypobetalipoproteinemiaProprotein Convertase 9Cardiology and Cardiovascular MedicineLipoprotein
researchProduct

A NOVEL LOSS OF FUNCTION MUTATION OF PCSK9 GENE

2006

LDLR genePCSK9 gene; loss of function; missense mutation; LDLR gene; LDL-C; hypocholesterolemic effecthypocholesterolemic effectloss of functionPCSK9 genemissense mutationLDL-C
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

AMPA receptor GluA2 subunit defects are a cause of neurodevelopmental disorders.

2019

AMPA receptors (AMPARs) are tetrameric ligand-gated channels made up of combinations of GluA1-4 subunits encoded by GRIA1-4 genes. GluA2 has an especially important role because, following post-transcriptional editing at the Q607 site, it renders heteromultimeric AMPARs Ca2+-impermeable, with a linear relationship between current and trans-membrane voltage. Here, we report heterozygous de novo GRIA2 mutations in 28 unrelated patients with intellectual disability (ID) and neurodevelopmental abnormalities including autism spectrum disorder (ASD), Rett syndrome-like features, and seizures or developmental epileptic encephalopathy (DEE). In functional expression studies, mutations lead to a dec…

Male[SDV.GEN] Life Sciences [q-bio]/GeneticsIon channels in the nervous systemCohort Studiesfluids and secretionsLoss of Function MutationReceptorsAMPAAMPA receptorlcsh:ScienceChildreproductive and urinary physiologyAMPA receptor GluA2 neurodevelopmental disorders autism spectrum disorder glutamatergic synaptic transmission GRIA2neurodevelopmental disordersDevelopmental disordersQNeurodevelopmental disordersBrainMagnetic Resonance ImagingSettore MED/26 - NEUROLOGIAGluA2Child PreschoolFemaleAdultHeterozygoteAdolescentScienceautism spectrum disorderArticleYoung Adult[SDV.MHEP.PED] Life Sciences [q-bio]/Human health and pathology/PediatricsMESH: Intellectual Disability/genetics; Neurodevelopmental Disorders/genetics; Receptors AMPA/genetics; HeterozygoteIntellectual Disabilitymental disordersAdolescent; Adult; Brain; Child; Child Preschool; Cohort Studies; Female; Heterozygote; Humans; Infant; Intellectual Disability; Loss of Function Mutation; Magnetic Resonance Imaging; Male; Neurodevelopmental Disorders; Receptors AMPA; Young AdultHumansReceptors AMPAGRIA2PreschoolIon channel in the nervous system Developmental disorders Synaptic development NG sequencing[SDV.GEN]Life Sciences [q-bio]/Genetics[SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/Pediatricsglutamatergic synaptic transmission[SCCO.NEUR]Cognitive science/Neuroscience[SCCO.NEUR] Cognitive science/NeuroscienceInfantNG sequencingSynaptic developmentIon channel in the nervous systemNext-generation sequencinglcsh:Q
researchProduct

12q21 Interstitial Deletions: Seven New Syndromic Cases Detected by Array-CGH and Review of the Literature.

2022

Interstitial deletions of the long arm of chromosome 12 are rare, with a dozen patients carrying a deletion in 12q21 being reported. Recently a critical region (CR) has been delimited and could be responsible for the more commonly described clinical features, such as developmental delay/intellectual disability, congenital genitourinary and brain malformations. Other, less frequent, clinical signs do not seem to be correlated to the proposed CR. We present seven new patients harboring non-recurrent deletions ranging from 1 to 18.5 Mb differentially scattered across 12q21. Alongside more common clinical signs, some patients have rarer features such as heart defects, hearing loss, hypotonia an…

dysmorphismsComparative Genomic Hybridization12q21 deletiongenetic counselingcopy number variants (CNVs)DNA Copy Number Variationscongenital anomaliesarray-CGH; 12q21 deletion; copy number variants (CNVs); variation intolerant genes; loss of function; developmental delay/intellectual disability (DD/ID); congenital anomalies; dysmorphisms; genetic counseling; patient management12q21 deletion array-CGH congenital anomalies copy number variants (CNVs) developmental delay/intellectual disability (DD/ID) dysmorphisms genetic counseling loss of function patient management variation intolerant genesdevelopmental delay/intellectual disability (DD/ID)variation intolerant genesloss of functionSettore MED/03 - Genetica MedicaChromosome Structuresarray-CGHIntellectual DisabilityGeneticsHumansChromosome Deletionpatient managementGenetics (clinical)Genes
researchProduct