Search results for " mutations"

showing 10 items of 127 documents

The roles of whole-genome and small-scale duplications in the functional specialization of Saccharomyces cerevisiae genes

2013

Researchers have long been enthralled with the idea that gene duplication can generate novel functions, crediting this process with great evolutionary importance. Empirical data shows that whole-genome duplications (WGDs) are more likely to be retained than small-scale duplications (SSDs), though their relative contribution to the functional fate of duplicates remains unexplored. Using the map of genetic interactions and the re-sequencing of 27 Saccharomyces cerevisiae genomes evolving for 2,200 generations we show that SSD-duplicates lead to neo-functionalization while WGD-duplicates partition ancestral functions. This conclusion is supported by: (a) SSD-duplicates establish more genetic i…

0106 biological sciencesCancer ResearchGenome evolutionlcsh:QH426-470ArabidopsisSaccharomyces cerevisiaeBiology01 natural sciencesGenomeDivergenceEvolution Molecular03 medical and health sciencesMolecular evolutionPhylogeneticsGene DuplicationGene duplicationGeneticsMads-Box genesBiologyMolecular BiologyGenePhylogenyGenetics (clinical)Ecology Evolution Behavior and Systematics030304 developmental biologySmall-scale duplicationsGeneticsEvolutionary BiologyEvolutionary Theory0303 health sciencesAdaptive conflictHuman evolutionary geneticsNull mutationsSaccharomyces cerevisiae genomeProtein-Protein interactionslcsh:GeneticsEvolutionary biologyDiversificationEpistasisMolecular evolutionWhole-genome duplicationsGenome FungalYeast genomeInteractions revealResearch Article010606 plant biology & botany
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Genome-wide association meta-analysis highlights light-induced signaling as a driver for refractive error

2018

Skin affections after sulfur mustard (SM) exposure include erythema, blister formation and severe inflammation. An antidote or specific therapy does not exist. Anti-inflammatory compounds as well as substances counteracting SM-induced cell death are under investigation. In this study, we investigated the benzylisoquinoline alkaloide berberine (BER), a metabolite in plants like berberis vulgaris, which is used as herbal pharmaceutical in Asian countries, against SM toxicity using a well-established in vitro approach. Keratinocyte (HaCaT) mono-cultures (MoC) or HaCaT/THP-1 co-cultures (CoC) were challenged with 100, 200 or 300 mM SM for 1 h. Post-exposure, both MoC and CoC were treated with 1…

0301 basic medicineAdultMaleCell typeResearchInstitutes_Networks_Beacons/MICRAIn silicotaittovirheetGenome-wide association studyRetinal Pigment EpitheliumBiologyBlindnessPolymorphism Single NucleotideSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]ArticleRetinaWhite People03 medical and health sciencesHIGH-GRADE MYOPIA ; RETINAL-PIGMENT EPITHELIUM ; SEROTONIN PATHWAY GENES ; FORM-DEPRIVATION MYOPIA ; COMMON VARIANTS ; OCULAR GROWTH ; RETINITIS-PIGMENTOSA ; GENOTYPE IMPUTATION ; MISSENSE MUTATIONS ; DOPAMINE-RECEPTORSAsian Peoplerefractive errorsRetinitis pigmentosaGeneticsmedicineMyopiaJournal ArticleHumansGenetic Predisposition to Disease610 Medicine & healthRegulation of gene expressionRetinaRetinal pigment epitheliummedicine.diseaseRefractive Errors030104 developmental biologymedicine.anatomical_structureManchester Institute for Collaborative Research on AgeingGene Expression Regulationgenetic factorsEye disorderFemalesense organsgeneettiset tekijätNeuroscienceGenome-Wide Association StudySignal Transduction
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Quantitative Imaging of D-2-Hydroxyglutarate in Selected Histological Tissue Areas by a Novel Bioluminescence Technique

2016

Abstract Patients with malignant gliomas have a poor prognosis with average survival of less than one year. Whereas in other tumor entities the characteristics of tumor metabolism are successfully used for therapeutic approaches, such developments are very rare in brain tumors, notably in gliomas. One metabolic feature characteristic of gliomas, in particular diffuse astrocytomas and oligodendroglial tumors, is the variable content of D-2-hydroxyglutarate (D2HG), a metabolite, which was discovered first in this tumor entity. D2HG is generated in large amounts due to various “gain-of–function” mutations in the isocitrate dehydrogenases IDH-1 and IDH-2. Meanwhile, D2HG has been detected in se…

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyMetabolite610 MedizinBiology03 medical and health scienceschemistry.chemical_compoundmedicineBioluminescence imagingBioluminescenceOligodendroglial TumorOriginal Researchddc:610D-2 hydroxyglutarateglioblastomaMyeloid leukemiaCancerACUTE MYELOID-LEUKEMIA; ISOCITRATE DEHYDROGENASE 1; IDH2 MUTATIONS; CHROMATOGRAPHY/MASS SPECTROMETRY; MAGNETIC-RESONANCE; 2-HYDROXYGLUTARATE; CANCER; GLIOMAS; L-2-HYDROXYGLUTARATE; METABOLITES; D-2 hydroxyglutarate; IDH mutations; bioluminescence imaging; oncometabolite; glioblastomabioluminescence imagingIDH mutationsmedicine.diseaseoncometaboliteLymphoma030104 developmental biologychemistryOncologyChondrosarcoma
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Frequency and prognostic impact of ALK amplifications and mutations in the European Neuroblastoma Study Group (SIOPEN) high-risk neuroblastoma trial …

2021

Purpose: In neuroblastoma (NB), the ALK receptor tyrosine kinase can be constitutively activated through activating point mutations or genomic amplification. We studied ALK genetic alterations in high-risk (HR) patients on the HR-NBL1/SIOPEN trial to determine their frequency, correlation with clinical parameters, and prognostic impact. Materials and methods: Diagnostic tumor samples were available from 1,092 HR-NBL1/SIOPEN patients to determine ALK amplification status (n = 330), ALK mutational profile (n = 191), or both (n = 571). Results: Genomic ALK amplification (ALKa) was detected in 4.5% of cases (41 out of 901), all except one with MYCN amplification (MNA). ALKa was associated with …

0301 basic medicineCancer ResearchPrognostic ImpactAnaplastic Lymphoma Kinase/genetics; Child Preschool; Clinical Trials Phase III as Topic; Europe; Female; Follow-Up Studies; Gene Amplification; Humans; Infant; Male; Mutation Rate; N-Myc Proto-Oncogene Protein/genetics; Neuroblastoma/genetics; Prognosis; Randomized Controlled Trials as Topic; Risk Factors; Survival RateEuropean Neuroblastoma Study GroupSIOPENRELAPSE03 medical and health sciencesNeuroblastoma0302 clinical medicineText miningNeuroblastomahemic and lymphatic diseasesREVEALSMedicine and Health SciencesKINASEMedicineHigh risk neuroblastomaHETEROGENEITYCRIZOTINIBSEGMENTAL CHROMOSOMAL ALTERATIONSACTIVATING MUTATIONSPEDIATRIC-PATIENTSbusiness.industryALK receptor tyrosine kinasePoint mutationREARRANGEMENTSCHEMOTHERAPYmedicine.diseaseDoenças Genéticas030104 developmental biologyALKOncology030220 oncology & carcinogenesisCancer researchbusiness
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Abstract IA06: Targeting the mutanome for individualized cancer immunotherapy

2016

Abstract Mutations are regarded as ideal targets for cancer immunotherapy. As neo-epitopes with strict lack of expression in any healthy tissue, they are expected to be safe. The systematic use of mutations for vaccine approaches, however, is hampered by the uniqueness of the repertoire of mutations (the mutanome) in every patient's tumor. We have recently proposed a personalized immunotherapy approach targeting the spectrum of individual mutations. Preclinically we could show in three independent murine tumor models that a considerable fraction of non-synonymous cancer mutations is immunogenic and that unexpectedly the immunogenic mutanome is pre-dominantly recognized by CD4+ T cells (the …

0301 basic medicineCancer Researchbusiness.industryRepertoiremedicine.medical_treatmentImmunologyCancerImmunotherapymedicine.diseaseEpitopeVaccination03 medical and health sciences030104 developmental biology0302 clinical medicineCancer immunotherapy030220 oncology & carcinogenesisImmunologymedicineCancer mutationsbusinessExome sequencingCancer Immunology Research
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Shank3 Mice Carrying the Human Q321R Mutation Display Enhanced Self-Grooming, Abnormal Electroencephalogram Patterns, and Suppressed Neuronal Excitab…

2019

Shank3, a postsynaptic scaffolding protein involved in regulating excitatory synapse assembly and function, has been implicated in several brain disorders, including autism spectrum disorders (ASD), Phelan-McDermid syndrome, schizophrenia, intellectual disability, and mania. Here we generated and characterized a Shank3 knock-in mouse line carrying the Q321R mutation (Shank3Q321R mice) identified in a human individual with ASD that affects the ankyrin repeat region (ARR) domain of the Shank3 protein. Homozygous Shank3Q321R/Q321R mice show a selective decrease in the level of Shank3a, an ARR-containing protein variant, but not other variants. CA1 pyramidal neurons in the Shank3Q321R/Q321R hip…

0301 basic medicineHippocampusautism spectrum disorderBiologyNeurotransmissionElectroencephalographyInhibitory postsynaptic potentiallcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceExcitatory synapse assembly0302 clinical medicinePostsynaptic potentialexcitabilitymedicineself-groomingEEGMolecular Biologylcsh:Neurosciences. Biological psychiatry. Neuropsychiatrypatient mutationsOriginal Researchmedicine.diagnostic_testanxiety-like behaviorseizure susceptibilitymedicine.disease030104 developmental biologyShank3SchizophreniaExcitatory postsynaptic potentialNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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Further delineation of the clinical spectrum of de novo TRIM8 truncating mutations.

2018

IF 2.264; International audience; De novo mutations of the TRIM8 gene, which codes for a tripartite motif protein, have been identified using whole exome sequencing (WES) in two patients with epileptic encephalopathy (EE), but these reports were not sufficient to conclude that TRIM8 was a novel gene responsible for EE. Here we report four additional patients presenting with EE and de novo truncating mutations of TRIM8 detected by WES, and give further details of the patient previously reported by the Epi4K consortium. Epilepsy of variable severity was diagnosed in children aged 2 months to 3.5 years of age. All patients had developmental delay of variable severity with no or very limited la…

0301 basic medicineMaleAdolescentNerve Tissue ProteinsBioinformaticswhole exome sequencing03 medical and health sciencesEpilepsyTripartite MotifGeneticsmedicineHumansTRIM8Amino Acid SequenceChildGeneGenetics (clinical)De novo mutationsExome sequencingbusiness.industrynephrotic syndromeEpileptic encephalopathyInfant NewbornInfantmedicine.diseasePhenotype3. Good health030104 developmental biologyepileptic encephalopathy[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolMutationFemalebusinessCarrier ProteinsNephrotic syndromeAmerican journal of medical genetics. Part A
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Benign nocturnal alternating hemiplegia of childhood

2018

Objective: To describe the clinical spectrum of benign nocturnal alternating hemiplegia of childhood (BNAHC) including long-term follow-up data of previously published cases and to propose an underlying genetic cause of this disorder. Methods: We studied the medical data of two novel patients, reviewed the literature on BNAHC, and gathered information of the most recent follow-up of published cases regarding the course of episodes, further development, attempted drugs, ancillary investigations, and sequelae. Results: All patients, i.e. two novel cases and twelve patients identified in the literature (13 boys, 1 girl, age at onset four months to three years), experienced episodes of hemipleg…

0301 basic medicineMaleExome sequencingPediatricsmedicine.medical_specialtyHeterozygoteHemiplegiaNerve Tissue ProteinsPATIENTSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]03 medical and health sciences0302 clinical medicinePRRT2 MUTATIONSmedicineHumansIctalPAROXYSMAL KINESIGENIC DYSKINESIAFamily historyPRRT2 geneExome sequencingCryingbusiness.industryAlternating hemiplegia of childhoodInfantMembrane ProteinsGeneral MedicineParoxysmal dyskinesiamedicine.diseaseDisorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]GENESleep deprivation030104 developmental biologyPhenotypeTreatment OutcomeSYNAPTIC-TRANSMISSIONMigraineMIGRAINEChild PreschoolPediatrics Perinatology and Child HealthDisease ProgressionNeurology (clinical)medicine.symptombusinessINFANTILE CONVULSIONS030217 neurology & neurosurgeryGene DeletionBenign nocturnal alternating hemiplegia of childhoodEuropean Journal of Paediatric Neurology
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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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A possible role of FANCM mutations in male breast cancer susceptibility: Results from a multicenter study in Italy

2018

Abstract Introduction Breast cancer (BC) in men is a rare disease, whose etiology appears to be associated with genetic factors. Inherited mutations in BRCA1/2 genes account for about 10–15% of all cases. FANCM, functionally linked to BRCA1/2, has been suggested as a novel BC susceptibility gene. Our aim was to test if FANCM germline mutations could further explain male BC (MBC) susceptibility. Methods We screened the entire coding region of FANCM in 286 MBCs by a multi-gene panel analysis, and compared these data with available whole exome sequencing data from 415 men used as population controls. Moreover, we genotyped the two most frequent FANCM mutations (c.5101C>T and c.5791C>T) in 506 …

0301 basic medicineMaleMutation rateSettore MED/06 - Oncologia MedicaDNA Helicasemedicine.disease_causeBRCA1/2; Breast cancer susceptibility; FANCM; Germline mutations; Male breast cancer; Adult; Aged; Aged 80 and over; Biomarkers Tumor; Breast Neoplasms Male; Case-Control Studies; DNA Helicases; Genetic Predisposition to Disease; Genotype; Germ-Line Mutation; Humans; Italy; Male; Middle Aged; Risk Factors; Whole Genome Sequencing; Young Adult; Surgery0302 clinical medicineFANCMRisk Factorshemic and lymphatic diseasesGermline mutationGenotypeBRCA1/2; Breast cancer susceptibility; FANCM; Germline mutations; Male breast cancer; SurgeryFANCMMutation frequencyGeneticsAged 80 and overeducation.field_of_studyMutationGeneral MedicineMiddle AgedItaly030220 oncology & carcinogenesisMale breast cancerCase-Control StudieHumanAdultcongenital hereditary and neonatal diseases and abnormalitiesGenotypePopulationBreast Neoplasms Male03 medical and health sciencesYoung AdultGermline mutationBRCA1/2medicineBiomarkers TumorHumansGenetic Predisposition to DiseaseeducationGermline mutationsGerm-Line MutationAgedBreast cancer susceptibilityWhole Genome Sequencingbusiness.industryRisk FactorDNA Helicasesnutritional and metabolic diseasesmedicine.diseaseMale breast cancer030104 developmental biologyCase-Control StudiesSurgerybusiness
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