Search results for "deletion"

showing 10 items of 383 documents

Clinical manifestations and management of four children with Pearson syndrome.

2011

Pearson marrow-pancreas syndrome is a fatal disorder mostly diagnosed during infancy and caused by mutations of mitochondrial DNA. We hereby report on four children affected by Pearson syndrome with hematological disorders at onset. The disease was fatal to three of them and the fourth one, who received hematopoietic stem cell transplantation, died of secondary malignancy. In this latter patient transplantation corrected hematological and non-hematological issues like metabolic acidosis, and we therefore argue that it could be considered as a useful option in an early stage of the disease.

MalePediatricsmedicine.medical_specialtyMitochondrial DiseasesAnemiaMitochondrial diseasemedicine.medical_treatmenttrapianto cellule staminali emopoieticheHematopoietic stem cell transplantationDiseaseDNA MitochondrialLipid Metabolism Inborn Errorsmitochondrial disordersFatal OutcomeMuscular DiseasesCause of Deathhematopoietic stem cell transplantation; mitochondrial disorders; Pearson marrow-pancreas syndrome; trapianto cellule staminali emopoietiche; malattie mitocondriali; sindrome di PearsonGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansChildGenetics (clinical)Pearson marrow-pancreas syndromeCause of deathPearson syndromebusiness.industryAcyl-CoA Dehydrogenase Long-ChainHematopoietic Stem Cell TransplantationInfantMetabolic acidosissindrome di Pearsonmedicine.diseaseAnemia SideroblasticTransplantationChild PreschoolImmunologymalattie mitocondrialiFemalebusinessGene DeletionAmerican journal of medical genetics. Part A
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Sequence variation in couch potato and its effects on life-history traits in a northern malt fly, Drosophila montana

2011

Abstract Couch potato ( cpo ) has previously been connected to reproductive diapause in several insect species including Drosophila melanogaster , where it has been suggested to provide a link between the insulin signalling pathway and the hormonal control of diapause. In the first part of the study we sequenced nearly 3.6 kb of this gene in a northern Drosophila species ( Drosophila montana ) with a robust photoperiodically determined diapause and found several types of polymorphisms along the sequenced area. We also found variation among five Drosophila virilis group species in the length of the 5th exon of cpo and in the site of the stop codon at the end of this exon. The second part of …

MalePhysiologyAmino Acid MotifsMolecular Sequence DataPopulationDiapauseExonSpecies SpecificityAnimalsDrosophila ProteinsAmino Acid SequenceeducationGeneConserved SequenceSequence DeletionGeneticseducation.field_of_studyPolymorphism GeneticSequence Homology Amino AcidbiologyWild typeNuclear ProteinsExonsSequence Analysis DNAbiology.organism_classificationIntronsStop codonDrosophila virilisPhenotypeInsect ScienceDrosophilaFemaleDrosophila melanogasterSequence AlignmentJournal of Insect Physiology
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A novel two base pair deletion in the factor V gene associated with severe factor V deficiency

2001

We studied a family in which the proband, a 13-year-old boy, had unmeasurable plasma levels of coagulation factor V antigen and activity. Clinical symptoms were severe, with several episodes of haemorrhages in the mucosal tracts (gastrointestinal, nose and urinary) and recurrent haemarthroses that caused permanent arthropathy. Sequence analysis of the factor V gene demonstrated the presence of a novel 2 base pair (bp) homozygous deletion in exon 13 at positions 2833-2834. This mutation, present in the heterozygous state in the asymptomatic mother and absent in the healthy brother, introduced a frameshift and a premature stop at codon 900. This would predict the synthesis of a truncated fact…

MaleProbandFactor V DeficiencyAdolescentMutantBiologymedicine.disease_causeFrameshift mutationExonmedicineHumansRNA MessengerBase PairingGeneGeneticsMutationReverse Transcriptase Polymerase Chain ReactionHomozygoteFactor VFactor VSequence Analysis DNAHematologyMolecular biologybiology.proteinBlood Coagulation TestsFactor V DeficiencyGene DeletionBritish Journal of Haematology
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Targeted next-generation sequencing of deafness genes in hearing-impaired individuals uncovers informative mutations

2014

Purpose: Targeted next-generation sequencing provides a remarkable opportunity to identify variants in known disease genes, particularly in extremely heterogeneous disorders such as nonsyndromic hearing loss. The present study attempts to shed light on the complexity of hearing impairment. Methods: Using one of two next-generation sequencing panels containing either 80 or 129 deafness genes, we screened 30 individuals with nonsyndromic hearing loss (from 23 unrelated families) and analyzed 9 normal-hearing controls. Results: Overall, we found an average of 3.7 variants (in 80 genes) with deleterious prediction outcome, including a number of novel variants, in individuals with nonsyndromic h…

MaleProbandUsher syndromeGene DosageDeafnessBioinformaticsmedicine.disease_causesensorineural hearing lossConnexinsCohort Studiestargeted next-generation sequencingOriginal Research Articlemutational loadChildGenetics (clinical)Oligonucleotide Array Sequence AnalysisGeneticsMutationmedicine.diagnostic_testHomozygoteHigh-Throughput Nucleotide SequencingPedigreeConnexin 26Treatment OutcomeChild PreschoolFemalemedicine.symptomAdultAdolescentSequence analysisHearing lossdeafness gene panelMolecular Sequence DataBiologynonsyndromic hearing lossDNA sequencingYoung AdultAudiometryGenetic variationotorhinolaryngologic diseasesmedicineHumansGenetic Predisposition to DiseaseFamily HealthBase SequenceGenetic VariationInfantDNASequence Analysis DNAmedicine.diseaseMutationAudiometryGene DeletionGenetics in Medicine
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RNA cytosine methylation by Dnmt2 and NSun2 promotes tRNA stability and protein synthesis.

2012

The function of cytosine-C5 methylation, a widespread modification of tRNAs, has remained obscure, particularly in mammals. We have now developed a mouse strain defective in cytosine-C5 tRNA methylation, by disrupting both the Dnmt2 and the NSun2 tRNA methyltransferases. Although the lack of either enzyme alone has no detectable effects on mouse viability, double mutants showed a synthetic lethal interaction, with an underdeveloped phenotype and impaired cellular differentiation. tRNA methylation analysis of the double-knockout mice demonstrated complementary target-site specificities for Dnmt2 and NSun2 and a complete loss of cytosine-C5 tRNA methylation. Steady-state levels of unmethylate…

MaleRNA StabilityMutantBiologyNSun2MethylationCytosineMiceRNA TransferStructural BiologyProtein biosynthesism5CAnimalsDNA (Cytosine-5-)-MethyltransferasesMolecular BiologytRNACells CulturedMice KnockoutTRNA methylationRNACell DifferentiationMethylationMethyltransferasesTRNA MethyltransferasesBiochemistryProtein BiosynthesisTransfer RNADNA methylationDnmt2FemaleGene DeletionNature structuralmolecular biology
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RNA methylation by Dnmt2 protects transfer RNAs against stress-induced cleavage

2010

The covalent modification of nucleic acids plays an important role in regulating the functions of DNA and RNA. DNA modifications have been analyzed in considerable detail, and the characterization of (cytosine-5) DNA methylation has been crucial for understanding the molecular basis of epigenetic gene regulation (Klose and Bird 2006). (Cytosine-5) methylation has also been documented in various RNA species, including tRNA, but the function of RNA methylation has not been firmly established yet (Motorin et al. 2010). Dnmt2 proteins were originally assigned to the DNA methyltransferase family, because of their strong sequence conservation of catalytic DNA methyltransferase motifs (Okano et al…

MaleRNA methylationBiologyMethylationDNA methyltransferaseResearch CommunicationMiceRNA TransferStress PhysiologicalGeneticsAnimalsDrosophila ProteinsDNA (Cytosine-5-)-MethyltransferasesRNA-Directed DNA MethylationSequence DeletionTRNA methylationTRNA methyltransferase activityTRNA MethyltransferaseRibonuclease PancreaticMethylationSurvival AnalysisMolecular biologyDrosophila melanogasterDNA methylationRNAFemaleDevelopmental BiologyGenes & Development
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Association between the polymorphism of CCR5 and Alzheimer's disease: results of a study performed on male and female patients from Northern Italy.

2007

Alzheimer's disease (AD) is the most common cause of dementia in Western society. The prevalence of AD is greater in women than in men, largely due to longevity and survival differences favoring women. However, some studies suggest that incidence rates may really be increased in women. One possible factor influencing AD incidence in women is the loss of ovarian estrogens production after menopause, which might be involved in AD pathogenesis. Estrogens seem to influence some neuronal functions. Many of these actions appear beneficial (i.e., neuroprotective action against a variety of insults, as oxidative stress, and reduction of beta-amyloid plaques formation). Furthermore, several studies …

MaleReceptors CCR5DiseaseBiologyGeneral Biochemistry Genetics and Molecular BiologyCohort StudiesHistory and Philosophy of ScienceGene FrequencyPolymorphism (computer science)Alzheimer DiseaseGenotypemedicineDementiaHumansSex RatioAlleleAllele frequencyAllelesAgedSequence DeletionAged 80 and overInflammationPolymorphism GeneticGeneral NeuroscienceIncidence (epidemiology)Middle Agedmedicine.diseaseMenopauseItalyCase-Control StudiesImmunologyFemaleAnnals of the New York Academy of Sciences
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Disruption of the ASTN2 / TRIM32 locus at 9q33.1 is a risk factor in males for Autism Spectrum Disorders, ADHD and other neurodevelopmental phenotypes

2014

Rare copy number variants (CNVs) disrupting ASTN2 or both ASTN2 and TRIM32 have been reported at 9q33.1 by genome-wide studies in a few individuals with neurodevelopmental disorders (NDDs). The vertebrate-specific astrotactins, ASTN2 and its paralog ASTN1, have key roles in glial-guided neuronal migration during brain development. To determine the prevalence of astrotactin mutations and delineate their associated phenotypic spectrum, we screened ASTN2/TRIM32 and ASTN1 (1q25.2) for exonic CNVs in clinical microarray data from 89 985 individuals across 10 sites, including 64 114 NDD subjects. In this clinical dataset, we identified 46 deletions and 12 duplications affecting ASTN2. Deletions o…

MaleReceptors Cell Surface/geneticsAutismChild Development Disorders Pervasive/geneticsGene ExpressionGenome-wide association studyMedical and Health SciencesTripartite Motif ProteinsRisk FactorsReceptors2.1 Biological and endogenous factorsProtein IsoformsNerve Tissue Proteins/geneticsCopy-number variationAetiologyChildGenetics (clinical)Sequence DeletionPediatricGenetics & HeredityGeneticseducation.field_of_studySingle NucleotideArticlesGeneral MedicineExonsBiological SciencesMental HealthPhenotypeAutism spectrum disorderOrgan SpecificityCerebellar cortexChild PreschoolCell SurfaceSpeech delayFemalemedicine.symptomTranscription Initiation SiteAttention Deficit Disorder with Hyperactivity/geneticsChromosomes Human Pair 9HumanPair 9AdultPediatric Research InitiativeChild Development DisordersAdolescentDNA Copy Number VariationsIntellectual and Developmental Disabilities (IDD)Ubiquitin-Protein LigasesPopulationTranscription Factors/geneticsNerve Tissue ProteinsReceptors Cell SurfaceBiologyPolymorphism Single NucleotideChromosomesYoung AdultClinical ResearchProtein Isoforms/geneticsBehavioral and Social ScienceGeneticsmedicineAttention deficit hyperactivity disorderHumansGenetic Predisposition to DiseasePolymorphismPreschooleducationMolecular BiologyGenetic Association StudiesPervasiveGlycoproteinsHuman GenomeNeurosciencesInfant NewbornGlycoproteins/geneticsInfantNewbornmedicine.diseaseBrain DisordersAttention Deficit Disorder with HyperactivityChild Development Disorders PervasiveCase-Control StudiesAutismTranscription Factors
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The Drosophila ACP65A cuticle gene: deletion scanning analysis of cis-regulatory sequences and regulation by DHR38.

2005

The regulatory sequences of the Drosophila ACP65A cuticle gene were analyzed in vivo in transgenic flies, using both fusion genes constructs and transposase-mediated deletions within a P element containing ACP65A regulatory sequences fused to the lacZ gene (deletion scanning). The sequences located between −594 and +161 are sufficient to confer both temporal and spatial expression specificities, indicating the presence of tissue-specific enhancers and response elements to hormone-induced factors. In addition, timing of expression and tissue-specificity appear to be controlled by distinct cis-regulatory elements, which suggests the existence of independent hormonal and tissue-specific signal…

MaleReceptors SteroidTranscription GeneticTransgenelac operonReceptors Cytoplasmic and NuclearBiologyFusion geneP elementAnimals Genetically ModifiedEndocrinologyGeneticsNuclear Receptor Subfamily 4 Group A Member 1AnimalsDrosophila ProteinsEnhancerGeneCrosses GeneticSequence DeletionGeneticsBase SequenceActivator (genetics)fungiPupaCell BiologyDNA-Binding ProteinsGene Expression RegulationRegulatory sequenceInsect ProteinsDrosophilaFemaleTranscription FactorsGenesis (New York, N.Y. : 2000)
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Molecular Basis of Hereditary C1q Deficiency

1998

Abstract Complete selective deficiencies of the complement component C1q are rare genetic disorders which are associated with recurrent infections and a high prevalence of lupus erythematosus-like symptoms. The improvements in molecular biology techniques have facilitated the analysis of such genetic defects to a great extend. To date the basis of C1q deficiencies from 13 families have been studied at the genetic level. In each case single base mutations leading to either termination codons, frame shift or amino acid exchanges were thought to be responsible for these defects as no other aberrations were found. In addition to DNA analysis, conventional immunochemical and biochemical methods …

MaleRecurrent infectionsGenotypeTurkeyImmunologySaudi ArabiaBiologyAutoimmune DiseasesFrameshift mutationchemistry.chemical_compoundC1q DeficiencyGermanyComplement component C1qmedicineHumansLupus Erythematosus SystemicPoint MutationImmunology and AllergyGenetic Predisposition to DiseaseSequence DeletionGeneticsSystemic lupus erythematosusComplement C1qImmunologic Deficiency SyndromesHematologymedicine.diseaseStructure and functionAmino Acid SubstitutionchemistryChromosomes Human Pair 1Codon NonsenseFemaleDNAImmunobiology
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