Search results for "sequence deletion"

showing 10 items of 107 documents

Infant developmental profile of Crisponi syndrome due to compound heterozygosity for CRLF1 deletion.

2020

Crisponi syndrome/CISS1, is an autosomal recessive ciliary neurotrophic factor receptor (CNTFR)-related genodermatosis caused in 95% of cases by mutations in CRLF1 on chromosome 19p13. The CNTFR pathway is important for CNS development. Crisponi syndrome/ CISS1 can be suspected in the presence of the following clinical triad: camptodactyly with fisted hands, intermittent hyperthermia and muscular contractions with feeding difficulties.

MalePathologymedicine.medical_specialtyCrisponi syndromeCompound heterozygosityPathology and Forensic MedicineCamptodactylyDeath SuddenPeriodic feverMedicineHumansHyperhidrosisReceptors CytokineGenetics (clinical)Sequence DeletionDevelopmental profiledevelopmental delay thin corpus callosum clinical profilebusiness.industryInfant NewbornFaciesInfantCold-induced sweating syndromeGeneral MedicineThin corpus callosumPediatrics Perinatology and Child HealthTrismusAnatomymedicine.symptomDevelopmental DelayCold-induced sweating syndrome CamptodactylyThin corpus callosum Periodic feverbusinessHand Deformities CongenitalClinical dysmorphology
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A Paucisymptomatic Neuromuscular Disease Mimicking Type III 5q-SMA With Complex Rearrangements in the SMN Gene

2013

Spinal muscular atrophy is an autosomal-recessive neuromuscular disorder, causing progressive proximal weakness and atrophy of the voluntary muscles. More than 96% of the spinal muscular atrophy patients show a homozygous absence of exons 7 and 8, or exon 7 only, in SMN1, the telomeric copy of the SMN gene. We report a young male patient with neurogenic symptoms and sparse muscle fiber atrophy, suggestive of a mild form of type III spinal muscular atrophy. He was found to be a carrier of intragenic mutations in both copies of the SMN gene, exhibiting a homozygous duplication of exons 7 and 8 in SMN1 and a homozygous deletion of exon 8 as well as a heterozygous deletion of exon 7 in SMN2. H…

MalePathologymedicine.medical_specialtyNeuromuscular diseaseBiopsyDNA Mutational AnalysisSMN1Spinal Muscular Atrophies of ChildhoodBiologyQuadriceps MuscleDiagnosis DifferentialMice03 medical and health sciencesExonAtrophyGene duplicationmedicineAnimalsHumansChildSequence Deletion030304 developmental biology0303 health sciences030305 genetics & heredityNeuromuscular DiseasesSpinal muscular atrophymedicine.diseaseSMA*ImmunohistochemistrySurvival of Motor Neuron 1 ProteinMolecular biologynervous system diseasesSmn geneSurvival of Motor Neuron 2 ProteinMuscular AtrophyPhenotypeMutationPediatrics Perinatology and Child HealthNeurology (clinical)Journal of Child Neurology
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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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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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Identification of a novel mutation in the alpha-galactosidase A gene in patients with Fabry disease.

2012

Abstract Objectives Mutation analysis of the alpha-galactosidase A (GLA) gene is a valuable tool for the diagnosis of affected families. In our work, we analyze about one thousand samples per year from patients suspected of having Fabry disease (FD). Design and methods We carried out high resolution melting analysis (HRM) and DNA sequencing of all the exons of the GLA gene. We also assayed the alpha-galactosidase A activity in patients' blood. Results In some members of one family, we identified a new mutation in the GLA gene, c.614delC. This is a deletion of a single nucleotide, a cytosine, in exon 4 of the gene which causes a frameshift mutation. Conclusions Patients with the c.614delC mu…

MaleSettore MED/09 - Medicina InternaClinical BiochemistryDNA Mutational AnalysisHigh Resolution MeltFrameshift mutationExonmedicineHumansFrameshift MutationGeneSequence DeletionGeneticsFamily HealthAlpha-galactosidasebiologyBase Sequencealpha-galactosidase A geneGeneral MedicineExonsmedicine.diseaseMolecular biologyFabry diseasealpha-GalactosidaseMutation (genetic algorithm)Mutation testingbiology.proteinFabry DiseaseFemalemutationClinical biochemistry
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Intragenic deletions of IL1RAPL1: Report of two cases and review of the literature

2010

IL1RAPL1 (interleukin-1 receptor accessory protein-like 1) located at Xp21.3-22.1 has repeatedly been shown to be deleted in patients with a contiguous gene syndrome also affecting neighboring genes, in particular DMD (dystrophin), DAX-1 (NR0B1, nuclear receptor subfamily 0, group B, member 1), and GK (glycerol kinase). In contrast, intragenic deletions of IL1RAPL1 or other mutations or cytogenetic aberrations affecting IL1RAPL1 have only rarely been identified. Up to date, they have mostly been associated with nonspecific mental retardation (MRX). We report on two nonrelated patients with MR and additional dysmorphic features who both show intragenic deletions of IL1RAPL1, one of them bein…

MaleSubfamilyMicroarrayBiologyPolymerase Chain ReactionContiguous gene syndromeExonIntellectual DisabilityGeneticsmedicineHumansAbnormalities MultipleGeneIn Situ Hybridization FluorescenceGenetics (clinical)X chromosomeSequence DeletionGeneticsKaryotypeMicroarray Analysismedicine.diseasePhenotypePedigreePhenotypeKaryotypingInterleukin-1 Receptor Accessory ProteinAmerican Journal of Medical Genetics Part A
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