Search results for "DELE"

showing 10 items of 631 documents

Dominant variants in the splicing factor PUF60 cause a recognizable syndrome with intellectual disability, heart defects and short stature

2016

Item does not contain fulltext Verheij syndrome, also called 8q24.3 microdeletion syndrome, is a rare condition characterized by ante- and postnatal growth retardation, microcephaly, vertebral anomalies, joint laxity/dislocation, developmental delay (DD), cardiac and renal defects and dysmorphic features. Recently, PUF60 (Poly-U Binding Splicing Factor 60 kDa), which encodes a component of the spliceosome, has been discussed as the best candidate gene for the Verheij syndrome phenotype, regarding the cardiac and short stature phenotype. To date, only one patient has been reported with a de novo variant in PUF60 that probably affects function (c.505C>T leading to p.(His169Tyr)) associated wi…

0301 basic medicineMaleMESH: Heart Defects Congenital / physiopathologyMicrocephalyPathologyMESH: Heart Defects Congenital / geneticsMESH: Exome / genetics030105 genetics & heredityMESH: RNA Splicing / geneticsMicrophthalmia[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesMESH: ChildExomeMESH: RNA Splicing Factors / geneticsChildFrameshift MutationMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingColobomaMESH: Frameshift MutationHigh-Throughput Nucleotide SequencingMicrodeletion syndromeMicrocephaly Verheij syndrome PUF60ChemistryPhenotypeChild PreschoolDISEASESMicrocephalyMedical geneticsFemaleRNA Splicing Factorsmedicine.symptomChromosome DeletionChromosomes Human Pair 8MESH: Dwarfism / genetics*Heart Defects Congenitalmedicine.medical_specialtyGENESAdolescentRNA SplicingMESH: Chromosome DeletionDwarfismBiologyMESH: PhenotypeShort statureArticlePUF6003 medical and health sciencesInternal medicineIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansCraniofacialBiologyMESH: AdolescentNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]MESH: HumansMESH: Child Preschoolmedicine.diseaseMESH: Repressor Proteins / geneticsMESH: MaleRepressor Proteins030104 developmental biologyEndocrinologyMESH: Chromosomes Human Pair 8 / geneticsMESH: Dwarfism / physiopathologyMESH: Intellectual Disability / physiopathologyHuman medicineMESH: Intellectual Disability / geneticsVerheij syndromeMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Myeloid Cells Restrict MCMV and Drive Stress- Induced Extramedullary Hematopoiesis through STAT1

2019

Cytomegalovirus (CMV) has a high prevalence worldwide, is often fatal for immunocompromised patients, and causes bone marrow suppression. Deficiency of signal transducer and activator of transcription 1 (STAT1) results in severely impaired antiviral immunity. We have used cell- type restricted deletion of Stat1 to determine the importance of myeloid cell activity for the defense against murine CMV (MCMV). We show that myeloid STAT1 limits MCMV burden and infection- associated pathology in the spleen but does not affect ultimate clearance of infection. Unexpectedly, we found an essential role of myeloid STAT1 in the induction of extramedullary hematopoiesis (EMH). The EMH- promoting function…

0301 basic medicineMaleMuromegalovirusMyeloidIFN-II receptorReceptor Interferon alpha-betamonocytes signal transducer and activator of transcription Herpesviridae IFN-I receptor IFN-II receptor L-27 receptor TLR9 agonistmedicine.disease_causeVirus Replication0302 clinical medicineTLR9 agonistMyeloid CellsSTAT1Cells CulturedHerpesviridaeReceptors Interferonsignal transducer and activator of transcriptionvirus diseasesIL-27 receptorHerpesviridae InfectionsExtramedullary hematopoiesisKiller Cells NaturalHaematopoiesismedicine.anatomical_structureSTAT1 Transcription FactorBone marrow suppressionHematopoiesis ExtramedullaryFemalemonocytesBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.SpleenBiologyGeneral Biochemistry Genetics and Molecular BiologyHerpesviridaeArticle03 medical and health sciencesStress PhysiologicalmedicineAnimalsBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Receptors Interleukinmedicine.diseaseMice Inbred C57BL030104 developmental biologyImmunologySTAT proteinbiology.protein030217 neurology & neurosurgeryGene DeletionSpleenIFN-I receptor
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Maternal Inheritance of a Recessive RBP4 Defect in Canine Congenital Eye Disease

2018

SUMMARY Maternally skewed transmission of traits has been associated with genomic imprinting and oocyte-derived mRNA. We report canine congenital eye malformations, caused by an amino acid deletion (K12del) near the N terminus of retinol-binding protein (RBP4). The disease is only expressed when both dam and offspring are deletion homozygotes. RBP carries vitamin A (retinol) from hepatic stores to peripheral tissues, including the placenta and developing eye, where it is required to synthesize retinoic acid. Gestational vitamin A deficiency is a known risk factor for ocular birth defects. The K12del mutation disrupts RBP folding in vivo, decreasing its secretion from hepatocytes to serum. T…

0301 basic medicineMaleNon-Mendelian inheritanceProtein Foldingcongenital eye defectEye Diseasesgenetic structuresNATIVE DISULFIDE BONDSMedical PhysiologyRetinoic acidReproductive health and childbirth413 Veterinary scienceMicrophthalmiavitamin Achemistry.chemical_compoundPlasmaA-vitamiini2.1 Biological and endogenous factorsMicrophthalmosPrealbuminCRYSTAL-STRUCTUREAetiologyBase Pairinglcsh:QH301-705.5Sequence DeletionPediatricwhole genome sequencingVITAMIN-A-DEFICIENCYANOPHTHALMIAPenetrancePedigreemedicine.anatomical_structurePhenotypeFemalemedicine.medical_specialtyGenotypeENDOPLASMIC-RETICULUMGenes RecessiveMETABOLISMBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesDogscanine geneticsInternal medicinePlacentaRETINOL-BINDING-PROTEINGeneticsmedicineAnimalsHumansRecessiveMALFORMATIONSBIOCHEMICAL BASISAmino Acid SequenceAlleleEye Disease and Disorders of VisionNutritiongenome-wide association study030102 biochemistry & molecular biologywestern blottingMUTATIONSta1184RBP4maternal inheritancemedicine.diseaseRetinol-Binding ProteinsRetinol binding proteinnuclear magnetic resonance030104 developmental biologyEndocrinologychemistryGeneslcsh:Biology (General)microphthalmiaGenetic LociHela Cells1182 Biochemistry cell and molecular biologyCongenital Structural Anomalies3111 BiomedicineBiochemistry and Cell BiologyDigestive DiseasesGenomic imprintingRetinol-Binding Proteins PlasmaHeLa Cells
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Genetic deletion of osteopontin in TRAMP mice skews prostate carcinogenesis from adenocarcinoma to aggressive human-like neuroendocrine cancers

2015

// Giorgio Mauri 1 , Elena Jachetti 1 , Barbara Comuzzi 1 , Matteo Dugo 2 , Ivano Arioli 1 , Silvia Miotti 1 , Sabina Sangaletti 1 , Emma Di Carlo 3, 4 , Claudio Tripodo 5 , Mario P. Colombo 1 1 Molecular Immunology Unit, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale Tumori, 20133, Milano, Italy 2 Functional Genomics and Bioinformatics, Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale Tumori, 20133, Milano, Italy 3 Department of Medicine and Science of Aging, Section of Anatomic Pathology and Molecular Medicine, “G. d’Annunzio” University, 66100, Chieti, Italy 4 Ce.S.I. Aging Research Center, “G…

0301 basic medicineMalePathologyFluorescent Antibody Techniquemedicine.disease_causeImmunoenzyme TechniquesProstate cancerMice0302 clinical medicineOsteopontinProstate cancerbiologyReverse Transcriptase Polymerase Chain ReactionExtracellular matrixNeuroendocrine TumorsCell Transformation NeoplasticNeuroendocrineOncology030220 oncology & carcinogenesisDisease ProgressionAdenocarcinomaTrampResearch Papermedicine.medical_specialtyBlotting WesternMice TransgenicAdenocarcinomaSettore MED/08 - Anatomia PatologicaReal-Time Polymerase Chain Reaction03 medical and health sciencesstomatognathic systemmedicineAnimalsHumansExtracellular matrix; Neuroendocrine; Osteopontin; Prostate cancer; OncologyRNA Messengerbusiness.industryGene Expression ProfilingCancerProstatic Neoplasmsmedicine.diseaseMolecular medicineMice Inbred C57BLDisease Models Animal030104 developmental biologyTumor progressionbiology.proteinOsteopontinCarcinogenesisbusinessGene Deletion
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Expanding the phenotype of reciprocal 1q21.1 deletions and duplications: a case series

2017

Abstract Background Recurrent reciprocal 1q21.1 deletions and duplications have been associated with variable phenotypes. Phenotypic features described in association with 1q21.1 microdeletions include developmental delay, craniofacial dysmorphism and congenital anomalies. The 1q21.1 reciprocal duplication has been associated with macrocephaly or relative macrocephaly, frontal bossing, hypertelorism, developmental delay, intellectual disability and autism spectrum disorder. Methods Our study describes seven patients, who were referred to us for developmental delay/intellectual disability, dysmorphic features and, in some cases, congenital anomalies, in whom we identified 1q21.1 CNVs by arra…

0301 basic medicineMalePediatricsmedicine.medical_specialtyArray-CGHDevelopmental delayTrigonocephaly03 medical and health sciencesFrontal BossingPregnancyPrenatal DiagnosisGene duplicationIntellectual disabilityMedicineHumansAbnormalities MultipleMegalencephalyHypertelorismChild1q21.1 deletionGeneticsbusiness.industryResearchMacrocephalylcsh:RJ1-570Infantlcsh:Pediatricsmedicine.diseaseMegalencephalyDysmorphism030104 developmental biologyPhenotypeAutism spectrum disorderChromosomes Human Pair 1Female1q21.1 duplicationmedicine.symptomChromosome DeletionbusinessItalian Journal of Pediatrics
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9q33.3q34.11 microdeletion: new contiguous gene syndrome encompassing STXBP1, LMX1B and ENG genes assessed using reverse phenotyping

2016

International audience; The increasing use of array-CGH in malformation syndromes with intellectual disability could lead to the description of new contiguous gene syndrome by the analysis of the gene content of the microdeletion and reverse phenotyping. Thanks to a national and international call for collaboration by Achropuce and Decipher, we recruited four patients carrying de novo overlapping deletions of chromosome 9q33.3q34.11, including the STXBP1, the LMX1B and the ENG genes. We restrained the selection to these three genes because the effects of their haploinsufficency are well described in the literature and easily recognizable clinically. All deletions were detected by array-CGH …

0301 basic medicineMale[ SDV.MHEP.PED ] Life Sciences [q-bio]/Human health and pathology/PediatricsHaploinsufficiencycerebral hypomyelinationwest-syndromeBioinformaticsCraniofacial Abnormalities0302 clinical medicineIntellectual disabilitySTXBP1ChildGenetics (clinical)Nail patella syndromeGeneticsEndoglinSyndrome3. Good healthdevelopmental delayPhenotypeintellectual disabilityMedical geneticsFemaleChromosome DeletionHaploinsufficiencyChromosomes Human Pair 9medicine.medical_specialtyAdolescentLIM-Homeodomain ProteinsBiologyContiguous gene syndromeArticle03 medical and health sciencesMunc18 ProteinsGenetic linkageGeneticsmedicineHumansde-novo mutations[SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/PediatricsdiseaseEpilepsyinfantile epileptic encephalopathyassociationdeletionsmedicine.diseaseHuman genetics030104 developmental biologynail-patella syndrome030217 neurology & neurosurgeryTranscription Factors
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Age-related regulation of bone formation by the sympathetic cannabinoid CB1 receptor.

2017

The endocannabinoid (eCB) system, including its receptors, ligands, and their metabolizing enzymes, plays an important role in bone physiology. Skeletal cannabinoid type 1 (CB1) receptor signaling transmits retrograde signals that restrain norepinephrine (NE) release, thus transiently stimulating bone formation following an acute challenge, suggesting a feedback circuit between sympathetic nerve terminals and osteoblasts. To assess the effect of chronic in vivo occurrence of this circuit, we characterized the skeletal phenotype of mice with a conditional deletion of the CB1 receptor in adrenergic/noradrenergic cells, including sympathetic nerves. Whereas the deletion of the CB1 receptor did…

0301 basic medicineMalemedicine.medical_specialtySympathetic nervous systemAgingHistologyCannabinoid receptorSympathetic Nervous SystemPhysiologyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentDopamine beta-HydroxylaseBone resorptionBone remodeling03 medical and health sciencesNorepinephrineNorepinephrineReceptor Cannabinoid CB1OsteogenesisInternal medicinemedicineAnimalsNeuropeptide YBone ResorptionReceptorMice KnockoutChemistryEndocannabinoid systemMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEndocrinologyCannabinoidReceptors Adrenergic beta-2Gene Deletionmedicine.drugEndocannabinoidsBone
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Genetic Polymorphism in Wine Yeasts: Mechanisms and Methods for Its Detection

2017

The processes of yeast selection for using as wine fermentation starters have revealed a great phenotypic diversity both at interspecific and intraspecific level, which is explained by a corresponding genetic variation among different yeast isolates. Thus, the mechanisms involved in promoting these genetic changes are the main engine generating yeast biodiversity. Currently, an important task to understand biodiversity, population structure and evolutionary history of wine yeasts is the study of the molecular mechanisms involved in yeast adaptation to wine fermentation, and on remodeling the genomic features of wine yeast, unconsciously selected since the advent of winemaking. Moreover, the…

0301 basic medicineMicrobiology (medical)lcsh:QR1-502SNPinterspecific hybridizationReviewBiologyAliments MicrobiologiaMicrobiologylcsh:Microbiology03 medical and health sciencesGenetic variationWinemakingGeneticsWineFermentation in winemakingStrain (biology)gene horizontal transferdeletionsfood and beveragesHibridacióYeastYeast in winemaking030104 developmental biologyNGSinsertionsViniculturaPCR-based methodsploidy changesAdaptationFrontiers in Microbiology
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Whole Exome Sequencing Is the Preferred Strategy to Identify the Genetic Defect in Patients With a Probable or Possible Mitochondrial Cause

2018

Mitochondrial disorders, characterized by clinical symptoms and/or OXPHOS deficiencies, are caused by pathogenic variants in mitochondrial genes. However, pathogenic variants in some of these genes can lead to clinical manifestations which overlap with other neuromuscular diseases, which can be caused by pathogenic variants in non-mitochondrial genes as well. Mitochondrial pathogenic variants can be found in the mitochondrial DNA (mtDNA) or in any of the 1,500 nuclear genes with a mitochondrial function. We have performed a two-step next-generation sequencing approach in a cohort of 117 patients, mostly children, in whom a mitochondrial disease-cause could likely or possibly explain the phe…

0301 basic medicineMitochondrial DNANuclear genelcsh:QH426-470DISORDERSMitochondrial diseaseBiologyMOLECULAR DIAGNOSISMtDNA sequencingDNA sequencingDISEASEDiagnostic yield03 medical and health sciencesmedicineGeneticsDNA DELETIONSGenetics(clinical)whole-exome sequencingTRANSFER-RNA-SYNTHETASELACTIC-ACIDOSISGeneGenetics (clinical)Exome sequencingOriginal ResearchGeneticsmtDNA sequencingGenetic heterogeneityMUTATIONSASSEMBLY FACTORSmedicine.diseasePhenotypeMitochondrial diseaselcsh:Geneticsmitochondrial disease030104 developmental biologyHUMAN COMPLEX-IWhole-exome sequencingdiagnostic yieldNext-generation sequencingMolecular Medicinenext-generation sequencingLEIGH-SYNDROMEFrontiers in Genetics
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Different rates of spontaneous mutation of chloroplastic and nuclear viroids as determined by high-fidelity ultra-deep sequencing

2017

[EN] Mutation rates vary by orders of magnitude across biological systems, being higher for simpler genomes. The simplest known genomes correspond to viroids, subviral plant replicons constituted by circular non-coding RNAs of few hundred bases. Previous work has revealed an extremely high mutation rate for chrysanthemum chlorotic mottle viroid, a chloroplastreplicating viroid. However, whether this is a general feature of viroids remains unclear. Here, we have used high-fidelity ultra-deep sequencing to determine the mutation rate in a common host (eggplant) of two viroids, each representative of one family: the chloroplastic eggplant latent viroid (ELVd, Avsunviroidae) and the nuclear pot…

0301 basic medicineMutation rateChloroplastsViroidvirusesPospiviroidaeArtificial Gene Amplification and ExtensionPlant ScienceSelf-CleavageVirus ReplicationBiochemistryPolymerase Chain ReactionGenomeDatabase and Informatics MethodsSequencing techniquesRibozymeNucleic AcidsRibozymesBiology (General)GeneticsHigh-Throughput Nucleotide Sequencingfood and beveragesRNA sequencingViroidsEnzymesAvsunviroidaeDeletion MutationVirusesPhysical SciencesRNA ViralIn-VivoSequence AnalysisResearch ArticleSubstitution MutationHammerhead RibozymesQH301-705.5Materials by StructureBioinformaticsEvolutionMaterials ScienceImmunologyPlant PathogensGenerationReplicationBiologyMicrobiology03 medical and health sciencesSequence Motif AnalysisVirologyGeneticsSolanum melongenaRNA-PolymeraseMolecular BiologyPotato spindle tuber viroidPlant DiseasesMatter030102 biochemistry & molecular biologyPoint mutationOrganismsBiology and Life SciencesProteinsRNAReverse Transcriptase-Polymerase Chain ReactionRC581-607Plant Pathologybiology.organism_classificationVirologyResearch and analysis methodsMolecular biology techniques030104 developmental biologyMutagenesisOligomersMutationEnzymologyRNAMotifParasitologyImmunologic diseases. AllergyPLOS Pathogens
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