Search results for " deletion"

showing 10 items of 361 documents

Tetraspanin CD151 Promotes Initial Events in Human Cytomegalovirus Infection.

2016

ABSTRACT Human cytomegalovirus (HCMV), a betaherpesvirus, can cause life-threatening disease in immunocompromised individuals. Viral envelope glycoproteins that mediate binding to and penetration into target cells have been identified previously. In contrast, cellular proteins supporting HCMV during entry are largely unknown. In order to systematically identify host genes affecting initial steps of HCMV infection, a targeted RNA interference screen of 96 cellular genes was performed in endothelial cells by use of a virus strain expressing the full set of known glycoprotein H and L (gH/gL) complexes. The approach yielded five proviral host factors from different protein families and eight an…

0301 basic medicineHuman cytomegalovirusvirusesImmunologyCytomegalovirusBiologyTetraspanin 24MicrobiologyVirus03 medical and health sciencesViral envelopeTetraspaninViral Envelope ProteinsRNA interferenceVirologymedicineHuman Umbilical Vein Endothelial CellsHumansRNA Small InterferingTropismCells CulturedHost factorchemistry.chemical_classificationFibroblastsVirus Internalizationmedicine.diseaseVirologyVirus-Cell Interactions030104 developmental biologychemistryInsect ScienceRNA InterferenceGlycoproteinGene DeletionJournal of virology
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Oligodendrocytes control potassium accumulation in white matter and seizure susceptibility

2018

Oligodendrocytes Control Potassium Accumulation in White Matter and Seizure Susceptibility.Larson VA, Mironova Y, Vanderpool KG, Waisman A, Rash JE, Agarwal A, Bergles DE. Elife. 2018 Mar 29;7. pii: e34829. doi: 10.7554/eLife.34829.The inwardly rectifying K+ channel Kir4.1 is broadly expressed by central nervous system glia and deficits in Kir4.1 lead to seizures and myelin vacuolization. However, the role of oligodendrocyte Kir4.1 channels in controlling myelination and K+ clearance in white matter has not been defined. Here, we show that selective deletion of Kir4.1 from oligodendrocyte progenitors or mature oligodendrocytes did not impair their development or disrupt the structure of mye…

0301 basic medicineKir4.1QH301-705.5seizureScienceMice TransgenicGeneral Biochemistry Genetics and Molecular BiologyWhite matterMice03 medical and health sciencesEpilepsyMyelin0302 clinical medicineSeizuresmedicineExtracellularAnimalsHomeostasisBiology (General)Potassium Channels Inwardly RectifyingProgenitor cellMyelin SheathMice KnockoutGeneral Immunology and MicrobiologyChemistryGeneral NeuroscienceQRGeneral Medicinemedicine.diseaseWhite MatterCurrent Literature in Basic ScienceOligodendrocyteCell biologymyelinOligodendroglia030104 developmental biologymedicine.anatomical_structureVacuolizationPotassiumepilepsyMedicineoligodendrocyteGene Deletion030217 neurology & neurosurgeryHomeostasiseLife
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Intratumoral immunosuppression profiles in 11q-deleted neuroblastomas provide new potential therapeutic targets

2021

In this issue, Coronado et al. attempt to improve our understanding of the factors affecting the response to immunotherapy in a large subset of high‐risk neuroblastoma with hemizygous deletion of chromosome 11q. By using several computational approaches, the authors study potential transcriptional and post‐transcriptional pathways that may affect the response to immunotherapy and further be leveraged therapeutically in a biomarker‐directed fashion.

0301 basic medicineMaleCancer Researchmedicine.medical_treatmentRetinoic acidchemistry.chemical_compoundNeuroblastoma0302 clinical medicineTumor Microenvironment11q deletion anti-GD2 immunotherapy combination immunotherapy immune cell infiltration miRNAs neuroblastomaMedicineeducation.field_of_studyimmune cell infiltration11q deletionImmunosuppressionGeneral Medicinelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPatologiaNeoplasm ProteinsmicroRNAsSurvival Rateanti‐GD2 therapyOncology030220 oncology & carcinogenesiscombination immunotherapymiRNAsMolecular Medicineimmune checkpoint inhibitionFemaleImmunotherapyChromosome Deletionanti‐GD2 immunotherapyPopulationlcsh:RC254-282Disease-Free Survival03 medical and health sciencesImmune systemNeuroblastomaGeneticsImmune ToleranceHumanseducationRetrospective Studiesbusiness.industryChromosomes Human Pair 11Immunotherapymedicine.diseaseImmune checkpointBlockade030104 developmental biologychemistryCancer researchCommentarybusiness
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Heterozygous deletion of the LRFN2 gene is associated with working memory deficits

2016

International audience; Learning disabilities (LDs) are a clinically and genetically heterogeneous group of diseases. Array-CGH and high-throughput sequencing have dramatically expanded the number of genes implicated in isolated intellectual disabilities and LDs, highlighting the implication of neuron-specific post-mitotic transcription factors and synaptic proteins as candidate genes. We report a unique family diagnosed with autosomal dominant learning disability and a 6p21 microdeletion segregating in three patients. The 870 kb microdeletion encompassed the brain-expressed gene LRFN2, which encodes for a synaptic cell adhesion molecule. Neuropsychological assessment identified selective w…

0301 basic medicineMaleCandidate genefamilyspeechHippocampal formationRats Sprague-Dawley0302 clinical medicineBorderline intellectual functioningNeuropsychological assessmentChilddisordersGenetics (clinical)Cells Culturedadhesion-like moleculesMembrane Glycoproteinsmedicine.diagnostic_testLearning DisabilitiesBrainMagnetic Resonance Imaging3. Good healthPedigreeMemory Short-TermBrain sizeFemaleAdultHeterozygotenmda receptorautismNerve Tissue ProteinsBiologyReceptors N-Methyl-D-AspartateArticle03 medical and health sciencesFluorodeoxyglucose F18[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyexpressionGeneticsmedicineAnimalsHumansMemory DisorderslanguageGenetic heterogeneityWorking memoryMembrane Proteinsdown-syndromeRats030104 developmental biologyEndophenotypePositron-Emission TomographySynapsesshort-termRadiopharmaceuticalsNeuroscience030217 neurology & neurosurgeryGene Deletion[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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12q14.3 microdeletion involving HMGA2 gene cause a Silver-Russell syndrome-like phenotype: a case report and review of the literature

2020

Abstract Background Silver-Russell Syndrome (SRS) is a genetic disorder characterized by intrauterine and postnatal growth restriction and normal head circumference with consequent relative macrocephaly. Addictional findings are protruding forehead in early life, body asymmetry (of upper and lower limbs) and substantial feeding difficulties. Although several genetic mechanisms that cause the syndrome are known, more than 40% of patients with a SRS-like phenotype remain without an etiological diagnosis. In the last few years, different clinical reports have suggested that mutations or deletions of the HMGA2 gene can be responsible for a SRS-like phenotype in patients with negative results of…

0301 basic medicineMaleCase Report030105 genetics & heredityBioinformaticsHMGA2 gene03 medical and health sciencesHMGA2parasitic diseasesmedicineHumansGeneChromosome 12biologybusiness.industrySilver–Russell syndromeNetchine-Harbison clinical scoring systemHMGA2 Proteinlcsh:RJ1-570Genetic disorderlcsh:PediatricsFailure to thrivemedicine.diseasePhenotypeSilver-Russell Syndrome030104 developmental biologyPhenotypeSettore MED/03 - Genetica MedicaChild PreschoolFailure to thriveEtiologybiology.proteinmedicine.symptombusinessGene DeletionItalian Journal of Pediatrics
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Endothelial Dab1 signaling orchestrates neuro-glia-vessel communication in the central nervous system.

2018

Developing the bloodbrain barrier During development, signals need to be dynamically integrated by endothelial cells, neurons, and glia to achieve functional neuro-glia-vascular units in the central nervous system. During cortical development, neuronal Dab1 and ApoER2 receptors respond to a guidance cue called reelin. Studying mice, Segarra et al. found that Dab1 and ApoER2 are also expressed in endothelial cells (see the Perspective by Thomas). The integration of reelin signaling in endothelial cells and neurons facilitates the communication between vessels, glia, and neurons that is necessary for the correct positioning of neurons during cortical development. This integration is also impo…

0301 basic medicineMaleCell signalingLow-density lipoprotein receptor-related protein 8EndotheliumCell Adhesion Molecules NeuronalCentral nervous systemNeovascularization PhysiologicNerve Tissue ProteinsCell Communication03 medical and health sciencesMiceCell MovementmedicineAnimalsReelinLDL-Receptor Related ProteinsCerebral CortexMice KnockoutNeuronsRetinaExtracellular Matrix ProteinsMultidisciplinarybiologyIntegrin beta1Serine EndopeptidasesRetinal VesselsDAB1Reelin Protein030104 developmental biologymedicine.anatomical_structurenervous systemCerebral cortexBlood-Brain Barrierbiology.proteinFemaleEndothelium VascularLamininNeuroscienceNeurogliaGene DeletionSignal TransductionScience (New York, N.Y.)
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Functional hypoxia drives neuroplasticity and neurogenesis via brain erythropoietin.

2020

Erythropoietin (EPO), named after its role in hematopoiesis, is also expressed in mammalian brain. In clinical settings, recombinant EPO treatment has revealed a remarkable improvement of cognition, but underlying mechanisms have remained obscure. Here, we show with a novel line of reporter mice that cognitive challenge induces local/endogenous hypoxia in hippocampal pyramidal neurons, hence enhancing expression of EPO and EPO receptor (EPOR). High-dose EPO administration, amplifying auto/paracrine EPO/EPOR signaling, prompts the emergence of new CA1 neurons and enhanced dendritic spine densities. Single-cell sequencing reveals rapid increase in newly differentiating neurons. Importantly, i…

0301 basic medicineMaleDendritic spineGeneral Physics and AstronomyHippocampal formationVARIANTSADULT NEUROGENESIS0302 clinical medicineCognitionhemic and lymphatic diseasesReceptors ErythropoietinHypoxialcsh:ScienceNEURONSMultidisciplinaryNeuronal PlasticityPyramidal CellsNeurogenesisQBrainCell DifferentiationHEMATOPOIETIC PROGENITOR CELLSFemalemedicine.symptomProto-Oncogene Proteins c-fosmedicine.drugEXPRESSIONScienceDendritic SpinesNeurogenesisModels NeurologicalBiologyMotor ActivityGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesParacrine signallingPhysical Conditioning AnimalNeuroplasticitymedicineAnimalsHumansErythropoietinMEMORYCognitive neuroscienceGeneral ChemistryHypoxia (medical)RECOMBINANT-HUMAN-ERYTHROPOIETINCellular neuroscienceErythropoietin receptorMice Inbred C57BLMICE030104 developmental biologyErythropoietinPhysical EnduranceIDENTITYlcsh:QTranscriptomeNeuroscience030217 neurology & neurosurgeryGene Deletion
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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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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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