Search results for "genetics [Transcriptome]"

showing 10 items of 3033 documents

Myeloid leukemia with transdifferentiation plasticity developing from T-cell progenitors

2016

Unfavorable patient survival coincides with lineage plasticity observed in human acute leukemias. These cases are assumed to arise from hematopoietic stem cells, which have stable multipotent differentiation potential. However, here we report that plasticity in leukemia can result from instable lineage identity states inherited from differentiating progenitor cells. Using mice with enhanced c-Myc expression, we show, at the single-cell level, that T-lymphoid progenitors retain broad malignant lineage potential with a high capacity to differentiate into myeloid leukemia. These T-cell-derived myeloid blasts retain expression of a defined set of T-cell transcription factors, creating a lymphoi…

0301 basic medicineMyeloidBone Marrow CellsBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceshemic and lymphatic diseasesmedicineCell LineageProgenitor cellMolecular BiologyGeneral Immunology and MicrobiologyGeneral NeuroscienceTransdifferentiationMyeloid leukemiaCell DifferentiationArticlesmedicine.diseaseHematopoietic Stem CellsHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureImmunologyCancer researchLymphoid Progenitor CellsStem cell
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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An imbalance between specialized pro-resolving lipid mediators and pro-inflammatory leukotrienes promotes instability of atherosclerotic plaques

2016

Chronic unresolved inflammation plays a causal role in the development of advanced atherosclerosis, but the mechanisms that prevent resolution in atherosclerosis remain unclear. Here, we use targeted mass spectrometry to identify specialized pro-resolving lipid mediators (SPM) in histologically-defined stable and vulnerable regions of human carotid atherosclerotic plaques. The levels of SPMs, particularly resolvin D1 (RvD1), and the ratio of SPMs to pro-inflammatory leukotriene B4 (LTB4), are significantly decreased in the vulnerable regions. SPMs are also decreased in advanced plaques of fat-fed Ldlr−/− mice. Administration of RvD1 to these mice during plaque progression restores the RvD1:…

0301 basic medicineNecrosisLeukotriene B4ScienceGeneral Physics and AstronomyInflammationmedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compoundAtherosclerosis--EtiologymedicineCarotid artery--DiseasesEfferocytosisInflammationAtherosclerotic plaqueMultidisciplinarybusiness.industryQGeneral ChemistryLipid signalingAtherosclerosisResolvin d1030104 developmental biologyTargeted mass spectrometrychemistryCancer researchMedicinemedicine.symptombusinessOxidative stressNature Communications
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NFATc1 supports imiquimod-induced skin inflammation by suppressing IL-10 synthesis in B cells

2016

Epicutaneous application of Aldara cream containing the TLR7 agonist imiquimod (IMQ) to mice induces skin inflammation that exhibits many aspects of psoriasis, an inflammatory human skin disease. Here we show that mice depleted of B cells or bearing interleukin (IL)-10-deficient B cells show a fulminant inflammation upon IMQ exposure, whereas ablation of NFATc1 in B cells results in a suppression of Aldara-induced inflammation. In vitro, IMQ induces the proliferation and IL-10 expression by B cells that is blocked by BCR signals inducing NFATc1. By binding to HDAC1, a transcriptional repressor, and to an intronic site of the Il10 gene, NFATc1 suppresses IL-10 expression that dampens the pro…

0301 basic medicineNecrosisScienceGeneral Physics and AstronomyInflammationHuman skinImiquimodBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesPsoriasismedicineddc:610Multidisciplinaryintegumentary systemQInterleukinGeneral ChemistryTLR7medicine.diseaseInterleukin 10030104 developmental biologyImmunologyCancer researchmedicine.symptommedicine.drugNature Communications
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Anisakis sensitization in different population groups and public health impact. A systematic review

2018

Anisakis simplex spp. sensitization rates have increased worldwide, with a significant impact on health-care systems. To date, no clear-cut diagnostic criteria and laboratory algorithm have been established, so anisakiasis still represents an under-reported health problem whose clinical manifestations, when present, mimic the much more common allergic and digestive disorders. Aim of the study was to systematically review the available literature on the prevalence of sensitization against Anisakis in the general population and in specific population groups, taking into account the impact of the different available diagnostic techniques on the epidemiological data. Following the Preferred Rep…

0301 basic medicineNematodaUrticarialcsh:MedicineSettore MED/42 - Igiene Generale E ApplicataAnisakisGeographical locations0302 clinical medicineAllergiesEpidemiologyMedicine and Health SciencesantibodiesEnzyme-Linked Immunoassayslcsh:SciencehumanshelminthSensitizationeducation.field_of_studyMultidisciplinaryAllergic DiseasesbiologyShellfish allergyEukaryotaanimals; anisakis; antibodies helminth; enzyme-linked immunosorbent assay; humans; hypersensitivity; occupational exposureClinical Laboratory SciencesEuropeanimalsClinical Laboratoriesmedicine.anatomical_structureSystematic reviewhypersensitivityResearch Articlemedicine.medical_specialtyImmunologyImmunoblotting030231 tropical medicinePopulationFood AllergiesAntibodies HelminthMolecular Probe TechniquesDermatologyResearch and Analysis Methods03 medical and health sciencesDiagnostic MedicineEnvironmental healthmedicineEuropean UnionImmunoassaysMolecular Biology TechniqueseducationMolecular BiologyBiochemistry Genetics and Molecular Biology (all)business.industryPublic healthlcsh:RAnisakis simplexOrganismsBiology and Life Sciencesoccupational exposureanisakismedicine.diseasebiology.organism_classificationInvertebrates030104 developmental biologyAgricultural and Biological Sciences (all)SpainImmunologic TechniquesClinical Immunologylcsh:Qenzyme-linked immunosorbent assayClinical MedicinePeople and placesbusiness
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Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function

2016

Reduced glomerular filtration rate defines chronic kidney disease and is associated with cardiovascular and all-cause mortality. We conducted a meta-analysis of genome-wide association studies for estimated glomerular filtration rate (eGFR), combining data across 133,413 individuals with replication in up to 42,166 individuals. We identify 24 new and confirm 29 previously identified loci. Of these 53 loci, 19 associate with eGFR among individuals with diabetes. Using bioinformatics, we show that identified genes at eGFR loci are enriched for expression in kidney tissues and in pathways relevant for kidney development and transmembrane transporter activity, kidney structure, and regulation o…

0301 basic medicineNephrologyGenetics and Molecular Biology (all)estimated glomerular filtration rateestimated glomerular filtration rate chronic kidney disease genetic determinantsGeneral Physics and AstronomyKidney developmentGenome-wide association studyBiochemistrySettore MED/14 - NEFROLOGIARenal InsufficiencyChronicGeneticsAGEN Consortiumddc:616education.field_of_studyKidneyStage renal-diseaseMultidisciplinaryGenome-wide associationCHARGe-Heart Failure GroupGene Expression Regulation; Genome-Wide Association Study; Genotype; Humans; Renal Insufficiency Chronic; Genetic Predisposition to Disease; Biochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)QChemistry (all)MetaanalysisGene Expression Regulation; Genetic Predisposition to Disease; Genome-Wide Association Study; Genotype; Humans; Renal Insufficiency Chronic/geneticsBiological sciencesSerum creatininemedicine.anatomical_structureEfficientRonyons -- FisiologiaHypertensionICBP ConsortiumTransmembrane transporter activitygenetic association loci kidney functionCARDIOGRAMHumanmedicine.medical_specialtyGenotypeSciencePopulationRenal functionECHOGen ConsortiumReplicationBiologyEnvironmentResearch SupportGeneral Biochemistry Genetics and Molecular BiologyN.I.H.genetic determinants03 medical and health sciencesPhysics and Astronomy (all)GENOME-WIDE ASSOCIATION ; FALSE DISCOVERY RATES ; STAGE RENAL-DISEASE ; SERUM CREATININE ; METAANALYSIS ; VARIANTS ; INDIVIDUALS ; POPULATION ; RISK ; HYPERTENSIONKidney functionResearch Support N.I.H. ExtramuralInternal medicineMD MultidisciplinarymedicineGeneticsJournal ArticleHumanseGFRcrea; eGFRcysGenetic Predisposition to Diseaseddc:610GenetikRenal Insufficiency ChronicMortalityeducationddc:613Biochemistry Genetics and Molecular Biology (all)urogenital systemIndividualsExtramuralGeneral Chemistryta3121medicine.diseaseR1030104 developmental biologyGene Expression RegulationBiochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)570 Life sciences; biologyGenèticachronic kidney diseaseKidney diseaseGenome-Wide Association StudyMeta-Analysis
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Genetic regulation and function of epidermal growth factor receptor signalling in patterning of the embryonicDrosophilabrain

2016

The specification of distinct neural cell types in central nervous system development crucially depends on positional cues conferred to neural stem cells in the neuroectoderm. Here, we investigate the regulation and function of the epidermal growth factor receptor (EGFR) signalling pathway in early development of theDrosophilabrain. We find that localized EGFR signalling in the brain neuroectoderm relies on a neuromere-specific deployment of activating (Spitz, Vein) and inhibiting (Argos) ligands. Activated EGFR controls the spatially restricted expression of all dorsoventral (DV) patterning genes in a gene- and neuromere-specific manner. Further, we reveal a novel role of DV genes—ventral …

0301 basic medicineNervous system197brain neuroblastsrhomboidBasic Helix-Loop-Helix Transcription FactorsDrosophila ProteinsEpidermal growth factor receptorPhosphorylationlcsh:QH301-705.5NeuregulinsNeural PlateGeneral NeuroscienceNeurogenesisBrainGene Expression Regulation DevelopmentalNuclear ProteinsAnatomyargosNeural stem cellHedgehog signaling pathwayCell biologyErbB ReceptorsDrosophila melanogastermedicine.anatomical_structureResearch ArticleSignal Transduction1001NeurogenesisImmunologyNerve Tissue ProteinsBiology133General Biochemistry Genetics and Molecular Biology03 medical and health sciencesNeuroblastveindorsoventral patterning genesmedicineAnimalsEye ProteinsReceptors Invertebrate PeptideBody PatterningHomeodomain ProteinsEpidermal Growth FactorNeuroectodermResearchMembrane Proteins58Embryonic stem cell030104 developmental biologylcsh:Biology (General)biology.proteinepidermal growth factor receptorTranscription FactorsOpen Biology
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction

2016

Myelination of axons facilitates rapid impulse propagation in the nervous system. The axon/myelin-unit becomes impaired in myelin-related disorders and upon normal aging. However, the molecular cause of many pathological features, including the frequently observed myelin outfoldings, remained unknown. Using label-free quantitative proteomics, we find that the presence of myelin outfoldings correlates with a loss of cytoskeletal septins in myelin. Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that extend longitudinally along myelinated axons. By confoca…

0301 basic medicineNervous systemCentral Nervous SystemProteomicsScaffoldMouseProteomeNeural ConductionSeptinNerve Fibers MyelinatedMyelinGene Knockout TechniquesMiceContractile ProteinsAxonBiology (General)CytoskeletonMicroscopy ImmunoelectronCytoskeletonMyelin SheathMicroscopy ConfocalGeneral NeuroscienceQRGeneral MedicineAnatomyCell biologyglial cellsmedicine.anatomical_structureGene TargetingMedicineResearch ArticleQH301-705.5ScienceCentral nervous systemmyelinated axonsmacromolecular substancesBiologyGeneral Biochemistry Genetics and Molecular Biologymyelin structure03 medical and health sciencesSeptin/anillin filaments; central nervous system; myelinlabel-free proteomicsmedicineAnimalsneuropathologyGeneral Immunology and Microbiology030104 developmental biologynervous systemseptin cytoskeletonProtein MultimerizationSeptinsSeptin cytoskeletonNeuroscienceeLife
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Engineering of Adult Neurogenesis and Gliogenesis

2016

Neural stem/progenitor cells (NSPCs) retain their ability to generate newborn neurons throughout life in the mammalian brain. Here, we describe how recently developed virus- and transgenesis-based techniques will help us (1) to understand the functional effects of neurogenesis in health and disease, (2) to design novel approaches to harness the potential for NSPC-associated endogenous repair, and (3) to induce the generation of neurons outside the main neurogenic niches in the adult brain.

0301 basic medicineNeurogenesisCellular differentiationPhysiology610 Medicine & healthBiologyGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciencesNeural Stem Cells1300 General Biochemistry Genetics and Molecular BiologyAnimalsHumansProgenitor cellCell ProliferationGliogenesis10242 Brain Research InstituteNeurogenesisBrainCell DifferentiationMammalian brainTechniquesNeural stem cell030104 developmental biology570 Life sciences; biologyNeuroscience
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