Search results for "Regulatory"

showing 10 items of 740 documents

Longevity-related molecular pathways are subject to midlife “switch” in humans

2019

Emerging evidence indicates that molecular aging may follow nonlinear or discontinuous trajectories. Whether this occurs in human neuromuscular tissue, particularly for the noncoding transcriptome, and independent of metabolic and aerobic capacities, is unknown. Applying our novel RNA method to quantify tissue coding and long noncoding RNA (lncRNA), we identified ~800 transcripts tracking with age up to ~60 years in human muscle and brain. In silico analysis demonstrated that this temporary linear “signature” was regulated by drugs, which reduce mortality or extend life span in model organisms, including 24 inhibitors of the IGF‐1/PI3K/mTOR pathway that mimicked, and 5 activators that oppos…

0301 basic medicineAgingved/biology.organism_classification_rank.speciesMuscle Fibers SkeletallihaksetTranscriptome0302 clinical medicineGene expressionGene Regulatory NetworksRNA-Seqmedia_commonCerebral CortexNeuronsreactive oxygen speciesihoTOR Serine-Threonine Kinasesmitochondrial complex 1LongevityBrainNon-coding RNAAlzheimer'sECSITCell biologytranskriptio (biologia)mTORRNA Long NoncodingOriginal ArticleaivotSignal TransductionAdultTranscriptional ActivationskinIn silicomedia_common.quotation_subjectLongevityBiology03 medical and health sciencesHumanslong noncoding RNAskeletal muscleModel organismGeneSirolimusved/biologyagingRNACell BiologyTwins MonozygoticOriginal Articles030104 developmental biologyikääntyminenRNATranscriptome030217 neurology & neurosurgery
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Distinctive Histogenesis and Immunological Microenvironment Based on Transcriptional Profiles of Follicular Dendritic Cell Sarcomas

2017

Abstract Follicular dendritic cell (FDC) sarcomas are rare mesenchymal tumors with variable clinical, morphologic, and phenotypic characteristics. Transcriptome analysis was performed on multiple FDC sarcomas and compared with other mesenchymal tumors, microdissected Castleman FDCs, and normal fibroblasts. Using unsupervised analysis, FDC sarcomas clustered with microdissected FDCs, distinct from other mesenchymal tumors and fibroblasts. The specific endowment of FDC-related gene expression programs in FDC sarcomas emerged by applying a gene signature of differentially expressed genes (n = 1,289) between microdissected FDCs and fibroblasts. Supervised analysis comparing FDC sarcomas with mi…

0301 basic medicineAlgorithms; B7-H1 Antigen; Castleman Disease; Chromatin; Cluster Analysis; Dendritic Cell Sarcoma Follicular; Gene Expression Profiling; Gene Expression Regulation Neoplastic; Humans; Programmed Cell Death 1 Ligand 2 Protein; Programmed Cell Death 1 Receptor; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Up-Regulation; Gene Regulatory Networks; Molecular Biology; Oncology; Cancer ResearchCancer ResearchProgrammed Cell Death 1 ReceptorDendritic Cell Sarcoma FollicularBiologyT-Lymphocytes RegulatoryB7-H1 AntigenTranscriptome03 medical and health sciencesmedicineCluster AnalysisHumansGene Regulatory NetworksMolecular BiologyRegulation of gene expressionCluster AnalysiGene Regulatory NetworkFollicular dendritic cellsCastleman DiseaseGene Expression ProfilingMesenchymal stem cellT-Lymphocytes Helper-InducerProgrammed Cell Death 1 Ligand 2 Proteinmedicine.diseaseChromatinUp-RegulationAlgorithmGene Expression Regulation NeoplasticGene expression profiling030104 developmental biologyOncologyCancer researchImmunohistochemistrySarcomaAlgorithmsHumanSignal TransductionExtracellular matrix organizationMolecular Cancer Research
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Mechanisms of the Development of Allergy (MeDALL) : Introducing novel concepts in allergy phenotypes

2017

Asthma, rhinitis, and eczema are complex diseases with multiple genetic and environmental factors interlinked through IgE-associated and non–IgE-associated mechanisms. Mechanisms of the Development of ALLergy (MeDALL; EU FP7-CP-IP; project no: 261357; 2010-2015) studied the complex links of allergic diseases at the clinical and mechanistic levels by linking epidemiologic, clinical, and mechanistic research, including in vivo and in vitro models. MeDALL integrated 14 European birth cohorts, including 44,010 participants and 160 cohort follow-ups between pregnancy and age 20 years. Thirteen thousand children were prospectively followed after puberty by using a newly standardized MeDALL Core Q…

0301 basic medicineAllergyGenome-wide association studyComorbidityImmunoglobulin Emedicine.disease_causeCohort StudiesTranslational Research Biomedical0302 clinical medicineAllergenREGULATORY B-CELLSPRECISION MEDICINEMedicineBIRTH COHORT INFANTSATOPIC-DERMATITISImmunology and Allergy[SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/AllergologyChildmedia_commonbiologyatopic dermatitisAtopic dermatitis3. Good healthEuropeMulticenter StudyCHRONIC RESPIRATORY-DISEASESrhinitiPhenotypeINNER-CITY CHILDRENBiomarker (medicine)Femaleatopic dermatitiAdolescentEUROPEAN INNOVATION PARTNERSHIPImmunologyreview03 medical and health sciencesEARLY-LIFEYoung AdultrhinitisAllergy ; Asthma ; Atopic Dermatitis ; RhinitisHypersensitivityJournal Articlemedia_common.cataloged_instanceAnimalsHumansEuropean unionAsthmaMOUNTAIN CEDAR POLLINOSISbusiness.industryGene Expression ProfilingCHILDHOOD ASTHMAAllergensImmunoglobulin Emedicine.diseaseallergyAsthma030104 developmental biology030228 respiratory systemImmunologybiology.proteinImmunizationbusinessGenome-Wide Association StudyJournal of Allergy and Clinical Immunology
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Peripheral artery disease, redox signaling, oxidative stress – Basic and clinical aspects

2017

Reactive oxygen and nitrogen species (ROS and RNS, e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. At higher concentrations, ROS and RNS lead to oxidative stress and oxidative damage of biomolecules (e.g. via formation of peroxynitrite, fenton chemistry). Peripheral artery disease (PAD) is characterized by severe ischemic conditions in the periphery leading to intermittent claudication and critical limb ischemia (end stage). It is well known that redox biology and oxidative stress play an important role in this setting. We here discuss the major pathways of oxidative stress and re…

0301 basic medicineAntioxidantRedox signalingmedicine.medical_treatmentCellular differentiationClinical BiochemistryReview Article030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeBiochemistrychemistry.chemical_compound0302 clinical medicineGene Regulatory Networks610 Medicine & healthlcsh:QH301-705.5chemistry.chemical_classificationlcsh:R5-920Anticholesteremic AgentsReactive Nitrogen Speciesmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionPeroxynitriteSignal Transductionmedicine.medical_specialtyCell signalingAntioxidant therapy610 Medicine & healthNitric oxide03 medical and health sciencesPeripheral Arterial DiseasemedicineHumansExerciseReactive oxygen speciesbusiness.industryOrganic ChemistryClaudication and critical limb ischemiaWalking distanceIntermittent claudicationSurgeryOxidative Stress030104 developmental biologychemistrylcsh:Biology (General)Peripheral artery (occlusive) diseasebusinessReactive Oxygen SpeciesOxidative stressRedox Biology
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Disruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in mice

2019

The CC chemokine 1 (CCL1, also called I-309 or TCA3) is a potent chemoattractant for leukocytes that plays an important role in inflammatory processes and diseases through binding to its receptor CCR8. Here, we investigated the role of the CCL1-CCR8 axis in atherosclerosis. We found increased expression of CCL1 in the aortas of atherosclerosis-prone fat-fed apolipoprotein E (Apoe)-null mice; moreover, in vitro flow chamber assays and in vivo intravital microscopy demonstrated an essential role for CCL1 in leukocyte recruitment. Mice doubly deficient for CCL1 and Apoe exhibited enhanced atherosclerosis in aorta, which was associated with reduced plasma levels of the anti-inflammatory interle…

0301 basic medicineApolipoprotein Emedicine.medical_specialtyRegulatory T cellCCL1030204 cardiovascular system & hematologyCCR8T-Lymphocytes RegulatoryReceptors CCR8Chemokine CCL1Mice03 medical and health sciencesApolipoproteins ETh2 Cells0302 clinical medicineInternal medicineLeukocytesmedicineSplenocyteAnimalsMolecular BiologyInflammationMice KnockoutChemistryTh1 CellsAtherosclerosisInterleukin-10Mice Inbred C57BLTregInterleukin 10030104 developmental biologyEndocrinologymedicine.anatomical_structureIL-10CytokinesCardiology and Cardiovascular MedicineCCR8Intravital microscopyCCL1LipoproteinJournal of Molecular and Cellular Cardiology
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The European regulatory environment of rna-based vaccines

2016

A variety of different mRNA-based drugs are currently in development. This became possible, since major breakthroughs in RNA research during the last decades allowed impressive improvements of translation, stability and delivery of mRNA. This article focuses on antigen-encoding RNA-based vaccines that are either directed against tumors or pathogens. mRNA-encoded vaccines are developed both for preventive or therapeutic purposes. Most mRNA-based vaccines are directly administered to patients. Alternatively, primary autologous cells from cancer patients are modified ex vivo by the use of mRNA and then are adoptively transferred to patients. In the EU no regulatory guidelines presently exist t…

0301 basic medicineAutologous cellMessenger RNAVaccinesAnticancer vaccinationGenetically modified medicinal productsbusiness.industryGenetic enhancementmRNARNAGenetic therapy03 medical and health sciences030104 developmental biology0302 clinical medicineAntigenPreventive and therapeutic approachesInfectious disease (medical specialty)030220 oncology & carcinogenesisAdvanced therapy medicinal products (ATMP)ImmunologyMedicineVaccination against infectious diseasebusinessRegulatory framework in the EUEx vivo
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Progranulin overexpression in sensory neurons attenuates neuropathic pain in mice: Role of autophagy

2016

Peripheral or central nerve injury is a frequent cause of chronic pain and the mechanisms are not fully understood. Using newly generated transgenic mice we show that progranulin overexpression in sensory neurons attenuates neuropathic pain after sciatic nerve injury and accelerates nerve healing. A yeast-2-hybrid screen revealed putative interactions of progranulin with autophagy-related proteins, ATG12 and ATG4b. This was supported by colocalization and proteomic studies showing regulations of ATG13 and ATG4b and other members of the autophagy network, lysosomal proteins and proteins involved in endocytosis. The association of progranulin with the autophagic pathway was functionally confi…

0301 basic medicineAutophagy-Related ProteinsMiceProgranulinsGanglia SpinalDorsal root gangliaGranulinsPain MeasurementCD11b AntigenMicrofilament ProteinsChronic painSciatic nerve injuryCysteine Endopeptidasesmedicine.anatomical_structureNociceptionNeurologyNeuropathic painIntercellular Signaling Peptides and Proteinsmedicine.symptomMicrotubule-Associated ProteinsNerve injuryProgranulinSensory Receptor CellsGreen Fluorescent ProteinsPainMice Transgeniclcsh:RC321-571ATG1203 medical and health sciencesLysosomal-Associated Membrane Protein 1mental disordersmedicineAutophagyAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryActivating Transcription Factor 3Sensory neuronbusiness.industryAutophagyCalcium-Binding ProteinsNerve injurymedicine.diseaseSensory neuronMice Inbred C57BLDisease Models Animal030104 developmental biologyGene OntologyNeuralgiabusinessApoptosis Regulatory ProteinsNeuroscienceNeurobiology of Disease
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Dynamics and predicted drug response of a gene network linking dedifferentiation with β-catenin dysfunction in hepatocellular carcinoma

2019

Background & Aims Alterations of individual genes variably affect the development of hepatocellular carcinoma (HCC). Thus, we aimed to characterize the function of tumor-promoting genes in the context of gene regulatory networks (GRNs). Methods Using data from The Cancer Genome Atlas, from the LIRI-JP (Liver Cancer – RIKEN, JP project), and from our transcriptomic, transfection and mouse transgenic experiments, we identify a GRN which functionally links LIN28B-dependent dedifferentiation with dysfunction of β-catenin (CTNNB1). We further generated and validated a quantitative mathematical model of the GRN using human cell lines and in vivo expression data. Results We found that LIN28B and C…

0301 basic medicineBeta-cateninCarcinoma HepatocellularHepatocellular carcinomaLIN28BCellGene regulatory networkPrincipal component analysisMice TransgenicBiologyTransfectionTranscriptomeCohort Studies03 medical and health sciencesMice0302 clinical medicineMathematical modelmicroRNAmedicineAnimalsHumansGene Regulatory NetworksCTNNB1Genebeta CateninHepatologySequence Analysis RNALiver NeoplasmsGene regulatory networkRNA-Binding ProteinsHGF/MET pathwayMicroRNAHep G2 CellsHCCSModels TheoreticalPrognosisPersonalized medicinedigestive system diseases030104 developmental biologymedicine.anatomical_structureCancer researchSMARCA4biology.protein030211 gastroenterology & hepatologyTranscriptome
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Mast cells contribute to autoimmune diabetes by releasing interleukin-6 and failing to acquire a tolerogenic IL-10+ phenotype

2017

Mast cells (MCs) are innate immune cells that exert positive and negative immune modulatory functions capable to enhance or limit the intensity and/or duration of adaptive immune responses. Although MCs are crucial to regulate T cell immunity, their action in the pathogenesis of autoimmune diseases is still debated. Here we demonstrate that MCs play a crucial role in T1D pathogenesis so that their selective depletion in conditional MC knockout NOD mice protects them from the disease. MCs of diabetic NOD mice are overly inflammatory and secrete large amounts of IL-6 that favors differentiation of IL-17-secreting T cells at the site of autoimmunity. Moreover, while MCs of control mice acquire…

0301 basic medicineBlood GlucoseAutoimmune diabeteAutoimmunityNodmedicine.disease_causeT-Lymphocytes RegulatoryAutoimmunityImmune toleranceSettore MED/13 - EndocrinologiaMiceAutoimmune diabetes0302 clinical medicineMice Inbred NODImmunology and AllergyNOD miceMice KnockoutInterleukin-17Forkhead Transcription FactorsFlow CytometryImmunohistochemistryhumanitiesInterleukin-10Interleukin 10Tumor necrosis factor alphaImmunologySettore MED/50 - Scienze Tecniche Mediche ApplicateMice TransgenicLaser Capture MicrodissectionReal-Time Polymerase Chain Reactionbehavioral disciplines and activities03 medical and health sciencesIslets of LangerhansImmune systemChymasesmedicineAnimalsInflammationInnate immune systembusiness.industryInterleukin-6Immune toleranceSettore MED/46 - Scienze Tecniche di Medicina di LaboratorioAutoimmune diabetes; Immune tolerance; Interleukin-10; Interleukin-6; Mast cells030104 developmental biologyDiabetes Mellitus Type 1ImmunologyMast cellsTh17 CellsMast cells; Autoimmune diabetes; Interleukin-6; Immune tolerance; Interleukin-10business030215 immunology
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Reciprocal regulation of the Il9 locus by counteracting activities of transcription factors IRF1 and IRF4.

2017

The T helper 9 (Th9) cell transcriptional network is formed by an equilibrium of signals induced by cytokines and antigen presentation. Here we show that, within this network, two interferon regulatory factors (IRF), IRF1 and IRF4, display opposing effects on Th9 differentiation. IRF4 dose-dependently promotes, whereas IRF1 inhibits, IL-9 production. Likewise, IRF1 inhibits IL-9 production by human Th9 cells. IRF1 counteracts IRF4-driven Il9 promoter activity, and IRF1 and IRF4 have opposing function on activating histone modifications, thus modulating RNA polymerase II recruitment. IRF1 occupancy correlates with decreased IRF4 abundance, suggesting an IRF1-IRF4-binding competition at the I…

0301 basic medicineCD4-Positive T-LymphocytesScienceCellular differentiationAntigen presentationGeneral Physics and AstronomyRNA polymerase IIMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciences0302 clinical medicineInterferonmedicineAnimalsHumansInterleukin 9Transcription factorMice KnockoutMultidisciplinaryGene Expression ProfilingQInterleukin-9Cell DifferentiationGeneral ChemistryT-Lymphocytes Helper-InducerCell biologyMice Inbred C57BL030104 developmental biologyIRF1Interferon Regulatory Factorsbiology.protein030215 immunologyInterferon regulatory factorsmedicine.drugInterferon Regulatory Factor-1Nature communications
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