Search results for "TUMOR-SUPPRESSOR"

showing 4 items of 4 documents

Transcription factor NRF2 as a therapeutic target for chronic diseases: a systems medicine approach

2018

Systems medicine has a mechanism-based rather than a symptom- or organ-based approach to disease and identifies therapeutic targets in a nonhypothesis-driven manner. In this work, we apply this to transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) by cross-validating its position in a protein-protein interaction network (the NRF2 interactome) functionally linked to cytoprotection in low-grade stress, chronic inflammation, metabolic alterations, and reactive oxygen species formation. Multiscale network analysis of these molecular profiles suggests alterations of NRF2 expression and activity as a common mechanism in a subnetwork of diseases (the NRF2 diseasome). This netw…

0301 basic medicineRMSystems AnalysisNF-E2-Related Factor 2MedicinaNF-KAPPA-BAnti-Inflammatory AgentsTYPE-2 DIABETES-MELLITUSGENE PROMOTER POLYMORPHISMDiseaseComputational biologyInteractomeenvironment and public healthGLYCOGEN-SYNTHASE KINASETUMOR-SUPPRESSOR PTENNRF203 medical and health sciencesDrug DiscoveryAnimalsHumansTherapeutic targetsMedicineMolecular Targeted TherapyBardoxolone methylPLACEBO-CONTROLLED PHASE-3PharmacologyMechanism (biology)Drug discoverybusiness.industryDrug RepositioningRChronic inflammationrespiratory systemHEME OXYGENASE 1PROTEIN-PROTEIN INTERACTION3. Good healthSystems medicineDrug repositioning030104 developmental biologyDrug developmentEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISChronic DiseaseSystems medicineMolecular MedicineFUMARIC-ACID ESTERSbusiness
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Menopause and adipose tissue: miR-19a-3p is sensitive to hormonal replacement

2018

Tissue-specific effects of 17 beta-estradiol are delivered via both estrogen receptors and microRNAs (miRs). Menopause is known to affect the whole-body fat distribution in women. This investigation aimed at identifying menopause-and hormone replacement therapy (HRT)-associated miR profiles and miR targets in subcutaneous abdominal adipose tissue and serum from the same women. A discovery phase using array technology was performed in 13 women, including monozygotic twin pairs discordant for HRT and premenopausal young controls. Seven miRs, expressed in both adipose tissue and serum, were selected for validation phase in 34 women from a different cohort. An age/menopause-related increase of …

0301 basic medicinevaihdevuodetmedicine.medical_treatmentmenopauseAdipose tissueEstrogen receptorMonozygotic twinTHERAPYchemistry.chemical_compoundestrogen therapyAdipocyteTUMOR-SUPPRESSORADIPOCYTE DIFFERENTIATIONmicroRNAestrogeenihoitota3141miR-19a-3pHormone replacement therapy (menopause)ta31423142 Public health care science environmental and occupational healthmicroRNAsadipose tissueMenopauseOncologyhormonihoitoSKELETAL-MUSCLEESTROGEN-RECEPTOR-ALPHASTEM-CELLSResearch PaperEXPRESSIONestrogeenitmedicine.medical_specialtyBODY-COMPOSITION3122 Cancersrasvakudokset03 medical and health sciencesInternal medicinemedicineBREAST-CANCERbusiness.industryagingmedicine.diseasehormonitMONOZYGOTIC TWIN PAIRSikääntyminen030104 developmental biologyEndocrinologychemistrybusinessEstrogen receptor alphaHormoneOncotarget
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Lysosomal Signaling Licenses Embryonic Stem Cell Differentiation via Inactivation of Tfe3

2019

International audience; Self-renewal and differentiation of pluripotent murine embryonic stem cells (ESCs) is regulated by extrinsic signaling pathways. It is less clear whether cellular metabolism instructs developmental progression. In an unbiased genome-wide CRISPR/Cas9 screen, we identified components of a conserved amino-acid-sensing pathway as critical drivers of ESC differentiation. Functional analysis revealed that lysosome activity, the Ragulator protein complex, and the tumor-suppressor protein Folliculin enable the Rag GTPases C and D to bind and seclude the bHLH transcription factor Tfe3 in the cytoplasm. In contrast, ectopic nuclear Tfe3 represses specific developmental and met…

MaleTranscription GeneticGTPaseGTP PhosphohydrolasesPATHWAYMice0302 clinical medicineNeural Stem CellsCRISPRTUMOR-SUPPRESSORCell Self RenewalPhosphorylationSPECIFICATIONdevelopmental disorder0303 health sciencesGenomeBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell DifferentiationMouse Embryonic Stem CellsFlcndifferentiationCell biologymedicine.anatomical_structuremTORMolecular MedicineFemaleSignal transductionProtein BindingSignal TransductionRECRUITMENTBiology03 medical and health sciencesRag GTPasesLysosomeGeneticsmedicineAnimalsHumansPoint MutationNAIVE PLURIPOTENCYAMINO-ACID LEVELSTranscription factorAllelesPI3K/AKT/mTOR pathway030304 developmental biologyCOMPLEXFOLLICULINRagulatorCell Biologypluripotencyembryonic stem cellEmbryonic stem cellTfe3[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsCytoplasmLysosomes030217 neurology & neurosurgeryCell Stem Cell
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Focal DNA Copy Number Changes in Neuroblastoma Target MYCN Regulated Genes

2013

Neuroblastoma is an embryonic tumor arising from immature sympathetic nervous system cells. Recurrent genomic alterations include MYCN and ALK amplification as well as recurrent patterns of gains and losses of whole or large partial chromosome segments. A recent whole genome sequencing effort yielded no frequently recurring mutations in genes other than those affecting ALK. However, the study further stresses the importance of DNA copy number alterations in this disease, in particular for genes implicated in neuritogenesis. Here we provide additional evidence for the importance of focal DNA copy number gains and losses, which are predominantly observed in MYCN amplified tumors. A focal 5 kb…

TRANSCRIPTIONAL TARGETNeuroblastoma/geneticsPsychologie appliquéeMedizinlcsh:MedicineChromosomal DisordersNeuroblastoma0302 clinical medicineRGS Proteins/geneticsGene duplicationMolecular Cell BiologyBasic Cancer ResearchTUMOR-SUPPRESSORALK KINASElcsh:ScienceNeurological TumorsGeneticsRegulation of gene expressionOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinACTIVATING MUTATIONSMultidisciplinaryCancer Risk FactorsHomozygoteChromosomal Deletions and DuplicationsNuclear ProteinsGenomicsSciences bio-médicales et agricolesSignaling in Selected DisciplinesCANCEROncogene Proteins/geneticsGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisMedicineRNA Long NoncodingBiologieResearch ArticleSignal TransductionEXPRESSIONDNA Copy Number VariationsGenetic Causes of CancerDown-RegulationGenomicsBiologyMolecular Genetics03 medical and health sciencesGenome Analysis ToolsNeuroblastomaCell Line TumormicroRNAmedicineGeneticsCancer GeneticsHumansGene RegulationGeneneoplasmsBiology030304 developmental biologyOncogenic SignalingN-MYCTHERAPEUTIC TARGETRECEPTORMICRORNAlcsh:RBiology and Life SciencesChromosomeCancers and NeoplasmsHuman Geneticsmedicine.diseaseNuclear Proteins/geneticsMicroRNAs/geneticsMicroRNAsPediatric Oncologylcsh:QGenome Expression AnalysisN-MycRGS ProteinsPLoS ONE
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