Search results for "Basic Helix-Loop-Helix Transcription Factor"

showing 10 items of 45 documents

Incomplete penetrance and phenotypic variability of 6q16 deletions including SIM1.

2015

International audience; 6q16 deletions have been described in patients with a Prader-Willi-like (PWS-like) phenotype. Recent studies have shown that certain rare single-minded 1 (SIM1) loss-of-function variants were associated with a high intra-familial risk for obesity with or without features of PWS-like syndrome. Although SIM1 seems to have a key role in the phenotype of patients carrying 6q16 deletions, some data support a contribution of other genes, such as GRIK2, to explain associated behavioural problems. We describe 15 new patients in whom de novo 6q16 deletions were characterised by comparative genomic hybridisation or single-nucleotide polymorphism (SNP) array analysis, including…

AdultMaleAdolescent[SDV]Life Sciences [q-bio]PenetranceBioinformaticsPolymorphism Single NucleotideArticlePregnancyGRIK2Basic Helix-Loop-Helix Transcription FactorsGeneticsHumansSNPObesityChildGeneGenetic Association StudiesGenetics (clinical)GeneticsComparative Genomic Hybridizationbiology[ SDV ] Life Sciences [q-bio]InfantPenetrancePhenotypeRepressor ProteinsChild PreschoolAborted FetusSIM1biology.proteinChromosomes Human Pair 6FemaleHaploinsufficiencyPrader-Willi SyndromeComparative genomic hybridization
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A meta-analysis of Hodgkin lymphoma reveals 19p13.3 TCF3 as a novel susceptibility locus

2014

Contains fulltext : 137763.pdf (Publisher’s version ) (Open Access) Recent genome-wide association studies (GWAS) of Hodgkin lymphoma (HL) have identified associations with genetic variation at both HLA and non-HLA loci; however, much of heritable HL susceptibility remains unexplained. Here we perform a meta-analysis of three HL GWAS totaling 1,816 cases and 7,877 controls followed by replication in an independent set of 1,281 cases and 3,218 controls to find novel risk loci. We identify a novel variant at 19p13.3 associated with HL (rs1860661; odds ratio (OR)=0.81, 95% confidence interval (95% CI)=0.76-0.86, Pcombined=3.5 x 10(-10)), located in intron 2 of TCF3 (also known as E2A), a regul…

AdultMaleAdolescent[SDV]Life Sciences [q-bio]TRANSCRIPTION FACTOR E2AGENETIC-ASSOCIATIONGeneral Physics and AstronomyLocus (genetics)Genome-wide association studyHuman leukocyte antigenBiologyGeneral Biochemistry Genetics and Molecular BiologyArticleDISEASEYoung AdultBasic Helix-Loop-Helix Transcription FactorsHumansTOOLGenetic Predisposition to DiseaseAlleleGENOME-WIDE ASSOCIATIONEPSTEIN-BARR-VIRUSGenetic associationAgedGeneticsAged 80 and overRISKMultidisciplinaryCELL-TYPECase-control studyGenetic VariationGeneral ChemistryOdds ratioGenomicsMiddle AgedALLELESHodgkin DiseaseCANCERMalaltia de HodgkinHodgkin lymphoma (HL)GenòmicaGenetic epidemiologyCase-Control StudiesUrological cancers Radboud Institute for Health Sciences [Radboudumc 15]Hodgkin's diseaseChromosomes Human Pair 19Genome-Wide Association Study
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Whole-exome sequencing identifies the first French MODY 6 family with a new mutation in the NEUROD1 gene

2020

Abstract Aim The aim of the present study was to identify the affected gene in a French family with maturity-onset diabetes of the young (MODY) using whole-exome sequencing (WES). Methods WES was performed in one patient with MODY, and candidate variants were confirmed in members of the immediate family by Sanger sequencing. Results In the proband, a new heterozygous missense mutation (c.340A>C) was identified in the NEUROD1 gene by WES analysis and confirmed by Sanger sequencing. Additional Sanger sequencing of the proband's sister and mother revealed the same heterozygous mutation. The proband and his sister displayed typical clinical characteristics of MODY, while their mother had the sa…

AdultMaleProbandHeterozygoteEndocrinology Diabetes and Metabolism[SDV]Life Sciences [q-bio]Mutation MissenseMothers030209 endocrinology & metabolism030204 cardiovascular system & hematologyBiology03 medical and health sciencessymbols.namesake0302 clinical medicineEndocrinologyDiabetic NeuropathiesExome SequencingBasic Helix-Loop-Helix Transcription FactorsInternal MedicinemedicineHumansHypoglycemic AgentsInsulinMissense mutationDiabetic NephropathiesAge of OnsetGeneExome sequencingAgedSanger sequencingGeneticsDiabetic RetinopathySiblingsGeneral Medicinemedicine.disease[SDV] Life Sciences [q-bio]Diabetes Mellitus Type 2Mutation (genetic algorithm)symbolsFemaleFranceMODY 6NEUROD1 Gene
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Reprogramming of Pericyte-Derived Cells of the Adult Human Brain into Induced Neuronal Cells

2012

SummaryReprogramming of somatic cells into neurons provides a new approach toward cell-based therapy of neurodegenerative diseases. A major challenge for the translation of neuronal reprogramming into therapy is whether the adult human brain contains cell populations amenable to direct somatic cell conversion. Here we show that cells from the adult human cerebral cortex expressing pericyte hallmarks can be reprogrammed into neuronal cells by retrovirus-mediated coexpression of the transcription factors Sox2 and Mash1. These induced neuronal cells acquire the ability of repetitive action potential firing and serve as synaptic targets for other neurons, indicating their capability of integrat…

AdultNeurogenesisCellular differentiationInduced Pluripotent Stem CellsAction PotentialsBiologySynaptic TransmissionMiceNeural Stem CellsSOX2Basic Helix-Loop-Helix Transcription FactorsGeneticsmedicineAnimalsHumansInduced pluripotent stem cellCells CulturedCerebral CortexNeuronsSOXB1 Transcription FactorsNeurogenesisCell DifferentiationNeurodegenerative DiseasesCell BiologyCellular ReprogrammingNeural stem cellCell biologyRetroviridaemedicine.anatomical_structureImmunologyMolecular MedicineNeuronPericyteNerve NetPericytesReprogrammingStem Cell TransplantationCell Stem Cell
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Chronic exposure of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces an obesogenic effect in C57BL/6J mice fed a high fat diet

2017

IF 3.582; International audience; Contaminant involvement in the pathophysiology of obesity is widely recognized. It has been shown that low dose and chronic exposure to endocrine disruptor compounds (EDCs) potentiated diet- induced obesity. High and acute exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a persistent organic pollutant (POP) and an EDC with anti-estrogenic property, causes wasting syndrome . However at lower doses, the TCDD metabolic effects remain poorly understood. We investigated the obesogenic effect during chronic exposure of TCDD at 1μg/kg body weight (bw)/week in adult C57BL/6J mice fed with a high fat diet (HFD) and exposed from 10 to 42 weeks old to TCDD or e…

Blood GlucoseLeptinMale0301 basic medicineTCDDPolychlorinated DibenzodioxinsTime FactorsAdipose tissue010501 environmental sciencesToxicology01 natural sciencesBasic Helix-Loop-Helix Transcription FactorsInsulinAdiposity2. Zero hunger[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism3. Good healthLiverEndocrine disruptorReceptors AndrogenCytokinesEnvironmental PollutantsFemaleInflammation Mediatorsmedicine.symptomStearoyl-CoA Desaturasemedicine.medical_specialtyLipolysisInflammationchronic exposureIntra-Abdominal FatDiet High-FatRisk Assessment03 medical and health sciencesSex FactorsobesogenInternal medicinemedicineAnimalsEndocrine systemObesityRNA MessengerWasting SyndromeTriglycerides0105 earth and related environmental sciencesbusiness.industrymedicine.diseaseObesityMice Inbred C57BL030104 developmental biologyEndocrinologyReceptors Aryl HydrocarbonInsulin ResistancebusinessBiomarkersObesogenDrug metabolism
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Meox2/Tcf15 Heterodimers Program the Heart Capillary Endothelium for Cardiac Fatty Acid Uptake

2015

Background— Microvascular endothelium in different organs is specialized to fulfill the particular needs of parenchymal cells. However, specific information about heart capillary endothelial cells (ECs) is lacking. Methods and Results— Using microarray profiling on freshly isolated ECs from heart, brain, and liver, we revealed a genetic signature for microvascular heart ECs and identified Meox2/Tcf15 heterodimers as novel transcriptional determinants. This signature was largely shared with skeletal muscle and adipose tissue endothelium and was enriched in genes encoding fatty acid (FA) transport–related proteins. Using gain- and loss-of-function approaches, we showed that Meox2/Tcf15 media…

CD36 AntigensHeterozygoteEndotheliumCD36Cardiac Output LowAdipose tissueLipoproteins VLDLBiologyFatty Acid-Binding ProteinsMicePhysiology (medical)Protein Interaction MappingBasic Helix-Loop-Helix Transcription FactorsmedicineAnimalsHumansRNA Small InterferingTranscription factorCells CulturedHomeodomain Proteinschemistry.chemical_classificationLipoprotein lipaseMyocardiumFatty AcidsEndothelial CellsFatty acidSkeletal muscleMetabolismCoronary VesselsCell biologyMice Inbred C57BLLipoprotein LipaseGlucosemedicine.anatomical_structureAdipose TissuechemistryBiochemistryTissue Array Analysisbiology.proteinTranscriptomeCardiology and Cardiovascular MedicineCirculation
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Nupr1-Aurora Kinase A Pathway Provides Protection against Metabolic Stress-Mediated Autophagic-Associated Cell Death

2012

Abstract Purpose: The limited supply of oxygen and nutrients is thought to result in rigorous selection of cells that will eventually form the tumor. Experimental Design: Nupr1 expression pattern was analyzed in human tissue microarray (TMA) and correlated with survival time of the patient. Microarray analysis was conducted on MiaPaCa2 cells subjected to metabolic stress in Nupr1-silenced conditions. DNA repair and cell cycle–associated gene expression was confirmed by real-time quantitative PCR (qRT-PCR). Nupr1 and AURKA protective role were analyzed using RNA interference (RNAi) silencing or overexpression. DNA damage and autophagy were analyzed by Western blot analysis and immunofluoresc…

Cancer ResearchProgrammed cell deathCell SurvivalDNA damageDNA repairAdenocarcinomaProtein Serine-Threonine KinasesBiologyAurora KinasesStress PhysiologicalCell Line TumorAutophagyBasic Helix-Loop-Helix Transcription FactorsHumansGene silencingAurora Kinase ARegulation of gene expressionGene knockdownMicroarray analysis techniquesAURKA GeneMolecular biologyCell HypoxiaNeoplasm ProteinsCell biologyGene Expression Regulation NeoplasticGlucoseOncologyRNA InterferenceCarcinoma Pancreatic DuctalClinical Cancer Research
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Haem oxygenase-1 induction reverses the actions of interleukin-1β on hypoxia-inducible transcription factors and human chondrocyte metabolism in hypo…

2013

HO-1 (haem oxygenase-1) catalyses the degradation of haem and possesses anti-inflammatory and cytoprotective properties. The role of inflammatory mediators in the pathogenesis of OA (osteoarthritis) is becoming increasingly appreciated. In the present study, we investigated the effects of HO-1 induction in OA and healthy HACs (human articular chondrocytes) in response to inflammatory cytokine IL-1 β (interleukin-1β) under hypoxic conditions. Hypoxia was investigated as it is a more physiological condition of the avascular cartilage. Hypoxic signalling is mediated by HIFs (hypoxia-inducible factors), of which there are two main isoforms, HIF-1α and HIF-2α. Normal and OA chondrocytes were sti…

Cartilage ArticularMaleSmall interfering RNAmedicine.medical_treatmentInterleukin-1betaBiologyMatrix metalloproteinaseChondrocytesOsteoarthritisBasic Helix-Loop-Helix Transcription FactorsmedicineHumansHypoxiaCollagen Type IITranscription factorAgedTumor Necrosis Factor-alphaCatabolismSOX9 Transcription FactorGeneral MedicineMiddle AgedHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCOPPMatrix MetalloproteinasesCell biologyCytokineBiochemistryFemaleTumor necrosis factor alphamedicine.symptomHeme Oxygenase-1Clinical Science
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Vascular niche factor PEDF modulates Notch-dependent stemness in the adult subependymal zone.

2009

We sought to address the fundamental question of how stem cell microenvironments can regulate self-renewal. We found that Notch was active in astroglia-like neural stem cells (NSCs), but not in transit-amplifying progenitors of the murine subependymal zone, and that the level of Notch transcriptional activity correlated with self-renewal and multipotency. Moreover, dividing NSCs appeared to balance renewal with commitment via controlled segregation of Notch activity, leading to biased expression of known (Hes1) and previously unknown (Egfr) Notch target genes in daughter cells. Pigment epithelium-derived factor (PEDF) enhanced Notch-dependent transcription in cells with low Notch signaling,…

Cell divisionTranscription GeneticNotch signaling pathwayGene ExpressionBiologyMicePEDFEpendymaSubependymal zoneBasic Helix-Loop-Helix Transcription FactorsAnimalsNuclear Receptor Co-Repressor 1Nerve Growth FactorsProgenitor cellHES1Receptor Notch1Eye ProteinsCells CulturedSerpinsHomeodomain ProteinsNeuronsTranscription Factor HES-1General NeuroscienceAge FactorsTranscription Factor RelACell DifferentiationNeural stem cellErbB ReceptorsAdult Stem CellsTranscription Factor HES-1NeuroscienceSignal TransductionNature neuroscience
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Hypoxia and HIF Signaling: One Axis with Divergent Effects

2020

The correct concentration of oxygen in all tissues is a hallmark of cellular wellness, and the negative regulation of oxygen homeostasis is able to affect the cells and tissues of the whole organism. The cellular response to hypoxia is characterized by the activation of multiple genes involved in many biological processes. Among them, hypoxia-inducible factor (HIF) represents the master regulator of the hypoxia response. The active heterodimeric complex HIF α/β, binding to hypoxia-responsive elements (HREs), determines the induction of at least 100 target genes to restore tissue homeostasis. A growing body of evidence demonstrates that hypoxia signaling can act by generating contrasting res…

CellInflammationReviewBiologyCatalysislcsh:ChemistryInorganic ChemistryImmune systemSettore BIO/13 - Biologia ApplicataOxygen homeostasisBasic Helix-Loop-Helix Transcription FactorsmedicineHumansRNA MessengerAcute and chronic diseasesPhysical and Theoretical ChemistryHypoxialcsh:QH301-705.5Molecular BiologySpectroscopyTissue homeostasisInflammationKidneyImmune cellsOrganic ChemistryHIF-αNuclear ProteinsGeneral MedicineHypoxia (medical)Cell HypoxiaComputer Science ApplicationsCell biologyDNA-Binding ProteinsOxygenmedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999Hypoxia-Inducible Factor 1medicine.symptomSignal transductionSignal TransductionTranscription FactorsInternational Journal of Molecular Sciences
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