Search results for "genetics [Mutation]"

showing 10 items of 3026 documents

Evaluation of in vivo and in vitro models of toxicity by comparison of toxicogenomics data with the literature.

2017

Toxicity affecting humans is studied by observing the effects of chemical substances in animal organisms (in vivo) or in animal and human cultivated cell lines (in vitro). Toxicogenomics studies collect gene expression profiles and histopathology assessment data for hundreds of drugs and pollutants in standardized experimental designs using different model systems. These data are an invaluable source for analyzing genome-wide drug response in biological systems. However, a problem remains that is how to evaluate the suitability of heterogeneous in vitro and in vivo systems to model the many different aspects of human toxicity. We propose here that a given model system (cell type or animal o…

0301 basic medicineCandidate geneCell typeDrug Evaluation PreclinicalBiologyBioinformaticsToxicogeneticsGeneral Biochemistry Genetics and Molecular BiologyIn vitroRats03 medical and health sciences030104 developmental biologyIn vivoToxicityHepatocytesAnimalsHumansToxicogenomicsTranscriptomeMolecular BiologyGeneFunction (biology)Cells CulturedMethods (San Diego, Calif.)
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Identification of loci of functional relevance to Barrett's esophagus and esophageal adenocarcinoma: Cross-referencing of expression quantitative tra…

2019

Esophageal adenocarcinoma (EA) and its precancerous condition Barrett's esophagus (BE) are multifactorial diseases with rising prevalence rates in Western populations. A recent meta-analysis of genome-wide association studies (GWAS) data identified 14 BE/EA risk loci located in non-coding genomic regions. Knowledge about the impact of non-coding variation on disease pathology is incomplete and needs further investigation. The aim of the present study was (i) to identify candidate genes of functional relevance to BE/EA at known risk loci and (ii) to find novel risk loci among the suggestively associated variants through the integration of expression quantitative trait loci (eQTL) and genetic…

0301 basic medicineCandidate geneEsophageal MucosaEsophageal NeoplasmsMedizinGene ExpressionGenome-wide association study0302 clinical medicineMathematical and Statistical TechniquesGeneticsMultidisciplinarySodium-Hydrogen Exchanger 3QStatisticsRGenomicsMetaanalysisGene Expression Regulation NeoplasticResearch Design030220 oncology & carcinogenesisPhysical SciencesMedicineResearch Articlemedicine.medical_specialtyScienceQuantitative Trait LociReplication StudiesContext (language use)BiologyAdenocarcinomaResearch and Analysis MethodsPolymorphism Single NucleotideMolecular Genetics03 medical and health sciencesBarrett EsophagusMolecular geneticsmedicineGeneticsGenome-Wide Association StudiesHumansGenetic Predisposition to DiseaseGene RegulationStatistical MethodsGeneMolecular BiologyGenetic associationProteinsBiology and Life SciencesComputational BiologyHuman Geneticsmedicine.diseaseGenome AnalysisRepressor Proteins030104 developmental biologyGenetic LociBarrett's esophagusExpression quantitative trait lociGenetics of DiseaseMathematicsGenome-Wide Association StudyPloS one
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Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis

2019

Summary MyD88, an adaptor molecule downstream of innate pathways, plays a significant tumor-promoting role in sporadic intestinal carcinogenesis of the Apcmin/+ model, which carries a mutation in the Apc gene. Here, we show that deletion of MyD88 in intestinal mesenchymal cells (IMCs) significantly reduces tumorigenesis in this model. This phenotype is associated with decreased epithelial cell proliferation, altered inflammatory and tumorigenic immune cell infiltration, and modified gene expression similar to complete MyD88 knockout mice. Genetic deletion of TLR4, but not interleukin-1 receptor (IL-1R), in IMCs led to altered molecular profiles and reduction of intestinal tumors similar to …

0301 basic medicineCarcinogenesisBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyExtracellular matrixMice03 medical and health sciences0302 clinical medicinemedicinetumor microenvironmentAnimalsHumansReceptorinnate immunityTumor microenvironmentInnate immune systemMesenchymal stem cellCell biologyIntestinesToll-Like Receptor 4030104 developmental biologyMyeloid Differentiation Factor 88Knockout mouseTLR4Carcinogenesiscancer-associated fibroblasts030217 neurology & neurosurgerySignal Transduction
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MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
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Daunorubicin reduces MBNL1 titration by expanded CUG repeat RNA and rescues cardiac dysfunctions in a Drosophila model of myotonic dystrophy

2018

International audience; Myotonic dystrophy (DM) is a dominantly inherited neuromuscular disorder caused by expression of mutant DMPK transcripts containing expanded CUG repeats. Pathogenic RNA sequesters the muscleblind-like (MBNL) proteins, causing alterations of RNA metabolism. Cardiac dysfunction represents the second most common cause of death in DM1 patients. However, the contribution of MBNL titration in DM1 cardiac dysfunction is unclear. We overexpressed Muscleblind (Mbl), Drosophila MBNL orthologue, in cardiomyocytes of DM1 model flies and observed a rescue of heart dysfunctions, which are characteristic of these model flies and resemble cardiac defects observed in patients. We als…

0301 basic medicineCardiac function curvecongenital hereditary and neonatal diseases and abnormalitiesDaunorubicin[SDV]Life Sciences [q-bio]Neuroscience (miscellaneous)Medicine (miscellaneous)BiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmunology and Microbiology (miscellaneous)medicineMBNL1Daunorubicin HydrochlorideRNAmedicine.diseaseTrinucleotide repeat disorder3. Good healthCell biology[SDV] Life Sciences [q-bio]030104 developmental biologychemistryTrinucleotide repeat expansion030217 neurology & neurosurgerymedicine.drug
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Few layer 2D pnictogens catalyze the alkylation of soft nucleophiles with esters

2019

Group 15 elements in zero oxidation state (P, As, Sb and Bi), also called pnictogens, are rarely used in catalysis due to the difficulties associated in preparing well–structured and stable materials. Here, we report on the synthesis of highly exfoliated, few layer 2D phosphorene and antimonene in zero oxidation state, suspended in an ionic liquid, with the native atoms ready to interact with external reagents while avoiding aerobic or aqueous decomposition pathways, and on their use as efficient catalysts for the alkylation of nucleophiles with esters. The few layer pnictogen material circumvents the extremely harsh reaction conditions associated to previous superacid–catalyzed alkylations…

0301 basic medicineCatàlisi heterogèniaScienceFOS: Physical sciencesGeneral Physics and Astronomy02 engineering and technologyAlkylationIonic liquidGeneral Biochemistry Genetics and Molecular BiologyArticleCatalysis03 medical and health scienceschemistry.chemical_compoundNucleophileOxidation stateAntimonenePhysics - Chemical PhysicsQUIMICA ANALITICAlcsh:ScienceMaterialsChemical Physics (physics.chem-ph)MultidisciplinaryAqueous solutionChemistryPnictogensPhosphoreneQGeneral Chemistry021001 nanoscience & nanotechnologyCombinatorial chemistryPhosphorene030104 developmental biologyReagentddc:540Ionic liquidlcsh:QCatalyst0210 nano-technologyNature Communications
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Toxicity and cell density monitoring in monolayer and three-dimensional cultures with the XTT assay

1998

The application of viability criteria (MTT and XTT tests) to monolayer cultures and immobilised cells in three-dimensional systems was investigated in order to assess cell viability and cell proliferation. The suitability and accuracy of these tests were compared with the conventional criteria (cellular protein and DNA content) used in monolayer cultures for the same purpose. The colorimetric assay based on the metabolic reduction of the tetrazolium salt XTT to a water-soluble formazan proved to be very useful, rapid and sensitive. This automated spectrophotometric enzymatic method, due to its lack of toxicity, also permits repeated nondestructive assays on a single cellular culture for the…

0301 basic medicineCell growthMonolayer cultureGeneral MedicineBiologyToxicologyGeneral Biochemistry Genetics and Molecular BiologyColorimetry (chemical method)In vitro03 medical and health sciencesMedical Laboratory Technology030104 developmental biology0302 clinical medicineBiochemistryCell densityMonolayerToxicityXtt assay030217 neurology & neurosurgery
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An actin network dispatches ciliary GPCRs into extracellular vesicles to modulate signaling

2017

Signaling receptors dynamically exit cilia upon activation of signaling pathways such as Hedgehog. Here, we find that when activated G protein-coupled receptors (GPCRs) fail to undergo BBSome-mediated retrieval from cilia back into the cell, these GPCRs concentrate into membranous buds at the tips of cilia before release into extracellular vesicles named ectosomes. Unexpectedly, actin and the actin regulators drebrin and myosin 6 mediate ectosome release from the tip of cilia. Mirroring signal-dependent retrieval, signal-dependent ectocytosis is a selective and effective process that removes activated signaling molecules from cilia. Congruently, ectocytosis compensates for BBSome defects as…

0301 basic medicineCell signalingBBSome*myosin 6*GPCR*exosomes*HedgehogBiologyKidneyGeneral Biochemistry Genetics and Molecular BiologyArticleCell LineReceptors G-Protein-Coupled03 medical and health sciencesExtracellular VesiclesMice0302 clinical medicine*BBSomeAnimalsHumans*ciliaCiliaReceptors SomatostatinHedgehog*actinActinG protein-coupled receptorCilium*extracellular vesiclesHedgehog signaling pathwayActinsCell biology030104 developmental biologyMicroscopy Electron ScanningSignal transduction*drebrin030217 neurology & neurosurgerySignal Transduction
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Evaluation of Planar-Cell-Polarity Phenotypes in Ciliopathy Mouse Mutant Cochlea

2016

In recent years, primary cilia have emerged as key regulators in development and disease by influencing numerous signaling pathways. One of the earliest signaling pathways shown to be associated with ciliary function was the non-canonical Wnt signaling pathway, also referred to as planar cell polarity (PCP) signaling. One of the best places in which to study the effects of planar cell polarity (PCP) signaling during vertebrate development is the mammalian cochlea. PCP signaling disruption in the mouse cochlea disrupts cochlear outgrowth, cellular patterning and hair cell orientation, all of which are affected by cilia dysfunction. The goal of this protocol is to describe the analysis of PCP…

0301 basic medicineCell signalingGeneral Chemical EngineeringStereocilia (inner ear)Cochlear ductBiologyGeneral Biochemistry Genetics and Molecular BiologyStereociliaMice03 medical and health sciencesHair Cells AuditorymedicineAnimalsCochleaGeneral Immunology and MicrobiologyGeneral NeuroscienceCiliumWnt signaling pathwayCell PolarityCochlear DuctEmbryo Mammalianmedicine.diseaseImmunohistochemistryCiliopathiesCochleaCell biologyDisease Models AnimalCiliopathyPhenotype030104 developmental biologymedicine.anatomical_structureMicroscopy Electron ScanningMedicinesense organsHair cellSignal TransductionJournal of Visualized Experiments
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EphrinB2 repression through ZEB2 mediates tumour invasion and anti-angiogenic resistance.

2016

Diffuse invasion of the surrounding brain parenchyma is a major obstacle in the treatment of gliomas with various therapeutics, including anti-angiogenic agents. Here we identify the epi-/genetic and microenvironmental downregulation of ephrinB2 as a crucial step that promotes tumour invasion by abrogation of repulsive signals. We demonstrate that ephrinB2 is downregulated in human gliomas as a consequence of promoter hypermethylation and gene deletion. Consistently, genetic deletion of ephrinB2 in a murine high-grade glioma model increases invasion. Importantly, ephrinB2 gene silencing is complemented by a hypoxia-induced transcriptional repression. Mechanistically, hypoxia-inducible facto…

0301 basic medicineCell signalingScienceGeneral Physics and AstronomyRepressorDown-RegulationAngiogenesis InhibitorsEphrin-B2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleNeovascularization03 medical and health sciencesDownregulation and upregulationddc:570GliomamedicineGene silencingAnimalsHumansNeoplasm InvasivenessPsychological repressionZinc Finger E-box Binding Homeobox 2Regulation of gene expressionMice KnockoutMultidisciplinaryNeovascularization PathologicQGeneral ChemistryGliomamedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysCell HypoxiaCell biologyUp-RegulationBevacizumabGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyDrug Resistance Neoplasmmedicine.symptomNature communications
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