Search results for "FIBROBLASTS"

showing 10 items of 445 documents

Influence ofKi-ras-driven oncogenic transformation on the protein network of murine fibroblasts

2007

Ki-ras gene mutations that specifically occur in codons 12, 13 and 61 are involved in the carcinogenesis of acute myeloid leukemia, melanoma and different carcinomas. In order to define potential mutation-specific therapeutic targets, stable transfectants of NIH3T3 cells carrying different Ki-ras4B gene mutations were generated. Wild type Ki-ras transformants, mock transfectants and parental cells served as controls. These in vitro model systems were systematically analyzed for their protein expression pattern using two-dimensional gel electrophoresis followed by mass spectrometry and/or protein sequencing. Using this approach, a number of target molecules that are differentially but coordi…

Gel electrophoresismedicine.diagnostic_testWild typeFibroblastsBiologyGene mutationTransfectionmedicine.disease_causeProteomicsBiochemistryMolecular biologyMiceCell Transformation NeoplasticWestern blotHeat shock proteinNIH 3T3 Cellsras ProteinsmedicineAnimalsMitogen-Activated Protein KinasesCarcinogenesisMolecular BiologyGeneSignal TransductionPROTEOMICS
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Cytomegalovirus Interleukin-10 Expression in Infected Cells Does Not Impair MHC Class I Restricted Peptide Presentation on Bystanding Antigen-Present…

2006

Human cytomegalovirus (HCMV) has evolved strategies to counteract its surveillance by the immune system. Mitigation of antiviral immune responses is considered critical for establishment of viral latency and for spread. Recently, a gene encoding an interleukin-10 homologue (cmvIL-10) has been discovered in the HCMV genome. Using recombinant cmvIL-10, several mostly immunosuppressive functions of the molecule have been described. However, the role of cmvIL-10 in the context of viral infection was not addressed. To be able to analyze this issue, we generated cmvIL- 10-negative viral mutants. Using these mutants, we tested whether the expression of cmvIL-10 by infected cells would render bysta…

Gene Expression Regulation ViralHuman cytomegalovirusvirusesImmunologyCongenital cytomegalovirus infectionAntigen-Presenting CellsCytomegalovirusContext (language use)Viral ProteinsImmune systemVirologyMHC class ImedicineHumansAntigen-presenting cellCells CulturedAntigen PresentationbiologyHistocompatibility Antigens Class IBystander EffectFibroblastsmedicine.diseaseVirologyInterleukin-10CTL*Interleukin 10MutationImmunologybiology.proteinMolecular MedicineGene DeletionViral Immunology
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Epigenetic modifiers are necessary but not sufficient for reprogramming non-myelinating cells into myelin gene-expressing cells.

2010

Background Modifications on specific histone residues and DNA methylation play an essential role in lineage choice and cellular reprogramming. We have previously shown that histone modifications or combinatorial codes of transcription factors (TFs) are critical for the differentiation of multipotential progenitors into myelinating oligodendrocytes. In this study we asked whether combining global manipulation of DNA methylation and histone acetylation together with the expression of oligodendrocyte- specific TFs, was sufficient to switch the identity of fibroblasts into myelin gene-expressing cells. Methodology/Principal Findings Transfection of six oligodendrocyte-specific TFs (Olig1, Olig2…

Gene Expressionlcsh:MedicineBiologyCell LineEpigenesis GeneticHistones03 medical and health sciencesMice0302 clinical medicineHistone H1Histone methylationHistone H2ANeuroscience/Neuronal Signaling MechanismsHistone codeAnimalsCell Lineagelcsh:ScienceCells Cultured030304 developmental biologyEpigenomics0303 health sciencesMultidisciplinaryNeuroscience/Neuronal and Glial Cell BiologyMultipotent Stem Cellslcsh:RAcetylationCell DifferentiationDNA MethylationFibroblastsMolecular biologyChromatinChromatinRatsOligodendrogliaHomeobox Protein Nkx-2.2Histone methyltransferaseNIH 3T3 Cellslcsh:QNeuroscience/Neurobiology of Disease and RegenerationChromatin immunoprecipitation030217 neurology & neurosurgeryMyelin ProteinsResearch ArticleNeuroscienceTranscription FactorsPLoS ONE
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Expression of the gene of the alpha-smooth muscle-actin isoform in rat liver and in rat fat-storing (ITO) cells.

1990

Fat storing cells (FSCs) in the liver represent the main site of vitamin A deposition in the body. These cells are considered to play an important role during scar formation and fibrogenesis in the liver. The putative descent of FSCs from the fibroblastic or from the myofibroblastic system have not been determined yet by morphological or immunohistochemical studies. To further define the origin of these liver cells, we analysed the pattern of expression of three structural proteins: vimentin, desmin and the α-smooth muscle (SM)-actin isoform in FSCs of the rat liver, in smooth muscle cells (SMCs) from the aorta and in rat skin fibroblasts. FSCs were studied by immunohistochemical methods im…

Gene isoformPathologymedicine.medical_specialtyFluorescent Antibody TechniqueGene ExpressionVimentinmacromolecular substancesBiologyDesminImmunoenzyme TechniquesNecrosisGene expressionmedicineAnimalsVimentinNorthern blotActinAortaCells CulturedImmunoperoxidaseNucleic Acid HybridizationMuscle SmoothRats Inbred StrainsGeneral MedicineFibroblastsLipid MetabolismMolecular biologyActinsRatsLiverHepatic stellate cellbiology.proteinRNADesminFemaleVirchows Archiv. B, Cell pathology including molecular pathology
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DNA double-strand breaks trigger apoptosis in p53-deficient fibroblasts

2001

DNA double-strand breaks (DSBs) are induced by ionizing radiation (IR) and various radiomimetic agents directly, or indirectly as a consequence of DNA repair, recombination and replication of damaged DNA. They are ultimately involved in the generation of chromosomal aberrations and were reported to cause genomic instability, gene amplification and reproductive cell death. To address the question of whether DSBs act as a trigger of apoptosis, we induced DSBs by means of restriction enzyme electroporation and compared the effect with IR in mouse fibroblasts that differ in p53 status [wild-type (+/+) versus p53-deficient (-/-) cells]. We show that (i) electroporation of PVU:II is highly effici…

Genome instabilityCancer ResearchProgrammed cell deathTime FactorsDNA RepairDNA repairBlotting WesternApoptosisBiologymedicine.disease_causeCell LineMiceNecrosischemistry.chemical_compoundProto-Oncogene ProteinsRadiation IonizingmedicineAnimalsDeoxyribonucleases Type II Site-SpecificCells Culturedbcl-2-Associated X ProteinMice KnockoutRecombination GeneticMutationElectroporationDose-Response Relationship RadiationDNAGeneral MedicineTransfectionFibroblastsGenes p53Molecular biologyElectroporationProto-Oncogene Proteins c-bcl-2chemistryGamma RaysApoptosisComet AssayTumor Suppressor Protein p53DNADNA DamageCarcinogenesis
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MAD2 depletion triggers premature cellular senescence in human primary fibroblasts by activating a P53 pathway preventing aneuploid cells propagation.

2012

The spindle assembly checkpoint (SAC) is a cellular surveillance mechanism that ensures faithful chromosome segregation during mitosis and its failure can result in aneuploidy. Previously, it was suggested that reduction of the MAD2 gene, encoding a major component of the SAC, induced aneuploidy in human tumor cells. However, tumor cell lines contain multiple mutations that might affect or exacerbate the cellular response to Mad2 depletion. Thus, the scenario resulting by Mad2 depletion in primary human cells could be different and more complex that the one depicted so far. We used primary human fibroblasts (IMR90) and epithelial breast cells (MCF10A) to gain further insight on the effects …

Genome instabilityCyclin-Dependent Kinase Inhibitor p21Cell cycle checkpointMad2PhysiologyClinical BiochemistryMAD2 depletion Aneuploidy Premature cellular senescence TP53Cell Cycle ProteinsBiologyCyclin-dependent kinaseChromosome instabilityChromosomal InstabilityTumor Suppressor Protein p14ARFHumansGene SilencingRNA Small InterferingMitosisCells CulturedCellular SenescenceCell ProliferationCalcium-Binding ProteinsCell BiologyCell Cycle CheckpointsFibroblastsAneuploidybeta-GalactosidaseCell biologyRepressor ProteinsSpindle checkpointSettore BIO/18 - GeneticaGene Expression RegulationMad2 Proteinsbiology.proteinM Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Cell agingSignal Transduction
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Functional and genetic characterization of the non-lysosomal glucosylceramidase 2 as a modifier for Gaucher disease.

2013

Background: Gaucher disease (GD) is the most common inherited lysosomal storage disorder in humans, caused by mutations in the gene encoding the lysosomal enzyme glucocerebrosidase (GBA1). GD is clinically heterogeneous and although the type of GBA1 mutation plays a role in determining the type of GD, it does not explain the clinical variability seen among patients. Cumulative evidence from recent studies suggests that GBA2 could play a role in the pathogenesis of GD and potentially interacts with GBA1. Methods: We used a framework of functional and genetic approaches in order to further characterize a potential role of GBA2 in GD. Glucosylceramide (GlcCer) levels in spleen, liver and brain…

GenotypeDiseaseBiologymedicine.disease_causePolymorphism Single NucleotidePathogenesis03 medical and health sciencesMice0302 clinical medicineGenotypemedicineAnimalsGenetics(clinical)Pharmacology (medical)GeneGenetics (clinical)Cells Cultured030304 developmental biologyMedicine(all)Mice Knockout0303 health sciencesMutationGaucher DiseaseReverse Transcriptase Polymerase Chain ReactionResearchGeneral MedicineHematologyFibroblastsHuman genetics3. Good healthGlucosylceramidaseImmunologyGlucosylceramidaseGlucocerebrosidase030217 neurology & neurosurgery
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Yunis-Varón Syndrome Is Caused by Mutations in FIG4, Encoding a Phosphoinositide Phosphatase

2013

Yunis-Varón syndrome (YVS) is an autosomal-recessive disorder with cleidocranial dysplasia, digital anomalies, and severe neurological involvement. Enlarged vacuoles are found in neurons, muscle, and cartilage. By whole-exome sequencing, we identified frameshift and missense mutations of FIG4 in affected individuals from three unrelated families. FIG4 encodes a phosphoinositide phosphatase required for regulation of PI(3,5)P(2) levels, and thus endosomal trafficking and autophagy. In a functional assay, both missense substitutions failed to correct the vacuolar phenotype of Fig4-null mouse fibroblasts. Homozygous Fig4-null mice exhibit features of YVS, including neurodegeneration and enlarg…

GenotypePhosphataseMicrognathismMolecular Sequence DataLimb Deformities CongenitalMutation MissenseBiologyCompound heterozygositymedicine.disease_causeFrameshift mutation03 medical and health sciencesMice0302 clinical medicinePhosphatidylinositol PhosphatesEctodermal DysplasiaReportmedicineGeneticsMissense mutationAnimalsHumansExomeGenetic Predisposition to DiseaseGenetics(clinical)Yunis–Varon syndromeFrameshift MutationGenetics (clinical)030304 developmental biology0303 health sciencesMutationBone DevelopmentBase SequenceFlavoproteinsNeurodegenerationSequence Analysis DNAFibroblastsmedicine.diseaseMolecular biologyPhenotypePhosphoric Monoester HydrolasesCleidocranial Dysplasia030217 neurology & neurosurgeryThe American Journal of Human Genetics
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Isolation and characterization of a 60-70-kD plasma membrane glycoprotein involved in the contact-dependent inhibition of growth

1990

Previous studies have shown that plasma membrane compounds are involved in the contact-dependent inhibition of growth of human diploid fibroblasts. The purification of the active plasma membrane glycoprotein is described in this report. The glycoprotein has an apparent molecular mass of 60-70 kD and, due to differential sialylation, isoelectric points between pH 5.5. and 6.2. Treatment with sialidase yielded one spot in two-dimensional gel electrophoresis with an isoelectric point of 6.3. After removal of the N-glycosidically linked oligosaccharide chains, the apparent molecular mass is reduced by approximately 22 kD. Treatment was diluted NaOH, which removes the O-glycosidically linked por…

GlycanCell CommunicationCell LineAnimalsHumansPolyacrylamide gel electrophoresisCells CulturedCytoskeletonGel electrophoresischemistry.chemical_classificationMembrane GlycoproteinsbiologyMolecular massContact InhibitionCell MembraneContact inhibitionCell BiologyArticlesFibroblastsMolecular biologyMolecular WeightMicroscopy ElectronIsoelectric pointchemistryBiochemistryCell culturebiology.proteinChromatography GelElectrophoresis Polyacrylamide GelGlycoproteinCell DivisionThe Journal of Cell Biology
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Contact-dependent inhibition of growth of normal diploid human fibroblasts by plasma membrane glycoproteins.

1988

Homeostasis in vivo is maintained by a highly complex network of positive and negative signals. At the cellular level, this regulatory microenvironment can be divided, in a simplified fashion, into two major compartments: the humoral compartment, including compounds such as hormones, growth factors and nutrients, and the contact-environment compartment, including cell-cell and cell-matrix interactions. At least in cultures of diploid, non-transformed cells, cell-cell and cell-matrix interactions have been shown to be of major importance for the regulation of growth as well as of differentiation. Although until now the glycoprotein involved in the contact-dependent inhibition of growth has n…

GlycanCell CommunicationPlatelet Membrane GlycoproteinsBiochemistrychemistry.chemical_compoundmedicineCompartment (development)AnimalsHumansReceptors ImmunologicFibroblastReceptorCells Culturedchemistry.chemical_classificationMembrane GlycoproteinsbiologyContact InhibitionCell MembraneAntibodies MonoclonalBiological activityGeneral MedicineFibroblastsMembrane glycoproteinsmedicine.anatomical_structureCell Transformation NeoplasticchemistryBiochemistryPlatelet Glycoprotein GPIb-IX Complexbiology.proteinGrowth inhibitionGlycolipidsGlycoproteinCell DivisionBiochimie
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