Search results for "Gene expression"

showing 10 items of 4085 documents

MYC and EGR1 synergize to trigger tumor cell death by controlling NOXA and BIM transcription upon treatment with the proteasome inhibitor bortezomib

2014

The c-MYC (MYC afterward) oncogene is well known for driving numerous oncogenic programs. However, MYC can also induce apoptosis and this function of MYC warrants further clarification. We report here that a clinically relevant proteasome inhibitor significantly increases MYC protein levels and that endogenous MYC is necessary for the induction of apoptosis. This kind of MYC-induced cell death is mediated by enhanced expression of the pro-apoptotic BCL2 family members NOXA and BIM. Quantitative promoter-scanning chromatin immunoprecipitations (qChIP) further revealed binding of MYC to the promoters of NOXA and BIM upon proteasome inhibition, correlating with increased transcription. Both pr…

Programmed cell deathTranscription GeneticEGR1ApoptosisBiologyBortezomibProto-Oncogene Proteins c-mycMicehemic and lymphatic diseasesCell Line TumorProto-Oncogene ProteinsGeneticsmedicineAnimalsPromoter Regions GeneticTranscription factorCells CulturedEarly Growth Response Protein 1Zinc finger transcription factorBinding SitesOncogeneBcl-2-Like Protein 11Genes p16Gene regulation Chromatin and EpigeneticsMembrane ProteinsPromoterGenes p53Boronic AcidsChromatinddc:Gene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2PyrazinesCancer researchProteasome inhibitorApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
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Evidence for an instructive role of apoptosis during the metamorphosis of Hydractinia echinata (Hydrozoa)

2011

Apoptosis is a highly conserved mechanism of cell deletion that destroys redundant, dysfunctional, damaged, and diseased cells. Furthermore, apoptotic cell death is essential during the development of multicellular organisms. However, there are only a few examples where the occurrence of apoptosis has been shown to be a direct prerequisite for developmental processes. As described previously by our group, the degradation of larval tissue during the first half of the metamorphosis of Hydractinia echinata involves extensive cell death. A large number of cells are removed, and we observed several cellular features of apoptotic cell death in the dying tissue, e.g., nucleosomal DNA fragmentation…

Programmed cell deathmedia_common.quotation_subjectMolecular Sequence DataCellApoptosisContext (language use)Gene Expression Regulation EnzymologicHydractinia echinatamedicineAnimalsAmino Acid SequenceMetamorphosisConserved SequencePhylogenyCaspasemedia_commonbiologyGene Expression ProfilingMetamorphosis Biologicalbiology.organism_classificationCell biologyHydrozoamedicine.anatomical_structureApoptosisCaspasesGene Knockdown Techniquesbiology.proteinDNA fragmentationAnimal Science and ZoologySequence AlignmentZoology
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Berberine inhibits cell growth and mediates caspase-independent cell death in human pancreatic cancer cells.

2010

Pancreatic cancer is one of the most aggressive human malignancies with an increasing incidence worldwide. In addition to the poor survival rates, combinations using gemcitabine as a backbone have failed to show any benefit beyond monotherapy. These facts underscore an urgent need for novel therapeutic options and motivated us to study the effect of berberine on pancreatic cancer cells. Here, we undertook an mRNA-based gene expression profiling study in order to get deeper insight into the molecular targets mediating the growth inhibitory effects of berberine on pancreatic cancer cells compared to normal ones. Twenty-four hours after treatment, berberine showed preferential selectivity towa…

Programmed cell deathmedicine.medical_specialtyBerberineDNA damagePharmaceutical ScienceApoptosisAnalytical Chemistrychemistry.chemical_compoundBerberinePancreatic cancerInternal medicineCell Line TumorDrug DiscoverymedicineHumansRNA MessengerCell ProliferationOligonucleotide Array Sequence AnalysisPharmacologybiologyCell growthTopoisomeraseGene Expression ProfilingOrganic ChemistryCancermedicine.diseaseAntineoplastic Agents PhytogenicCaspase InhibitorsImmunohistochemistryEnzyme ActivationPancreatic NeoplasmsEndocrinologyComplementary and alternative medicinechemistryApoptosisCaspasesbiology.proteinCancer researchMolecular MedicineSignal TransductionPlanta medica
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Extracorporeal shock wave-mediated changes in proliferation, differentiation, and gene expression of human osteoblasts.

2008

The goal of this study was to determine whether cell proliferation, differentiation, and gene expression of primary human osteoblasts (hOB) are influenced by shock wave application (SWA).Osteoblast cultures were isolated from cancellous bone fragments and treated with 500 impulses of energy flux densities of 0.06 mJ/mm, 0.18 mJ/mm, 0.36 mJ/mm, and 0.50 mJ/mm. Twenty-four hours and 96 hours after SWA cell proliferation, alkaline phosphatase activity, and mineralization were analyzed. The global gene expression profiling was determined 96 hours after SWA employing Affymetrix HG-U133A microarrays.After 24 hours, hOB showed a dose-dependent increase in cell proliferation from 68.7% (at 0.06 mJ/…

Proliferation differentiationGene ExpressionIn Vitro TechniquesCritical Care and Intensive Care MedicineHigh-Energy Shock WavesBone DensityGene expressionmedicineHumansHigh-Density MicroarrayOligonucleotide Array Sequence AnalysisOsteoblastsCell growthbusiness.industryReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingOsteoblastCell DifferentiationAnatomyExtracorporeal shock waveAlkaline PhosphataseCell biologyGene expression profilingmedicine.anatomical_structureSurgerybusinessCancellous boneCell DivisionThe Journal of trauma
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Development of a second generation of inhibitors of microsomal prostaglandin E synthase 1 expression bearing the γ-hydroxybutenolide scaffold

2008

Petrosaspongiolide M (PM), a marine sesterterpene metabolite bearing the gamma-hydroxybutenolide scaffold and displaying a potent inhibitory activity toward PLA(2) enzyme, was selected by us as an attractive target in order to explore its mechanism of action at molecular level. In the course of our investigations we decided to synthetically modify the parent compound to clarify the structural determinants responsible for the activity; in fact, very recently, our research group reported the synthesis and the pharmacological properties of a first collection of PM analogues generated by Ludi approach. The synthesized compounds showed a poor or moderate activity toward PLA(2) enzymes, neverthel…

Prostaglandin AntagonistsStereochemistryMetaboliteClinical BiochemistryAnti-Inflammatory AgentsPharmaceutical ScienceIsomeraseProstaglandin E synthaseBiochemistryChemical synthesisCell LineMiceStructure-Activity Relationshipchemistry.chemical_compound4-ButyrolactoneMicrosomesDrug DiscoverymedicineAnimalsEnzyme InhibitorsProstaglandin E2Molecular BiologyProstaglandin-E Synthaseschemistry.chemical_classificationBinding SitesbiologyChemistryMacrophagesOrganic ChemistryIntramolecular OxidoreductasesPhospholipases A2EnzymeGene Expression RegulationMechanism of actionBiochemistryCyclooxygenase 2Enzyme inhibitorbiology.proteinMolecular Medicinelipids (amino acids peptides and proteins)medicine.symptommedicine.drugBioorganic & Medicinal Chemistry
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Enzymatically modified LDL induces cathepsin H in human monocytes: potential relevance in early atherogenesis.

2003

Objective—Modification with proteases and cholesterylesterase transforms LDL to a moiety that resembles lipoproteins isolated from atherosclerotic lesions and possesses atherogenic properties. To identify changes in monocyte-derived foam cells laden with enzymatically modified LDL (E-LDL), we compared patterns of the most abundant transcripts in these cells after incubation with LDL or E-LDL.Methods and Results—Serial analyses of gene expression (SAGE) libraries were constructed from human monocytes after treatment with LDL or E-LDL. Several tags were differentially expressed in LDL-treated versus E-LDL–treated cells, whereby marked selective induction by E-LDL of cathepsin H was conspicuou…

ProteasesCathepsin HCoronary Artery DiseaseBiologyCathepsin HCathepsin L1medicineMacrophageHumansFoam cellGene LibraryCathepsinMonocyteGene Expression ProfilingColocalizationSterol EsteraseMolecular biologyCathepsinsLipoproteins LDLCysteine Endopeptidasesmedicine.anatomical_structureCholesterolBiochemistryGene Expression Regulationlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineFoam CellsArteriosclerosis, thrombosis, and vascular biology
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Dominant role of paraoxonases in inactivation of the Pseudomonas aeruginosa quorum-sensing signal N-(3-oxododecanoyl)-L-homoserine lactone.

2008

Pseudomonas aeruginosa is an opportunistic bacterium which causes serious infections in immunocompromised and cystic fibrosis patients (10). As with many gram-negative bacteria, P. aeruginosa produces acyl-homoserine lactone (AHL) quorum-sensing (QS) signaling molecules termed autoinducers which allow the single-celled organisms to coordinate their actions (36). N-(3-Oxododecanoyl)-l-homoserine lactone (3OC12-HSL) is a key autoinducer synthesized by P. aeruginosa which regulates the expression of extracellular virulence factors and biofilm formation (5, 36). Rats and mice experimentally infected with P. aeruginosa mutants deficient in the ability to produce or respond to 3OC12-HSL exhibited…

ProteasesCell signalingImmunologyHomoserineBiologymedicine.disease_causeMicrobiologyMicrobiologychemistry.chemical_compoundMice4-ButyrolactonemedicineHomoserineLeukocyte proliferationAnimalsHumansLungEdetic AcidMice Inbred ICRPseudomonas aeruginosaAryldialkylphosphataseHydrolysisBiofilmEsterasesfood and beveragesQuorum SensingGene Expression Regulation BacterialMolecular PathogenesisQuorum sensingInfectious DiseasesBiochemistrychemistryLiverMetalsPseudomonas aeruginosaParasitologyAutoinducerInfection and immunity
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Morpholino knockdown of the ubiquitously expressed transmembrane serine protease TMPRSS4a in zebrafish embryos exhibits severe defects in organogenes…

2011

AbstractOver the past years the members of the type II transmembrane serine protease (TTSP) family have emerged as new players in mammalian biology. TMPRSS4 (transmembraneprotease/serine) is overexpressed in several human cancer tissues, promoting invasion, migration, and metastasis. However, the physiological function has not yet been elucidated. Here, we present morpholino knockdown studies targeting TMPRSS4a, a homolog of human TMPRSS4 in zebrafish embryos. By RT-PCR, we could demonstrate an expression of this protease already 5 h post-fertilization, suggesting important functions in the early stages of embryonic development. Indeed,in vivogene silencing caused severe defects in tissue d…

ProteasesEmbryo NonmammalianMorpholinoOrganogenesisCellular differentiationmedicine.medical_treatmentMolecular Sequence DataClinical BiochemistryBiologyBiochemistry03 medical and health sciences0302 clinical medicineCell AdhesionmedicineAnimalsHumansAmino Acid SequenceCell adhesionMolecular BiologyPhylogenyZebrafish030304 developmental biologySerine protease0303 health sciencesProteaseCell adhesion moleculeGene Expression ProfilingSerine EndopeptidasesProteolytic enzymesGene Expression Regulation DevelopmentalMembrane ProteinsCell DifferentiationZebrafish ProteinsMolecular biologyGene Knockdown Techniques030220 oncology & carcinogenesisbiology.proteinSequence AlignmentBiological Chemistry
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Bortezomib Partially Improves Laminin α2 Chain–Deficient Muscular Dystrophy

2014

Congenital muscular dystrophy, caused by mutations in LAMA2 (the gene encoding laminin α2 chain), is a severe and incapacitating disease for which no therapy is yet available. We have recently demonstrated that proteasome activity is increased in laminin α2 chain-deficient muscle and that treatment with the nonpharmaceutical proteasome inhibitor MG-132 reduces muscle pathology in laminin α2 chain-deficient dy(3K)/dy(3K) mice. Here, we explore the use of the selective and therapeutic proteasome inhibitor bortezomib (currently used for treatment of relapsed multiple myeloma and mantle cell lymphoma) in dy(3K)/dy(3K) mice and in congenital muscular dystrophy type 1A muscle cells. Outcome measu…

Proteasome Endopeptidase ComplexApoptosisBiologyPathology and Forensic MedicineBortezomibmedicineAnimalsMyocyteMuscular dystrophyCells CulturedMultiple myelomaMuscle CellsMyogenesisBortezomibMusclesBody WeightMuscular Dystrophy Animalmedicine.diseaseBoronic AcidsFibrosisSurvival AnalysisMice Inbred C57BLDisease Models AnimalMicroRNAsGene Expression RegulationOrgan SpecificityPyrazinesCongenital muscular dystrophyCancer researchProteasome inhibitorMantle cell lymphomaLamininLocomotionmedicine.drugThe American Journal of Pathology
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Glucocorticoids inhibit MAP kinase via increased expression and decreased degradation of MKP-1

2001

Glucocorticoids inhibit the proinflammatory activities of transcription factors such as AP-1 and NF-kappa B as well as that of diverse cellular signaling molecules. One of these signaling molecules is the extracellular signal-regulated kinase (Erk-1/2) that controls the release of allergic mediators and the induction of proinflammatory cytokine gene expression in mast cells. The mechanism of inhibition of Erk-1/2 activity by glucocorticoids is unknown. Here we report a novel dual action of glucocorticoids for this inhibition. Glucocorticoids increase the expression of the MAP kinase phosphatase-1 (MKP-1) gene at the promoter level, and attenuate proteasomal degradation of MKP-1, which we re…

Proteasome Endopeptidase ComplexCell signalingMitogen-Activated Protein Kinase 3Cell Cycle ProteinsBiologyDexamethasoneGene Expression Regulation EnzymologicArticleGeneral Biochemistry Genetics and Molecular BiologyCell LineImmediate-Early ProteinsProinflammatory cytokineMiceGlucocorticoid receptorMultienzyme ComplexesProtein Phosphatase 1Phosphoprotein PhosphatasesAnimalsEnzyme InhibitorsPhosphorylationMolecular BiologyTranscription factorDNA PrimersMitogen-Activated Protein Kinase 1Regulation of gene expressionMitogen-Activated Protein Kinase 3Base SequenceGeneral Immunology and MicrobiologyKinaseHydrolysisGeneral NeuroscienceDual Specificity Phosphatase 1Cell biologyMice Inbred C57BLCysteine EndopeptidasesMitogen-activated protein kinasebiology.proteinMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesThe EMBO Journal
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