Search results for "script"

showing 10 items of 5143 documents

Assessing the reliability of gene expression measurements in very-low-numbers of human monocyte-derived macrophages

2019

Abstract Tumor-derived primary cells are essential for in vitro and in vivo studies of tumor biology. The scarcity of this cellular material limits the feasibility of experiments or analyses and hence hinders basic and clinical research progress. We set out to determine the minimum number of cells that can be analyzed with standard laboratory equipment and that leads to reliable results, unbiased by cell number. A proof-of-principle study was conducted with primary human monocyte-derived macrophages, seeded in decreasing number and constant cell density. Gene expression of cells stimulated to acquire opposite inflammatory states was analyzed by quantitative PCR. Statistical analysis indicat…

Gene Expression ProfilingMacrophageslcsh:RPrimary Cell Culturelcsh:MedicineReal-Time Polymerase Chain ReactionArticle570 Life sciencesCNS cancerGene expression analysisHumanslcsh:QGene ontologylcsh:ScienceTranscriptomeCells Cultured570 Biowissenschaften
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Regulatory RNAs and beyond.

2011

The dynamic regulation of biological processes by RNA has emerged as a key field in recent years, and was the topic of the 62nd Mosbacher Colloquium of the German Society for Biochemistry and Molecular Biology (GBM). The 2011 Colloquium, held in April in the romantic Neckar-river region, was also a celebration of the tenth anniversary of the RNA Biochemistry study group within the GBM, which acts as platform for RNA biologists and chemists within Germany and in other European countries.

Gene Expression ProfilingRNARNA-Binding ProteinsBiologyRNA BiochemistryBioinformaticsBiochemistrylanguage.human_languageGermanUpfrontGene Expression RegulationRegulatory sequenceGeneticslanguageHumansRNAPost-transcriptional regulationMolecular BiologyClassicsEMBO reports
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Role for Tumor Necrosis Factor Alpha in Murine Cytomegalovirus Transcriptional Reactivation in Latently Infected Lungs

2004

ABSTRACT Interstitial pneumonia is a major clinical manifestation of primary or recurrent cytomegalovirus (CMV) infection in immunocompromised recipients of a bone marrow transplant. In a murine model, lungs were identified as a prominent site of CMV latency and recurrence. Pulmonary latency of murine CMV is characterized by high viral genome burden and a low incidence of variegated immediate-early (IE) gene expression, reflecting a sporadic activity of the major IE promoters (MIEPs) and enhancer. The enhancer-flanking promoters MIEP1/3 and MIEP2 are switched on and off during latency in a ratio of ∼2:1. MIEP1/3 latency-associated activity generates the IE1 transcript of the ie1/3 transcrip…

Gene Expression Regulation ViralHuman cytomegalovirusMuromegalovirusTranscription GeneticImmunologyBiologyMicrobiologyImmediate early proteinImmediate-Early ProteinsMiceViral ProteinsTransactivationVirologyGene expressionVirus latencymedicineAnimalsHumansEnhancerLungBone Marrow TransplantationMice Inbred BALB CTumor Necrosis Factor-alphaAlternative splicingPromoterHerpesviridae Infectionsmedicine.diseaseVirologyVirus LatencyVirus-Cell InteractionsDisease Models AnimalTransplantation IsogeneicInsect ScienceFemaleVirus ActivationJournal of Virology
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Enhancerless Cytomegalovirus Is Capable of Establishing a Low-Level Maintenance Infection in Severely Immunodeficient Host Tissues but Fails in Expon…

2010

ABSTRACT Major immediate-early transcriptional enhancers are genetic control elements that act, through docking with host transcription factors, as a decisive regulatory unit for efficient initiation of the productive virus cycle. Animal models are required for studying the function of enhancers paradigmatically in host organs. Here, we have sought to quantitatively assess the establishment, maintenance, and level of in vivo growth of enhancerless mutants of murine cytomegalovirus in comparison with those of an enhancer-bearing counterpart in models of the immunocompromised or immunologically immature host. Evidence is presented showing that enhancerless viruses are capable of forming restr…

Gene Expression Regulation ViralMutantImmunology/dk/atira/pure/subjectarea/asjc/2400/2406CytomegalovirusMice SCIDBiologyMicrobiologyVirusImmunocompromised HostMiceExponential growthIn vivoVirologyAnimalsHumans/dk/atira/pure/subjectarea/asjc/2400/2403EnhancerTranscription factorMice Inbred BALB CVirologyGenome Replication and Regulation of Viral Gene ExpressionEnhancer Elements GeneticInsect ScienceCytomegalovirus InfectionsHost-Pathogen InteractionsCytomegalovirus infections
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Oxidative stress inhibits IFN-α-induced antiviral gene expression by blocking the JAK–STAT pathway

2006

Abstract BACKGROUND/AIMS: Unresponsiveness to IFN-alpha is common in chronic hepatitis C. Since conditions associated with an increased oxidative stress (advanced age, steatosis, fibrosis, iron overload, and alcohol consumption) reduce the likelihood of response, we hypothesized that oxidative stress may affect the antiviral actions of IFN-alpha. METHODS: We examined in a human hepatocellular carcinoma cell line (Huh-7) the effect of hydrogen peroxide (H2O2), as a generator of oxidative stress, on the IFN-alpha signaling pathway. RESULTS: Pretreatment of Huh-7 cells with 0.5-1 mM H2O2 resulted in the suppression of the IFN-alpha-induced antiviral protein MxA and of IRF-9 mRNA expression. Th…

Gene Expression Regulation ViralMyxovirus Resistance ProteinsCarcinoma HepatocellularBlotting WesternAntiviral proteinProtein tyrosine phosphataseInterferon alpha-2Biologymedicine.disease_causechemistry.chemical_compoundGTP-Binding ProteinsCell Line TumormedicineHumansRNA NeoplasmHepatologyTyk-2Reverse Transcriptase Polymerase Chain ReactionSTATLiver NeoplasmsInterferon-alphaJAK-STAT signaling pathwayTyrosine phosphorylationHydrogen PeroxideJanus Kinase 1Flow CytometryInterferon-Stimulated Gene Factor 3 gamma SubunitRecombinant ProteinsIFN-aJAK-1Oxidative StressSTAT Transcription FactorsHydrogen peroxide; IFN-a; STAT; JAK-1; Tyk-2chemistryImmunologySTAT proteinCancer researchSignal transductionTyrosine kinaseOxidative stressSignal TransductionJournal of Hepatology
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Bacteriophage GIL01 gp7 interacts with host LexA repressor to enhance DNA binding and inhibit RecA-mediated auto-cleavage

2015

The SOS response in Eubacteria is a global response to DNA damage and its activation is increasingly associated with the movement of mobile genetic elements. The temperate phage GIL01 is induced into lytic growth using the host's SOS response to genomic stress. LexA, the SOS transcription factor, represses bacteriophage transcription by binding to a set of SOS boxes in the lysogenic promoter P1. However, LexA is unable to efficiently repress GIL01 transcription unless the small phage-encoded protein gp7 is also present. We found that gp7 forms a stable complex with LexA that enhances LexA binding to phage and cellular SOS sites and interferes with RecA-mediated auto-cleavage of LexA, the ke…

Gene Expression Regulation ViralSOS responsebacteriophagesTranscription GeneticvirusesRepressorBacillus PhagesBiologybakteriofagitBacteriophage03 medical and health sciencesSOS Response (Genetics)Viral ProteinsBacterial ProteinsLysogenic cycleGeneticsSOS responsePromoter Regions GeneticSOS Response GeneticsTranscription factor030304 developmental biologyGenetics0303 health sciences030306 microbiologyLexA repressorGene regulation Chromatin and EpigeneticsSerine Endopeptidasesta1182DNAbiochemical phenomena metabolism and nutritionbiology.organism_classification3. Good healthCell biologyRepressor Proteinsenzymes and coenzymes (carbohydrates)Rec A RecombinasesLytic cyclebacteriaRepressor lexAProtein BindingNucleic Acids Research
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Patchwork Pattern of Transcriptional Reactivation in the Lungs Indicates Sequential Checkpoints in the Transition from Murine Cytomegalovirus Latency…

1999

The lungs are a relevant organ site of primary and recurrent human cytomegalovirus (hCMV) disease (for overviews, see references 21, 22, 31, 34, 39, and 44). Murine CMV (mCMV) can serve us as a model for studying CMV pneumonia in acute infection (6, 27, 33, 37) as well as for studying viral latency, reactivation, and recurrence in the lungs (2, 17, 18, 42, 43). We have shown recently that transcription from the major immediate-early (MIE) transcription unit ie1-ie3 (hereafter referred to as ie1/3), which is driven by a strong MIE promoter-enhancer (MIEPE) (3), occurs during pulmonary latency of mCMV but fails to initiate the productive cycle (17). Notably, the paralogous MIEPE of hCMV can f…

Gene Expression Regulation ViralTranscriptional ActivationHuman cytomegalovirusvirusesImmunologyCytomegalovirusReplicationBiologyMicrobiologyMiceTransactivationTranscription (biology)VirologyGene expressionVirus latencymedicineAnimalsEnhancerGenes Immediate-EarlyLungTranscription factorMice Inbred BALB CEffectormedicine.diseaseVirologyVirus LatencyInsect ScienceCytomegalovirus InfectionsFemaleVirus ActivationTranscription FactorsJournal of Virology
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Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice

2002

The serine-threonine kinase Akt seems to be central in mediating stimuli from different classes of receptors. In fact, both IGF-1 and IL6-like cytokines induce hypertrophic and antiapoptotic signals in cardiomyocytes through PI3K-dependent Akt activation. More recently, it was shown that Akt is involved also in the hypertrophic and antiapoptotic effects of β-adrenergic stimulation. Thus, to determine the effects of Akt on cardiac function in vivo, we generated a model of cardiac-specific Akt overexpression in mice. Transgenic mice were generated by using the E40K, constitutively active mutant of Akt linked to the rat α-myosin heavy chain promoter. The effects of cardiac-selective Akt overex…

Gene ExpressionTransgenicGlycogen Synthase Kinase 3MiceGSK-3Receptorsgenetics/physiologycytology/metabolismMultidisciplinaryBiological SciencesProtein-Serine-Threonine KinasesDNA-Binding Proteinsenzymology/genetics/pathologyAdrenergicPhosphorylationSignal transductionMitogen-Activated Protein KinasesSignal Transductionmedicine.medical_specialtyCardiomyopathyAnimals; Calcium-Calmodulin-Dependent Protein Kinases; metabolism; Cardiomyopathy; Hypertrophic; enzymology/genetics/pathology; Cell Size; physiology; DNA-Binding Proteins; GATA4 Transcription Factor; Gene Expression; Glycogen Synthase Kinase 3; Mice; Transgenic; Mitogen-Activated Protein Kinases; Myocardial Contraction; Myocardium; cytology/metabolism; Point Mutation; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins; genetics/physiology; Rats; Receptors; Adrenergic; beta; Signal Transduction; Transcription FactorsMice TransgenicBiologyProtein Serine-Threonine KinasesContractilityIn vivoInternal medicineProto-Oncogene ProteinsReceptors Adrenergic betamedicineAnimalsPoint MutationGlycogen synthaseProtein kinase BPI3K/AKT/mTOR pathwayCell SizeMyocardiumCardiomyopathy HypertrophicMyocardial ContractionGATA4 Transcription FactorRatsEndocrinologyHypertrophicphysiologyCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinbetametabolismProto-Oncogene Proteins c-aktTranscription Factors
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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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Midregion PTHrP and Human Breast Cancer Cells

2010

PTHrP is a polyhormone undergoing proteolytic processing into smaller bioactive forms, comprising an N-terminal peptide, which is the mediator of the “classical” PTH-like effect, as well as midregion and C-terminal peptides. The midregion PTHrP domain (38-94)-amide was found to restrain growth and invasionin vitroof some breast cancer cell lines, causing striking toxicity and accelerating death; the most responsive being MDA-MB231, whose tumorigenesis was also attenuatedin vivo. In addition, midregion PTHrP appears to be imported in the nucleoplasm of cultured MDA-MB231 cells andin vitro, it can bind chromatin of metaphase spread preparations and also an isolated 20-mer oligonucleotide, the…

Gene Expressionlcsh:MedicineBreast NeoplasmsDNA FragmentationBiologymedicine.disease_causelcsh:TechnologyGeneral Biochemistry Genetics and Molecular BiologyTranscription (biology)Cell Line TumorPTHrP breast cancer cancer cell gene expression cytotoxicityGene expressionmedicineHumansSettore BIO/06 - Anatomia Comparata E CitologiaMDA-MB231lcsh:ScienceDNA statusGeneral Environmental ScienceMini-Review ArticleNucleoplasmlcsh:Tmidregion PTHrPlcsh:RParathyroid Hormone-Related ProteinapoptosisGeneral MedicineMolecular biologynuclear importIn vitroCell biologyChromatinPTHrP (38-94)Cancer cellprotein degradationFemalelcsh:QCarcinogenesisReprogrammingbreast cancer cellsThe Scientific World Journal
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