Search results for "Gene expression"

showing 10 items of 4085 documents

Functioning of DcuC as the C 4 -Dicarboxylate Carrier during Glucose Fermentation by Escherichia coli

1999

ABSTRACT The dcuC gene of Escherichia coli encodes an alternative C 4 -dicarboxylate carrier (DcuC) with low transport activity. The expression of dcuC was investigated. dcuC was expressed only under anaerobic conditions; nitrate and fumarate caused slight repression and stimulation of expression, respectively. Anaerobic induction depended mainly on the transcriptional regulator FNR. Fumarate stimulation was independent of the fumarate response regulator DcuR. The expression of dcuC was not significantly inhibited by glucose, assigning a role to DcuC during glucose fermentation. The inactivation of dcuC increased fumarate-succinate exchange and fumarate uptake by DcuA and DcuB, suggesting a…

Physiology and MetabolismMolecular Sequence DataMutantStimulationBiologymedicine.disease_causeMicrobiologyBacterial ProteinsFumaratesConsensus SequenceEscherichia colimedicineTranscriptional regulationDicarboxylic AcidsAnaerobiosisPromoter Regions GeneticMolecular BiologyEscherichia coliPsychological repressionDicarboxylic Acid TransportersBinding SitesBase SequenceEscherichia coli ProteinsSuccinatesGene Expression Regulation BacterialKineticsResponse regulatorGlucoseBiochemistryFermentationFermentationEffluxCarrier ProteinsRibosomesJournal of Bacteriology
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Regulation of aerobic and anaerobic D-malate metabolism of Escherichia coli by the LysR-type regulator DmlR (YeaT).

2010

ABSTRACT Escherichia coli K-12 is able to grow under aerobic conditions on d -malate using DctA for d -malate uptake and the d -malate dehydrogenase DmlA (formerly YeaU) for converting d -malate to pyruvate. Induction of dmlA encoding DmlA required an intact dmlR (formerly yeaT ) gene, which encodes DmlR, a LysR-type transcriptional regulator. Induction of dmlA by DmlR required the presence of d -malate or l - or meso -tartrate, but only d -malate supported aerobic growth. The regulator of general C 4 -dicarboxylate metabolism (DcuS-DcuR two-component system) had some effect on dmlA expression. The anaerobic l -tartrate regulator TtdR or the oxygen sensors ArcB-ArcA and FNR did not have a m…

Physiology and MetabolismRegulatorMalatesDehydrogenasemedicine.disease_causeMicrobiologyMalate dehydrogenaseMicrobiologyMalate DehydrogenasemedicineAnaerobiosisMolecular BiologyEscherichia coliTartratesChromatography High Pressure LiquidbiologyEscherichia coli K12Escherichia coli ProteinsMetabolismGene Expression Regulation Bacterialbiology.organism_classificationbeta-GalactosidaseAerobiosisBiochemistryMutationFermentationAnaerobic exerciseBacteriaJournal of bacteriology
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Arabidopsis copper transport protein COPT2 participates in the crosstalk between iron deficiency responses and low phosphate signaling

2013

[EN] Copper and iron are essential micronutrients for most living organisms because they participate as cofactors in biological processes, including respiration, photosynthesis, and oxidative stress protection. In many eukaryotic organisms, including yeast (Saccharomyces cerevisiae) and mammals, copper and iron homeostases are highly interconnected; yet, such interdependence is not well established in higher plants. Here, we propose that COPT2, a high-affinity copper transport protein, functions under copper and iron deficiencies in Arabidopsis (Arabidopsis thaliana). COPT2 is a plasma membrane protein that functions in copper acquisition and distribution. Characterization of the COPT2 expr…

PhysiologyArabidopsisPlant SciencePlant RootsMembranes Transport and BioenergeticsGene Expression Regulation PlantArabidopsisThalianaHomeostasisArabidopsis thalianaSLC31 ProteinsGene-expressionCation Transport ProteinsChlorosisbiologyRevealsIron DeficienciesMetal homeostasisPlantsPlants Genetically ModifiedUp-RegulationTransport proteinPhenotypeBiochemistrySignal TransductionIronRecombinant Fusion ProteinsSaccharomyces cerevisiaechemistry.chemical_elementSaccharomyces cerevisiaeModels BiologicalPhosphatesEthyleneGeneticsmedicineBIOQUIMICA Y BIOLOGIA MOLECULARFamilyIron deficiency (plant disorder)Arabidopsis ProteinsBiological TransportRoot elongationSequence Analysis DNAbiology.organism_classificationmedicine.diseaseCopperPlant LeavesAcquisitionchemistrySeedlingsStarvationMutationCopper deficiencyCopper
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A new gene superfamily of pathogen-response (repat) genes in Lepidoptera: Classification and expression analysis

2012

Repat (REsponse to PAThogens) genes were first identified in the midgut of Spodoptera exigua (Lepidoptera: Noctuidae) in response to Bacillus thuringiensis and baculovirus exposure. Since then, additional repat gene homologs have been identified in different studies. In this study the comprehensive larval transcriptome from S. exigua was analyzed for the presence of novel repat-homolog sequences. These analyses revealed the presence of at least 46 repat genes in S. exigua, establishing a new gene superfamily in this species. Phylogenetic analysis and studies of conserved motifs in these hypothetical proteins have allowed their classification in two main classes, αREPAT and βREPAT. Studies o…

PhysiologyBacillus thuringiensisGenes InsectSpodopteradigestive systemBiochemistryTranscriptomeHemolysin ProteinsBacterial ProteinsBacillus thuringiensisGene expressionExiguaAnimalsMolecular BiologyGeneGeneticsBacillus thuringiensis ToxinsbiologyGene Expression ProfilingStem CellsfungiMidgutbiology.organism_classificationMolecular biologyEndotoxinsIntestinesLepidopteraGene expression profilingLarvaMetagenomeComparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology
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Mapping Brain Response to Social Stress in Rodents With c-fos Expression: A Review

2002

Social defeat is an important event in the life of many animals, and forms part of the process of social control. Adapting to social defeat is thus an intrinsic part of social "homeostasis", and mal-adaptation may have pathological sequelae. Experimental models of social defeat (e.g. inter-male aggression) have existed for many years. However, very few studies have investigated the changes in brain activity in male animals exposed to the social stress of being defeated by another conspecific male, and in all these studies the expression of the immediate-early gene c-fos has been used as the marker of neuronal activity. In general, the results obtained inform that many areas of the brain, es…

PhysiologyBrain activity and meditationRodentiac-FosBrain mappingSocial defeatBehavioral NeurosciencemedicineAnimalsPremovement neuronal activityHabituationSocial stressBrain MappingbiologyEndocrine and Autonomic SystemsAggressionBrainGenes fosPsychiatry and Mental healthNeuropsychology and Physiological PsychologyGene Expression Regulationbiology.proteinmedicine.symptomPsychologyNeuroscienceStress PsychologicalStress
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The PVT-1 oncogene is a Myc protein target that is overexpressed in transformed cells

2007

The human PVT-1 gene is located on chromosome 8 telomeric to the c-Myc gene and it is frequently involved in the translocations occurring in variant Burkitt's lymphomas and murine plasmacytomas. It has been proposed that PVT-1 regulates c-Myc gene transcription over a long distance. To get new insights into the functional relationships between the two genes, we have investigated PVT-1 and c-Myc expression in normal human tissues and in transformed cells. Our findings indicate that PVT-1 expression is restricted to a relative low number of normal tissues compared to the wide distribution of c-Myc mRNA, whereas the gene is highly expressed in many transformed cell types including neuroblastom…

PhysiologyClinical BiochemistryBiologyCell LineProto-Oncogene Proteins c-mycGenes ReporterNeoplasmsC-MYCAnimalsHumansTissue DistributionPromoter Regions GeneticGeneGENE-EXPRESSIONRegulation of gene expressionReporter geneOncogeneProteinsCell BiologyTransfectionMolecular biologyPVT1Cell Transformation NeoplasticGene Expression RegulationPVT-1Cell cultureRNA Long NoncodingChromatin immunoprecipitationJournal of Cellular Physiology
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Type V collagen regulates the expression of apoptotic and stress response genes by breast cancer cells.

2004

Type V collagen is a "minor" component of normal human breast stroma, which is subjected to over-deposition in cases of ductal infiltrating carcinoma (DIC). We reported that, if used as a culture substrate for the DIC cell line 8701-BC, it exhibited poorly-adhesive properties and restrained the proliferative and motile behavior of the cell subpopulation able to attach onto it. Moreover, this collagen species was able to trigger DNA fragmentation and impair survival of 8701-BC cells. In this study, we have extended our investigation with the aim to obtain further evidence that the death induced by type V collagen was of the apoptotic type by (i) microscopic detection and quantitation of Apop…

PhysiologyClinical BiochemistryCellApoptosisBreast NeoplasmsEnzyme activatorCell Line TumormedicineHumansSettore BIO/06 - Anatomia Comparata E CitologiaCaspaseHeat-Shock ProteinsbiologyCarcinoma Ductal BreastCell BiologyMolecular biologyIn vitroEnzyme ActivationGene Expression Regulation Neoplasticmedicine.anatomical_structurecollagen breast cancer gene expressionApoptosisCell cultureCaspasesbiology.proteinDNA fragmentationHSP60FemaleCollagen Type VJournal of cellular physiology
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TLR4 abrogates the Th1 immune response through IRF1 and IFN-β to prevent immunopathology during L. infantum infection

2020

A striking feature of human visceral leishmaniasis (VL) is chronic inflammation in the spleen and liver, and VL patients present increased production levels of multiple inflammatory mediators, which contribute to tissue damage and disease severity. Here, we combined an experimental model with the transcriptional profile of human VL to demonstrate that the TLR4-IFN-β pathway regulates the chronic inflammatory process and is associated with the asymptomatic form of the disease. Tlr4-deficient mice harbored fewer parasites in their spleen and liver than wild-type mice. TLR4 deficiency enhanced the Th1 immune response against the parasite, which was correlated with an increased activation of de…

PhysiologyGene ExpressionWhite Blood CellsMiceCell SignalingAnimal CellsImmune PhysiologyZoonosesImmunopathologyMedicine and Health SciencesMembrane Receptor SignalingBiology (General)Immune ResponseLeishmaniasisProtozoansLeishmaniaMice Knockout0303 health sciencesbiologyT Cells030302 biochemistry & molecular biologyEukaryotaImmune Receptor SignalingInfectious Diseasesmedicine.anatomical_structureLeishmaniasis VisceralCellular Typesmedicine.symptomLeishmania infantumResearch ArticleSignal TransductionNeglected Tropical DiseasesQH301-705.5Leishmania InfantumImmune CellsImmunologySpleenInflammationLEISHMANIOSE VISCERALMicrobiology03 medical and health sciencesImmune systemVirologyParasitic DiseasesGeneticsmedicineAnimalsMolecular Biology030304 developmental biologyInflammationProtozoan InfectionsBlood CellsOrganismsBiology and Life SciencesCell BiologyInterferon-betaTh1 CellsRC581-607Tropical Diseasesmedicine.diseasebiology.organism_classificationParasitic ProtozoansToll-Like Receptor 4IRF1Visceral leishmaniasisImmunologyTLR4ParasitologyImmunologic diseases. AllergySpleenInterferon Regulatory Factor-1
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Paratransgenic manipulation of a tsetse microRNA alters the physiological homeostasis of the fly’s midgut environment

2021

Tsetse flies are vectors of parasitic African trypanosomes, the etiological agents of human and animal African trypanosomoses. Current disease control methods include fly-repelling pesticides, fly trapping, and chemotherapeutic treatment of infected people and animals. Inhibiting tsetse’s ability to transmit trypanosomes by strengthening the fly’s natural barriers can serve as an alternative approach to reduce disease. The peritrophic matrix (PM) is a chitinous and proteinaceous barrier that lines the insect midgut and serves as a protective barrier that inhibits infection with pathogens. African trypanosomes must cross tsetse’s PM in order to establish an infection in the fly, and PM struc…

PhysiologyGenes InsectBiochemistryAnimals Genetically ModifiedMedical ConditionsGene expressionMedicine and Health SciencesHomeostasisPeritrophic matrixBiology (General)Protozoans0303 health sciencesbiologyGene OntologiesSodalis glossinidiusEukaryotaCardiaGenomicsBody FluidsCell biologyIntestinesNucleic acidsBloodDigestionAnatomyResearch ArticleSymbiotic bacteriaTrypanosomaTsetse FliesQH301-705.5ImmunologyParatransgenesisMicrobiology03 medical and health sciencesVirologyParasitic DiseasesGeneticsAnimalsNon-coding RNAMolecular Biology030304 developmental biologyNatural antisense transcripts030306 microbiologyfungiOrganismsBiology and Life SciencesComputational BiologyTsetse flyMidgutRC581-607Genome Analysisbiology.organism_classificationParasitic ProtozoansGastrointestinal MicrobiomeInsect VectorsGene regulationGastrointestinal TractMicroRNAsTrypanosomiasis AfricanTrypanosomaRNAParasitologyGene expressionImmunologic diseases. AllergyPhysiological ProcessesDigestive SystemPLOS Pathogens
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Activin A and bone metastasis

2010

Activin A, is a multifunctional cytokine of the transforming growth factor-b superfamily of growth factors. This molecule has been shown to be implicated in the regulation of a broad range of important biological functions including bone remodelling. Therefore, a deregulation in the activin signalling pathway may result in disturbances of normal bone metabolism and, eventually, in the onset of severe pathological conditions associated with an altered bone resorption. These observations support the concept that Act A might also be implicated in the pathogenesis of bone metastasis. This review provides insight into the most recent advances in understanding the role of this growth factor in th…

PhysiologyGrowth factormedicine.medical_treatmentClinical BiochemistryBone metastasisBone NeoplasmsCell BiologyBiologymedicine.diseaseHedgehog signaling pathwayBone resorptionBone remodelingActivinsActivin bone metastasisPathogenesisGene Expression Regulation NeoplasticCytokineImmunologymedicineCancer researchAnimalsBone RemodelingActivin type 2 receptorsSignal Transduction
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