Search results for " Small Interfering"

showing 10 items of 211 documents

Tribolium castaneum immune defense genes are differentially expressed in response to Bacillus thuringiensis toxins sharing common receptor molecules …

2015

In Tribolium castaneum larvae we have demonstrated by RNA interference knockdown that the Bacillus thuringiensis Cry3Ba toxin receptors Cadherin-like and Sodium solute symporter proteins are also functional receptors of the less active Cry3Aa toxin. Differences in susceptibility to B. thuringiensis infection might not only rely on toxin-receptor interaction but also on host defense mechanisms. We compared the expression of the immune related genes encoding Apolipophorin-III and two antimicrobial peptides, Defensin3 and Defensin2 after B. thuringiensis challenge. All three genes were up-regulated following Cry3Ba spore-crystal intoxication whereas only Defensins gene expression was induced u…

Staphylococcus aureusImmunologyAntimicrobial peptidesBacterial ToxinsMolecular Sequence DataBacillus thuringiensisBiologymedicine.disease_causeMicrobiologyDefensinsHemolysin ProteinsImmune systemBacterial ProteinsRNA interferenceBacillus thuringiensisGene expressionCandida albicansmedicineEscherichia coliAnimalsAmino Acid SequenceRNA Small InterferingDefensinTriboliumInnate immune systemBacillus thuringiensis ToxinsSymportersToxinfungibiology.organism_classificationAnti-Bacterial AgentsEndotoxinsApolipoproteinsLarvaInsect ProteinsRNA InterferenceDevelopmental BiologyDevelopmental and comparative immunology
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Preeclampsia: a defect in decidualization is associated with deficiency of Annexin A2.

2020

Background Decidualization defects in the endometrium have been demonstrated at the time of delivery in women with severe preeclampsia and to linger for years, which suggests a maternal contribution to the pathogenesis of this condition. Global transcriptional profiling reveals alterations in gene expression, which includes down-regulation of Annexin A2 in severe preeclampsia patients with decidualization resistance. Objective We investigated the functional role of Annexin A2 deficiency during endometrial decidualization and its potential contribution to shallow trophoblast invasion during implantation and subsequent placentation using in vitro and in vivo modeling. Study Design Annexin A2 …

Stromal cellGene ExpressionEndometriumAndrology03 medical and health sciencesMice0302 clinical medicinePre-EclampsiaAnnexinCell MovementPregnancymedicineDeciduaAnimalsHumans030212 general & internal medicineEmbryo ImplantationRNA Small InterferingAnnexin A2Cells Cultured030219 obstetrics & reproductive medicinemedicine.diagnostic_testbusiness.industryObstetrics and GynecologyDecidualizationPlacentationTrophoblastActinsPlacentationProlactinTrophoblastsInsulin-Like Growth Factor Binding Protein 1Disease Models Animalmedicine.anatomical_structureFemaleStromal CellsbusinessAnnexin A2Endometrial biopsyAmerican journal of obstetrics and gynecology
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Topotecan triggers apoptosis in p53-deficient cells by forcing degradation of XIAP and survivin thereby activating caspase-3-mediated Bid cleavage.

2009

The topoisomerase I inhibitor topotecan (TPT) is used in the therapy of different tumors including high-grade gliomas. We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I. Here, we show that p53-deficient (p53(-/-)) fibroblasts undergo excessive mitochondrial apoptosis featuring H2AX phosphorylation, Bcl-x(L) decline, cytochrome c release, caspase-9/-3/-2 activation, and cleavage of Bid. In wt and apaf-1(-/-) cells, caspase-2 did not become activated and Bid was not cleaved. In addition, p53(-/-) cells cotreated with TPT and caspase-3 inhibitor showed neither caspase-2 acti…

SurvivinBlotting WesternDown-RegulationCaspase 3ApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyTopoisomerase-I InhibitorInhibitor of apoptosisTransfectionInhibitor of Apoptosis ProteinsHistonesMiceCell Line TumorSurvivinAnimalsHumansPhosphorylationRNA Small InterferingPharmacologyMice KnockoutCaspase 3Caspase 2TransfectionFibroblastsFlow CytometryMolecular biologyXIAPMice Inbred C57BLRepressor ProteinsApoptotic Protease-Activating Factor 1ApoptosisCancer researchMolecular MedicineApoptosomeTopoisomerase I InhibitorsTumor Suppressor Protein p53TopotecanMicrotubule-Associated ProteinsBH3 Interacting Domain Death Agonist ProteinThe Journal of pharmacology and experimental therapeutics
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cIAP1-dependent TRAF2 degradation regulates the differentiation of monocytes into macrophages and their response to CD40 ligand.

2008

AbstractPeripheral blood monocytes are plastic cells that migrate to tissues and differentiate into various cell types, including macrophages, dendritic cells, and osteoclasts. We have described the migration of cellular inhibitor of apoptosis protein 1 (cIAP1), a member of the IAP family of proteins, from the nucleus to the Golgi apparatus in monocytes undergoing differentiation into macrophages. Here we show that, once in the cytoplasm, cIAP1 is involved in the degradation of the adaptor protein tumor necrosis factor receptor–associated factor 2 (TRAF2) by the proteosomal machinery. Inhibition of cIAP1 prevents the decrease in TRAF2 expression that characterizes macrophage formation. We d…

TRAF2CytoplasmCellular differentiationImmunologyCD40 LigandDown-RegulationGene ExpressionGolgi ApparatusBiologyBiochemistryMonocytesProinflammatory cytokineInhibitor of Apoptosis ProteinsPhagocytes Granulocytes and MyelopoiesisPhagocytosisMacrophageHumansRNA Small InterferingCD40U937 cellMacrophagesSignal transducing adaptor proteinCell DifferentiationCell BiologyHematologyU937 CellsTNF Receptor-Associated Factor 2Molecular biologyCell biologybiology.proteinTumor necrosis factor alphaBlood
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Nickel induces intracellular calcium mobilization and pathophysiological responses in human cultured airway epithelial cells.

2009

Abstract Environmental exposure to nickel is associated to respiratory disorders and potential toxicity in the lung but molecular mechanisms remain incompletely explored. The extracellular Ca 2+ -sensing receptor (CaSR) is widely distributed and may be activated by divalent cations. In this study, we investigated the presence of CaSR in human cultured airway epithelial cells and its activation by nickel. Nickel transiently increased intracellular calcium (−log EC 50  = 4.67 ± 0.06) in A549 and human bronchial epithelial cells as measured by epifluorescence microscopy. Nickel (20 μM)-induced calcium responses were reduced after thapsigargin or ryanodine exposure but not by Ca 2+ -free medium…

ThapsigarginInterleukin-1betachemistry.chemical_elementRespiratory MucosaBiologyCalciumToxicologyCalcium in biologychemistry.chemical_compoundNickelExtracellularHumansRNA Small InterferingCells CulturedA549 cellRyanodine receptorRyanodineTumor Necrosis Factor-alphaInositol trisphosphateEpithelial CellsGeneral MedicineEnvironmental exposureIntercellular Adhesion Molecule-1Cell biologychemistryMicroscopy FluorescenceType C PhospholipasesImmunologyGTP-Binding Protein alpha Subunits Gq-G11ThapsigarginCalciumReceptors Calcium-SensingChemico-biological interactions
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Profilin1 regulates sternum development and endochondral bone formation.

2012

Bone development is a dynamic process that requires cell motility and morphological adaptation under the control of actin cytoskeleton. This actin cytoskeleton system is regulated by critical modulators including actin-binding proteins. Among them, profilin1 (Pfn1) is a key player to control actin fiber structure, and it is involved in a number of cellular activities such as migration. During the early phase of body development, skeletal stem cells and osteoblastic progenitor cells migrate to form initial rudiments for future skeletons. During this migration, these cells extend their process based on actin cytoskeletal rearrangement to locate themselves in an appropriate location within mic…

Time FactorsGenotypeMice Transgenicmacromolecular substancesBiologyTransfectionBiochemistryBone and BonesMiceProfilinsCell MovementOsteogenesisBone cellAnimalsProgenitor cellRNA Small InterferingCytoskeletonMolecular BiologyActinAllelesCytoskeletonMice KnockoutOsteoblastsMesenchymal stem cellGene Expression Regulation DevelopmentalCell migrationMesenchymal Stem CellsCell BiologyX-Ray MicrotomographyActin cytoskeletonCell biologyCartilageImmunologyNIH 3T3 CellsStem cellDevelopmental BiologyThe Journal of biological chemistry
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Role of SIRT1 and FOXO factors in eNOS transcriptional activation by resveratrol.

2013

Many of the cardiovascular protective effects of resveratrol are attributable to an enhanced production of nitric oxide (NO) by the endothelial NO synthase (eNOS). Resveratrol has been shown to enhance eNOS gene expression as well as eNOS enzymatic activity. The aim of the present study was to analyze the molecular mechanisms of eNOS transcriptional activation by resveratrol. Treatment of human EA.hy 926 endothelial cells with resveratrol led to a concentration-dependent upregulation of eNOS expression. In luciferase reporter gene assay, resveratrol enhanced the activity of human eNOS promoter fragments (3500, 1600, 633 and 263bp in length, respectively), indicating that the proximal promot…

Transcriptional ActivationCancer Researchendocrine system diseasesNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryFOXO1ResveratrolBiochemistryCell LineTransactivationchemistry.chemical_compoundSirtuin 1EnosStilbenesHumansRNA Small Interferingskin and connective tissue diseasesPromoter Regions GeneticTranscription factorGene knockdownAnalysis of VariancebiologySirtuin 1Chemistryorganic chemicalsfood and beveragesForkhead Transcription Factorsbiology.organism_classificationMolecular biologyUp-RegulationNitric oxide synthaseResveratrolGene Knockdown Techniquesbiology.proteinhormones hormone substitutes and hormone antagonistsNitric oxide : biology and chemistry
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Melatonin induces transcriptional regulation of Bim by FoxO3a in HepG2 cells

2012

Background: Melatonin induces apoptosis in many different cancer cell lines, including hepatocellular carcinoma cells. However, the responsible pathways have not been clearly elucidated. A member of the forkhead transcription factors' family, FoxO3a, has been implicated in the expression of the proapoptotic protein Bim (a Bcl-2-interacting mediator of cell death). In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate whether melatonin treatment induces Bim through regulation by the transcription factor FoxO3a. Methods: Cytotoxicity of melatonin was compared in HepG2 hepatoblastoma cells and primary human hepatocytes. Proapoptotic Bim expression was analys…

Transcriptional ActivationCancer Researchmedicine.medical_specialtyProgrammed cell deathSmall interfering RNACarcinoma HepatocellularTranscription GeneticApoptosisFoxO3amelatoninBiologyGenetics & GenomicsMelatoninDownregulation and upregulationCell Line TumorProto-Oncogene ProteinsInternal medicinemedicineTranscriptional regulationHumansGene silencingBimPhosphorylationRNA Small InterferingPromoter Regions GeneticTranscription factorBinding SitesBcl-2-Like Protein 11Forkhead Box Protein O3Membrane ProteinsForkhead Transcription FactorsHep G2 Cellshepatocellular carcinomaCell biologyEndocrinologyOncologyHepatocytesRNA Interferencebiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsChromatin immunoprecipitationProtein Bindingmedicine.drugBritish Journal of Cancer
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Epigenetic activation of a cryptic TBC1D16 transcript enhances melanoma progression by targeting EGFR

2015

Metastasis is respoMetastasis is responsible for most cancer-related deaths, and, among common tumor types, melanoma is one with great potential to metastasize. Here we study the contribution of epigenetic changes to the dissemination process by analyzing the changes that occur at the DNA methylation level between primary cancer cells and metastases. We found a hypomethylation event that reactivates a cryptic transcript of the Rab GTPase activating protein TBC1D16 (TBC1D16-47 kDa; referred to hereafter as TBC1D16-47KD) to be a characteristic feature of the metastatic cascade. This short isoform of TBC1D16 exacerbates melanoma growth and metastasis both in vitro and in vivo. By combining imm…

Transcriptional ActivationGTPase-activating proteinImmunoprecipitationMice NudeEditorials: Cell Cycle FeaturesBiologyBioinformaticsMethylationGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticMetastasisMetastasisEpigènesiMetàstasiCell Line TumormedicineAnimalsImmunoprecipitationProtein IsoformsRNA MessengerEpigeneticsNeoplasm MetastasisRNA Small InterferingPromoter Regions GeneticProteïnes supressores de tumorsProtein Kinase InhibitorsMelanomaMelanomaGTPase-Activating ProteinsGeneral MedicineMethylationDNA MethylationPrognosismedicine.diseaseTumor suppressor proteinErbB ReceptorsMolecular WeightTreatment Outcomerab GTP-Binding ProteinsDNA methylationDisease ProgressionCancer researchRabMetilacióProtein BindingSignal TransductionEpigenesisNature Medicine
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Role of reactive oxygen species in the regulation of HIF-1 by prolyl hydroxylase 2 under mild hypoxia

2012

The function and survival of eukaryotic cells depends on a constant and sufficient oxygen supply. Cells recognize and respond to hypoxia by accumulation of the transcription factor hypoxia-inducible factor 1 (HIF-1), composed of an oxygen-sensitive HIF-1α and a constitutive HIF-1β subunit. Besides physiology, HIF-1 induction is involved in major pathological processes such as cardiovascular disease, inflammation and cancer, which are associated with the formation of reactive oxygen species (ROS). ROS have been reported to affect HIF-1 activity but the role for ROS in regulating HIF-1 has not been definitely settled. In order to shed light on the redox-regulation of HIF-1 by ROS, we studied …

Transcriptional ActivationProcollagen-Proline DioxygenaseMedizinBiologyTransfectionBiochemistryHypoxia-Inducible Factor-Proline DioxygenasesTransactivationCell Line TumormedicineHumansRNA Small InterferingTranscription factorchemistry.chemical_classificationRegulation of gene expressionReactive oxygen speciesGene knockdownGeneral MedicineTransfectionHydrogen PeroxideHypoxia (medical)Cell HypoxiaCell biologyHypoxia-inducible factorschemistryBiochemistryHypoxia-Inducible Factor 1medicine.symptomReactive Oxygen SpeciesOxidation-Reduction
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