Search results for "Transcription factors"

showing 10 items of 848 documents

Cholesterol Starvation and Hypoxia Activate the FVII Gene via the SREBP1-GILZ Pathway in Ovarian Cancer Cells to Produce Procoagulant Microvesicles

2019

AbstractInteraction between the transcription factors, hypoxia-inducible factor (HIF1α and HIF2α) and Sp1, mediates hypoxia-driven expression of FVII gene encoding coagulation factor VII (fVII) in ovarian clear cell carcinoma (CCC) cells. This mechanism is synergistically enhanced in response to serum starvation, a condition possibly associated with tumor hypoxia. This transcriptional response potentially results in venous thromboembolism, a common complication in cancer patients by producing procoagulant extracellular vesicles (EVs). However, which deficient serum factors are responsible for this characteristic transcriptional mechanism is unknown. Here, we report that cholesterol deficien…

Serum0301 basic medicineLeucine zipper030204 cardiovascular system & hematologyMice03 medical and health sciences0302 clinical medicineCell-Derived MicroparticlesCell Line Tumorhemic and lymphatic diseasesAnimalsHumansHypoxiaTranscription factorOvarian NeoplasmsTumor hypoxiaCoagulantsChemistryHematologyFactor VIIChromatin Assembly and DisassemblyHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysMicrovesiclesChromatinCell biologySterol regulatory element-binding proteinCholesterol030104 developmental biologyFemaleSignal transductionSterol Regulatory Element Binding Protein 1Chromatin immunoprecipitationSignal TransductionTranscription FactorsThrombosis and Haemostasis
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OPLA scaffold, collagen I, and horse serum induce a higher degree of myogenic differentiation of adult rat cardiac stem cells

2009

In the last few years, a major goal of cardiac research has been to drive stem cell differentiation to replace damaged myocardium. Several research groups have attempted to differentiate potential cardiac stem cells (CSCs) using bi- or three-dimensional systems supplemented with growth factors or molecules acting as differentiating substances. We hypothesize that these systems failed to induce a complete differentiation because they lacked an architectural space. In the present study, we isolated a pool of small proliferating and fibroblast-like cells from adult rat myocardium. The phenotype of these cells was assessed and the characterized cells were cultured in a collagen I/OPLA scaffold …

SerumScaffoldPhysiologyCellular differentiationLIM-Homeodomain ProteinsClinical BiochemistryNerve Tissue ProteinsCell SeparationBiologyMuscle DevelopmentCollagen Type INestinRats Sprague-DawleyIntermediate Filament ProteinsMicroscopy Electron TransmissionTroponin TAnimalsMyocyteMyocytes CardiacHorsesTranscription factorHomeodomain ProteinsMyosin Heavy ChainsTissue ScaffoldsSettore BIO/16 - Anatomia UmanaMyocardiumCell DifferentiationCell BiologyAnatomyNestinPhenotypestem cell OPLA scaffoldActinsIn vitroClone CellsGATA4 Transcription FactorRatsCell biologyAdult Stem CellsProto-Oncogene Proteins c-kitConnexin 43FemaleStem cellTranscription FactorsJournal of Cellular Physiology
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miRNA Signature and Dicer Requirement during Human Endometrial Stromal Decidualization In Vitro

2012

Decidualization is a morphological and biochemical transformation of endometrial stromal fibroblast into differentiated decidual cells, which is critical for embryo implantation and pregnancy establishment. The complex regulatory networks have been elucidated at both the transcriptome and the proteome levels, however very little is known about the post-transcriptional regulation of this process. miRNAs regulate multiple physiological pathways and their de-regulation is associated with human disorders including gynaecological conditions such as endometriosis and preeclampsia. In this study we profile the miRNAs expression throughout human endometrial stromal (hESCs) decidualization and analy…

Sexual ReproductionRibonuclease IIISmall interfering RNAAnatomy and PhysiologyCellular differentiationGene ExpressionBioinformaticsCell morphologyTranscriptomeEndocrinologyMolecular Cell BiologyMultidisciplinarybiologyStem CellsQDeciduaRObstetrics and GynecologyCell DifferentiationForkhead Transcription FactorsCell biologyFemale Genital Diseasesmedicine.anatomical_structureMedicineFemaleResearch ArticleAdultScienceMolecular GeneticsYoung AdultmicroRNAGeneticsDeciduamedicineReproductive EndocrinologyHumansGene RegulationBiologyEmbryonic Stem CellsHomeodomain ProteinsGene Expression ProfilingReproductive SystemComputational BiologyDecidualizationFibroblastsFemale SubfertilityInsulin-Like Growth Factor Binding Protein 1MicroRNAsHomeobox A10 ProteinsGene Expression Regulationbiology.proteinStromal CellsDevelopmental BiologyDicerPLoS ONE
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The mitotic kinase Aurora-A promotes distant metastases by inducing epithelial-to-mesenchymal transition in ERα+ breast cancer cells

2013

In this study, we demonstrate that constitutive activation of Raf-1 oncogenic signaling induces stabilization and accumulation of Aurora-A mitotic kinase that ultimately drives the transition from an epithelial to a highly invasive mesenchymal phenotype in estrogen receptor α-positive (ERα(+)) breast cancer cells. The transition from an epithelial- to a mesenchymal-like phenotype was characterized by reduced expression of ERα, HER-2/Neu overexpression and loss of CD24 surface receptor (CD24(-/low)). Importantly, expression of key epithelial-to-mesenchymal transition (EMT) markers and upregulation of the stemness gene SOX2 was linked to acquisition of stem cell-like properties such as the ab…

Smad5 ProteinCancer ResearchEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemReceptor ErbB-2Active Transport Cell NucleusEstrogen receptorMice NudeBreast NeoplasmsBiologyArticleMicebreast cancerSOX2Cell MovementCell Line TumorGeneticsAnimalsHumansEpithelial–mesenchymal transitionKinase activityNeoplasm MetastasisPhosphorylationRNA Small InterferingMolecular BiologyAurora Kinase Ametastases mitosisSOXB1 Transcription FactorsEstrogen Receptor alphaCD24 AntigenXenograft Model Antitumor AssaysstemneGene Expression Regulation NeoplasticProto-Oncogene Proteins c-rafSettore BIO/18 - GeneticaTumor progressionembryonic structuresCancer researchMCF-7 CellsNeoplastic Stem CellsProto-Oncogene Proteins c-rafFemaleRNA InterferenceSignal transductionEstrogen receptor alphaNeoplasm Transplantation
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Response of yeast cells to high glucose involves molecular and physiological differences when compared to other osmostress conditions.

2015

Yeast cells can be affected by several causes of osmotic stress, such as high salt, sorbitol or glucose concentrations. The last condition is particularly interesting during natural processes where this microorganism participates. Response to osmostress requires the HOG (High Osmolarity Glycerol) pathway and several transcription factors, including Hot1, which plays a key role in high glucose concentrations. In this work, we describe how the yeast response to osmotic stress shows differences in accordance with the stress agent responsible for it. Compared with other conditions, under high glucose stress, delocalization of MAPK (Mitogen-Activated Protein Kinase) Hog1 is slower, induction of …

Snf3Saccharomyces cerevisiae ProteinsOsmotic shockTranscription GeneticSaccharomyces cerevisiaeChitinSaccharomyces cerevisiaeOsmosisApplied Microbiology and BiotechnologyMicrobiologychemistry.chemical_compoundOsmotic PressureGene Expression Regulation FungalSorbitolProtein kinase AbiologyGlycogenEthanolBenzenesulfonatesOsmolar ConcentrationGeneral Medicinebiology.organism_classificationYeastDNA-Binding ProteinsRepressor ProteinsBasic-Leucine Zipper Transcription FactorsGlucosechemistryBiochemistrySorbitolMitogen-Activated Protein KinasesTranscription FactorsFEMS yeast research
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PyCellBase

2019

Python package for easy retrieval of biological data from heterogeneous sources.

Software_GENERALHardware_GENERALComputer Science::Information RetrievalInformationSystems_INFORMATIONSTORAGEANDRETRIEVALTranscription factors and regulatory sitesComputer Science::Mathematical SoftwareComputingMethodologies_GENERAL
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CEND1 and NEUROGENIN2 Reprogram Mouse Astrocytes and Embryonic Fibroblasts to Induced Neural Precursors and Differentiated Neurons

2015

Summary Recent studies demonstrate that astroglia from non-neurogenic brain regions can be reprogrammed into functional neurons through forced expression of neurogenic factors. Here we explored the effect of CEND1 and NEUROG2 on reprogramming of mouse cortical astrocytes and embryonic fibroblasts. Forced expression of CEND1, NEUROG2, or both resulted in acquisition of induced neuronal cells expressing subtype-specific markers, while long-term live-cell imaging highlighted the existence of two different modes of neuronal trans-differentiation. Of note, a subpopulation of CEND1 and NEUROG2 double-transduced astrocytes formed spheres exhibiting neural stem cell properties. mRNA and protein exp…

Somatic cellCellular differentiationNerve Tissue ProteinsEndogenyBiologyBiochemistryArticleMiceNeural Stem CellsBasic Helix-Loop-Helix Transcription FactorsGeneticsAnimalslcsh:QH301-705.5NeuronsGene knockdownMessenger RNAlcsh:R5-920Membrane ProteinsCell DifferentiationCell BiologyFibroblastsCellular ReprogrammingEmbryo MammalianEmbryonic stem cellNeural stem cellCell biologylcsh:Biology (General)Astrocytesembryonic structureslcsh:Medicine (General)ReprogrammingDevelopmental BiologyStem Cell Reports
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The NUPR1/p73 axis contributes to sorafenib resistance in hepatocellular carcinoma

2021

The multikinase inhibitor sorafenib was the first drug approved by the FDA for treating patients with advanced hepatocellular carcinoma (HCC). However, sorafenib resistance remains a major challenge for improving the effectiveness of HCC treatment. Previously, we identified several genes modulated after sorafenib treatment of human HCC cells, including the stress-inducible nuclear protein 1 (NUPR1) gene. Multiple studies have shown that NUPR1 regulates autophagy, apoptosis, and chemoresistance. Here, we demonstrate that treatment of HCC cells with sorafenib resulted in the activation of autophagic flux. NUPR1 knock-down (KD) in HCC cells was associated with increased p62 expression, suggest…

SorafenibCancer ResearchCarcinoma HepatocellularSettore MED/09 - Medicina InternaHepatocellular carcinomap73Mice NudeApoptosisSettore BIO/11 - Biologia MolecolareMiceNSC5594In vivoPumaBasic Helix-Loop-Helix Transcription FactorsmedicineAutophagyNSC5994AnimalsHumansGene silencingneoplasmsbiologyActivator (genetics)business.industryLiver NeoplasmsAutophagyApoptosiTumor Protein p73Hep G2 CellsSorafenibbiology.organism_classificationmedicine.diseasedigestive system diseasesNeoplasm ProteinsOncologyDrug Resistance NeoplasmApoptosisHepatocellular carcinomaCancer researchFemalebusinessNUPR1medicine.drug
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Production of Norspermidine Contributes to Aminoglycoside Resistance in pmrAB Mutants of Pseudomonas aeruginosa

2019

Emergence of resistance to polymyxins in Pseudomonas aeruginosa is mainly due to mutations in two-components systems, that promote addition of 4-amino-4-deoxy-L-arabinose to the lipopolysaccharide (LPS) through upregulation of operon arnBCADTEF-ugd (arn) expression. Here, we demonstrate that mutations occurring in different domains of histidine kinase PmrB or in response regulator PmrA result in coresistance to aminoglycosides and colistin. All seventeen clinical strains tested exhibiting such a cross-resistance phenotype were found to be pmrAB mutants. As shown by gene deletion experiments, the decreased susceptibility of the mutants to aminoglycosides was independent from operon arn but r…

Spectrometry Mass Electrospray IonizationOperonSpermidineMutantMicrobial Sensitivity TestsMicrobiology03 medical and health scienceschemistry.chemical_compoundBacterial ProteinsMechanisms of Resistance[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]PolyaminesPharmacology (medical)GeneComputingMilieux_MISCELLANEOUS030304 developmental biologyPharmacology0303 health sciences030306 microbiologyColistinNorspermidineHistidine kinaseGene Expression Regulation Bacterial[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyAnti-Bacterial AgentsResponse regulatorInfectious DiseasesAminoglycosideschemistryPseudomonas aeruginosaEffluxBacterial outer membraneTranscription Factors
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The Molecular Basis of X-Linked Spondyloepiphyseal Dysplasia Tarda

2001

The X-linked form of spondyloepiphyseal dysplasia tarda (SEDL), a radiologically distinct skeletal dysplasia affecting the vertebrae and epiphyses, is caused by mutations in the SEDL gene. To characterize the molecular basis for SEDL, we have identified the spectrum of SEDL mutations in 30 of 36 unrelated cases of X-linked SEDL ascertained from different ethnic populations. Twenty-one different disease-associated mutations now have been identified throughout the SEDL gene. These include nonsense mutations in exons 4 and 5, missense mutations in exons 4 and 6, small (2–7 bp) and large (>1 kb) deletions, insertions, and putative splicing errors, with one splicing error due to a complex deleti…

Spondyloepiphyseal dysplasiaGenetic MarkersMaleX ChromosomeGenetic LinkageNonsense mutationDNA Mutational AnalysisMolecular Sequence DataBiologymedicine.disease_causeOsteochondrodysplasiasFrameshift mutation03 medical and health sciencesExonStructure-Activity Relationship0302 clinical medicinemedicineEthnicityGeneticsMissense mutationHumansGenetics(clinical)Genetic TestingRNA MessengerGenetics (clinical)X chromosome030304 developmental biologyGenetics0303 health sciencesMutationBone DevelopmentPolymorphism GeneticBase SequenceReverse Transcriptase Polymerase Chain ReactionRacial GroupsMembrane Transport ProteinsExonsArticlesmedicine.diseaseOsteochondrodysplasiaBody Height3. Good healthPhenotypeHaplotypesMutationCarrier Proteins030217 neurology & neurosurgeryTranscription FactorsThe American Journal of Human Genetics
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