Search results for " Transcription factor"

showing 10 items of 656 documents

Cellular Inhibitor of Apoptosis Protein-1 (cIAP1) Can Regulate E2F1 Transcription Factor-mediated Control of Cyclin Transcription

2011

International audience; The inhibitor of apoptosis protein cIAP1 (cellular inhibitor of apoptosis protein-1) is a potent regulator of the tumor necrosis factor (TNF) receptor family and NF-B signaling pathways in the cytoplasm. However, in some primary cells and tumor cell lines, cIAP1 is expressed in the nucleus, and its nuclear function remains poorly understood. Here, we show that the N-terminal part of cIAP1 directly interacts with the DNA binding domain of the E2F1 transcription factor. cIAP1 dramatically increases the transcriptional activity of E2F1 on synthetic and CCNE promoters. This function is not conserved for cIAP2 and XIAP, which are cytoplasmic proteins. Chromatin immunoprec…

Transcription GeneticCellular differentiation[SDV]Life Sciences [q-bio]Cyclin ACyclin A[SDV.BC]Life Sciences [q-bio]/Cellular BiologyResponse ElementsInhibitor of apoptosisBiochemistryInhibitor of Apoptosis ProteinsMice03 medical and health sciences0302 clinical medicineCyclin EAnimalsHumansE2F1Gene SilencingE2F[SDV.BC] Life Sciences [q-bio]/Cellular BiologyMolecular BiologyCell Proliferation030304 developmental biologyCell Nucleus0303 health sciencesbiologyE2F1 Transcription FactorCell BiologyCell cycleMolecular biologyProtein Structure Tertiary3. Good healthCell biology[SDV] Life Sciences [q-bio]030220 oncology & carcinogenesisbiology.proteinbiological phenomena cell phenomena and immunityChromatin immunoprecipitationE2F1 Transcription FactorHeLa Cells
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Transcriptional regulation of the stem cell leukemia gene by PU.1 and Elf-1.

1998

Abstract The SCL gene, also known astal-1, encodes a basic helix-loop-helix transcription factor that is pivotal for the normal development of all hematopoietic lineages. SCL is expressed in committed erythroid, mast, and megakaryocytic cells as well as in hematopoietic stem cells. Nothing is known about the regulation of SCL transcription in mast cells, and in other lineages GATA-1 is the only tissue-specific transcription factor recognized to regulate the SCL gene. We have therefore analyzed the molecular mechanisms underlyingSCL expression in mast cells. In this paper, we demonstrate that SCL promoter 1a was regulated by GATA-1 together with Sp1 and Sp3 in a manner similar to the situati…

Transcription GeneticDNA FootprintingBiologyBiochemistryCell LineMiceTranscription (biology)hemic and lymphatic diseasesProto-Oncogene ProteinsmedicineTranscriptional regulationBasic Helix-Loop-Helix Transcription FactorsAnimalsMast CellsPromoter Regions GeneticMolecular BiologyTranscription factorT-Cell Acute Lymphocytic Leukemia Protein 1DNA PrimersBase SequenceGATA2Nuclear ProteinsGATA1Cell BiologyMast cellMolecular biologyDNA-Binding ProteinsHaematopoiesismedicine.anatomical_structureGene Expression RegulationMutagenesis Site-DirectedTrans-ActivatorsStem cellTranscription FactorsThe Journal of biological chemistry
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Transcriptional activation of apurinic/apyrimidinic endonuclease (Ape, Ref-1) by oxidative stress requires CREB.

1999

Abstract Apurinic/apyrimidinic endonuclease (APE alias Ref-1) is a multifunctional enzyme involved in DNA repair and redox regulation of transcription factors (e.g., AP-1). It also acts as a repressor of its own and other genes. Recently, it was shown that the level of APE mRNA and protein is enhanced upon treatment of cells with oxidative agents, such as hydrogen peroxide (H 2 O 2 ), which gives rise to an adaptive response of cells to oxidative stress. Induction of APE is due to APE promoter activation. To elucidate the mechanism of transcriptional activation of APE by oxidative agents, we introduced mutations into the cloned human APE promoter and checked its activity in transient transf…

Transcription GeneticDNA repairProto-Oncogene Proteins c-junvirusesCarbon-Oxygen LyasesBiophysicsRepressorContext (language use)CHO CellsCREBTransfectionBiochemistryPolymerase Chain ReactionEndonucleasestomatognathic systemCricetinaeDNA-(Apurinic or Apyrimidinic Site) LyaseAnimalsHumansAP siteBinding siteCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticMolecular BiologyTranscription factorBinding SitesbiologyActivating Transcription Factor 2social sciencesCell BiologyHydrogen PeroxideOxidantsMolecular biologybody regionsOxidative Stressbiology.proteinMutagenesis Site-DirectedTranscription FactorsBiochemical and biophysical research communications
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Beclomethasone dipropionate and formoterol reduce oxidative/nitrosative stress generated by cigarette smoke extracts and IL-17A in human bronchial ep…

2013

Interleukin-17A (IL-17A), cigarette smoke and oxidative/nitrosative stress are involved in inflammatory airway diseases, and the mechanisms behind these processes are still poorly understood. We investigated whether recombinant human IL-17A (rhIL-17A), in combination with cigarette smoke extracts (CSE), increases the levels of inducibile nitric oxide synthase (iNOS), reactive oxygen species, nitrotyrosine (NT) and the activation of signal transducer and activator of transcription 1 (STAT-1) in normal human bronchial epithelial cells (16HBE). The effect of beclomethasone dipropionate (BDP), formoterol and their combination was also evaluated. We demonstrated that rhIL-17A or CSE alone increa…

Transcription GeneticNitric Oxide Synthase Type IIBronchiOxidative phosphorylationPharmacologyGene Expression Regulation EnzymologicCell Linechemistry.chemical_compoundFormoterol FumarateSmokeNitrilesmedicineButadienesGene silencingHumansGene SilencingPromoter Regions GeneticPharmacologychemistry.chemical_classificationReactive oxygen speciesbiologyNitrotyrosineInterleukin-17BeclomethasoneEpithelial CellsTobacco ProductsReactive Nitrogen SpeciesNitric oxide synthaseOxidative StressSTAT1 Transcription FactorchemistryEthanolaminesImmunologySTAT proteinbiology.proteinPhosphorylationFormoterolBiomarkersmedicine.drugEuropean journal of pharmacology
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Transcriptional Activity and Nuclear Localization of Cabut, the Drosophila Ortholog of Vertebrate TGF-β-Inducible Early-Response Gene (TIEG) Proteins

2011

Background Cabut (Cbt) is a C2H2-class zinc finger transcription factor involved in embryonic dorsal closure, epithelial regeneration and other developmental processes in Drosophila melanogaster. Cbt orthologs have been identified in other Drosophila species and insects as well as in vertebrates. Indeed, Cbt is the Drosophila ortholog of the group of vertebrate proteins encoded by the TGF-s-inducible early-response genes (TIEGs), which belong to Sp1-like/Kruppel-like family of transcription factors. Several functional domains involved in transcriptional control and subcellular localization have been identified in the vertebrate TIEGs. However, little is known of whether these domains and fu…

Transcription GeneticNuclear Localization SignalsActive Transport Cell Nucleuslcsh:MedicineGene ExpressionBiochemistrybehavioral disciplines and activities03 medical and health sciencesModel Organisms0302 clinical medicineTransforming Growth Factor betaMolecular Cell Biologymental disordersGeneticsTranscriptional regulationAnimalsDrosophila Proteinslcsh:ScienceBiology030304 developmental biologyGeneticsZinc finger transcription factor0303 health sciencesMultidisciplinarybiologySchneider 2 cellslcsh:RfungiProteinsAnimal Modelsbiology.organism_classificationFusion proteinCellular StructuresDorsal closure3. Good healthRepressor ProteinsDrosophila melanogasterGene Expression RegulationVertebrateslcsh:QDrosophila melanogaster030217 neurology & neurosurgeryDrosophila ProteinNuclear localization sequenceTranscription FactorsResearch ArticleDevelopmental BiologyPLoS ONE
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Characterization and DNA-binding properties of GRF, a novel monomeric binding orphan receptor related to GCNF and betaFTZ-F1

1999

0014-2956 (Print) Comparative Study Journal Article Research Support, Non-U.S. Gov't; A PCR approach has been used to isolate, from Bombyx mori, a cDNA encoding a novel orphan receptor (GRF) that is most closely related to Bombyx betaFTZ-F1 and to the vertebrate germ cell nuclear factor. The major GRF mRNA is detected in most tissues as an 8-kb transcript whose amount follows the circulating ecdysteroid concentration with a delay. The expression pattern of GRF is similar to that of the Bombyx homologue of the Drosophila early-late gene DHR3, and precedes that of betaFTZ-F1 in all stages and tissues examined. The GRF protein is thus likely to be required in many tissues, but in a temporally …

Transcription GeneticReceptors Cytoplasmic and NuclearFushi Tarazu Transcription FactorsSequence HomologyGenes InsectDevelopmental/drug effectsSteroidogenic Factor 1BiochemistryBombyx/*chemistry/growth & developmentDNA/*metabolismNuclear Receptor Subfamily 6 Group A Member 1ReceptorsCloning MolecularReceptorRegulation of gene expressionOrphan receptorbiologyGene Expression Regulation DevelopmentalDNA-Binding ProteinsEcdysterone/pharmacologyAmino AcidEcdysteroneInsect Proteins/genetics/*isolation & purification/metabolismInsect ProteinsRecombinant Fusion Proteins/metabolismTranscriptionProtein StructureRecombinant Fusion ProteinsGerm cell nuclear factorMolecular Sequence DataGeneticComplementary DNAAnimalsAmino Acid SequenceBinding siteBombyxHomeodomain ProteinsBinding Sitespurification/metabolismSequence Homology Amino AcidBase SequencefungiMolecularCytoplasmic and Nuclear/chemistryDNABombyxbiology.organism_classificationMolecular biologyProtein Structure TertiaryTranscription Factors/chemistry/genetics/*isolation &Nuclear receptorGene Expression RegulationGenesDNA-Binding Proteins/chemistry/genetics/*isolation &InsectSequence AlignmentTertiaryTranscription FactorsCloning
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Transcriptional Mechanisms of Proneural Factors and REST in Regulating Neuronal Reprogramming of Astrocytes

2015

Summary Direct lineage reprogramming induces dramatic shifts in cellular identity, employing poorly understood mechanisms. Recently, we demonstrated that expression of Neurog2 or Ascl1 in postnatal mouse astrocytes generates glutamatergic or GABAergic neurons. Here, we take advantage of this model to study dynamics of neuronal cell fate acquisition at the transcriptional level. We found that Neurog2 and Ascl1 rapidly elicited distinct neurogenic programs with only a small subset of shared target genes. Within this subset, only NeuroD4 could by itself induce neuronal reprogramming in both mouse and human astrocytes, while co-expression with Insm1 was required for glutamatergic maturation. Cu…

Transcription GeneticRepressorNerve Tissue ProteinsCell fate determinationBiologyDNA-binding proteinArticleMiceGlutamatergicBasic Helix-Loop-Helix Transcription FactorsGeneticsAnimalsHumansPromoter Regions GeneticTranscription factorCells CulturedNeuronsCell BiologyCellular ReprogrammingMolecular biologyCell biologyDNA-Binding ProteinsRepressor ProteinsASCL1Astrocytesembryonic structuresMolecular MedicineGABAergicReprogrammingTranscription FactorsCell Stem Cell
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An epistatic mini-circuitry between the transcription factors Snail and HNF4α controls liver stem cell and hepatocyte features exhorting opposite reg…

2011

Preservation of the epithelial state involves the stable repression of epithelial-to-mesenchymal transition program, whereas maintenance of the stem compartment requires the inhibition of differentiation processes. A simple and direct molecular mini-circuitry between master elements of these biological processes might provide the best device to keep balanced such complex phenomena. In this work, we show that in hepatic stem cell Snail, a transcriptional repressor of the hepatocyte differentiation master gene HNF4α, directly represses the expression of the epithelial microRNAs (miRs)-200c and-34a, which in turn target several stem cell genes. Notably, in differentiated hepatocytes HNF4α, p…

Transcription GeneticTranscription FactorCellular differentiationLiver Stem CellSnailMESH: Mice KnockoutMESH: HepatocytesMice0302 clinical medicineSnail; hnf4a; mir-200; mir-34a; stemness; hepatocyte differentiationHepatocyteMESH: AnimalsMice KnockoutHepatocyte differentiationmir-34a0303 health sciencesStemneStem CellsMicroRNACell DifferentiationMESH: Transcription FactorsCell biologySnailmir-200Hepatocyte Nuclear Factor 4Liver030220 oncology & carcinogenesisMiRs-200MESH: Hepatocyte Nuclear Factor 4Hepatocyte differentiation; HNF4a; MiR-34a; MiRs-200; Snail; Stemness; Animals; Cell Differentiation; Epithelial-Mesenchymal Transition; Hepatocyte Nuclear Factor 4; Hepatocytes; Liver; Mice; Mice Knockout; MicroRNAs; Snail Family Transcription Factors; Stem Cells; Transcription Factors; Transcription Genetic; Cell Biology; Molecular BiologyStem cellhnf4aMESH: Cell Differentiationhepatocyte differentiationEpithelial-Mesenchymal TransitionMESH: Stem Cells[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologystemness03 medical and health sciencesStem Cellbiology.animalAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEpithelial–mesenchymal transitionMESH: MiceMolecular BiologyTranscription factor030304 developmental biologyOriginal PaperAnimalMESH: Transcription GeneticSnail Family Transcription FactorCell BiologyMolecular biologyMicroRNAsMESH: Epithelial-Mesenchymal TransitionHepatocyte nuclear factor 4HepatocytesSnail Family Transcription FactorsMESH: MicroRNAsMESH: LiverTranscription FactorsCell Death & Differentiation
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Estrogens increase transcription of the human endothelial NO synthase gene: analysis of the transcription factors involved.

1998

Abstract —Estrogens have been found to reduce the incidence of cardiovascular disease that has been ascribed in part to an increased expression and/or activity of the vasoprotective endothelial NO synthase (NOS III). Some reports have shown that the level of expression of this constitutive enzyme can be upregulated by estrogens. The current study investigates the molecular mechanism of the NOS III upregulation in human endothelial EA.hy 926 cells. Incubation of EA.hy 926 cells with 17β-estradiol or the more stable 17α-ethinyl estradiol enhanced NOS III mRNA and protein expression up to 1.8-fold, without changing the stability of the NOS III mRNA. There was no enhancement of NOS III mRNA af…

Transcription Geneticmedicine.drug_classBiologyEthinyl EstradiolTransfectionCell LineDownregulation and upregulationDrug StabilityEstradiol CongenersTranscription (biology)Consensus SequenceInternal MedicinemedicineHumansRNA MessengerPromoter Regions GeneticTranscription factorCell NucleusSp1 transcription factorMessenger RNABase SequenceEstradiolTissue ExtractsTransfectionDNAMolecular biologyEndothelial stem cellIsoenzymesEstrogenEndothelium VascularNitric Oxide Synthasehormones hormone substitutes and hormone antagonistsTranscription FactorsHypertension (Dallas, Tex. : 1979)
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NFAT transcription factors control HIV-1 expression through a binding site downstream of TAR region.

2004

NFAT factors control HIV-1 transcription. We show here that, in addition to binding to two NF-kappaB/NFAT sites within the U3 HIV LTR, NFATc1 and NFATc2 bind to an NFAT site within the LTR's U5 region. Mutations in this site which abolish NFAT binding reduce the ability of NFATs to transactivate LTR-mediated transcription. Mutations in all three NFAT sites strongly interfered with LTR induction, but affected moderately the stimulatory effect of Tat.

Transcription GeneticvirusesImmunologyTransfectionJurkat cellsJurkat CellsTranscription (biology)Immunology and AllergyHumansNuclear proteinBinding siteTranscription factorHIV Long Terminal RepeatBinding SitesNFATC Transcription FactorsChemistryNuclear ProteinsNFATHematologyU937 CellsNFATC Transcription FactorsMolecular biologyDNA-Binding Proteinscardiovascular systemHIV-1HIV Long Terminal RepeatTranscription FactorsImmunobiology
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