Search results for "Transcription factor"

showing 10 items of 1493 documents

Transcription, apoptosis and p53: catch-22

2005

The tumor suppressor p53 is a transcription factor and is activated in response to DNA damage or oncogenic transformation through modification of its interaction with regulatory proteins. The transcription factor activity of p53 is thought to mediate its primary functions of cell-cycle arrest and apoptosis through the gene expression it regulates, and evidence to support this interpretation continues to accumulate. However, reports of transcription-independent activities of p53, especially in the induction of apoptosis, persist. In particular, recent studies suggest that cytosolic p53 directly interacts with members of the BCL-2 family of apoptosis regulators, thereby triggering mitochondri…

Transcription GeneticTumor suppressor geneDNA damageApoptosisBiologylaw.inventionTranscription (biology)ApoptosislawGene expressionGeneticsCancer researchAnimalsHumansSuppressorE2F1Tumor Suppressor Protein p53Transcription factorTrends in Genetics
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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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Targeting the aryl hydrocarbon receptor with a novel set of triarylmethanes

2020

International audience; The aryl hydrocarbon receptor (AhR) is a chemical sensor upregulating the transcription of responsive genes associated with endocrine homeostasis, oxidative balance and diverse metabolic, immunological and inflammatory processes, which have raised the pharmacological interest on its modulation. Herein, a novel set of 32 unsymmetrical triarylmethane (TAM) class of structures has been synthesized, characterized and their AhR transcriptional activity evaluated using a cell-based assay. Eight of the assayed TAM compounds (14, 15, 18, 19, 21, 22, 25, 28) exhibited AhR agonism but none of them showed antagonist effects. TAMs bearing benzotrifluoride, naphthol or heteroarom…

Transcriptional ActivationAgonistmedicine.drug_classStereochemistryIn silicoCYP1A101 natural sciences03 medical and health scienceschemistry.chemical_compoundTriarylmethaneDrug DiscoverymedicineHumans[CHIM]Chemical SciencesMolecular Targeted TherapyTranscription factor030304 developmental biologyADMEPharmacologyIndole test0303 health sciencesbiology010405 organic chemistryChemistryOrganic ChemistryQuinolineHep G2 CellsGeneral MedicineDruglikenessAryl hydrocarbon receptor3. Good health0104 chemical sciencesMolecular Docking SimulationReceptors Aryl HydrocarbonAh receptorbiology.proteinTranscription factorMethaneAgonistic activityProtein Binding
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Recruitment of HIF-1α and HIF-2α to common target genes is differentially regulated in neuroblastoma: HIF-2α promotes an aggressive phenotype

2006

In neuroblastoma specimens, HIF-2alpha but not HIF-1alpha is strongly expressed in well-vascularized areas. In vitro, HIF-2alpha protein was stabilized at 5% O2 (resembling end capillary oxygen conditions) and, in contrast to the low HIF-1alpha activity at this oxygen level, actively transcribed genes like VEGF. Under hypoxia (1% O2), HIF-1alpha was transiently stabilized and primarily mediated acute responses, whereas HIF-2alpha protein gradually accumulated and governed prolonged hypoxic gene activation. Knockdown of HIF-2alpha reduced growth of neuroblastoma tumors in athymic mice. Furthermore, high HIF-2alpha protein levels were correlated with advanced clinical stage and high VEGF expr…

Transcriptional ActivationCancer ResearchProcollagen-Proline DioxygenaseAggressive phenotypeCELLCYCLEBiologyMiceNeuroblastomaNeuroblastomaBasic Helix-Loop-Helix Transcription FactorsTumor Cells CulturedmedicineAnimalsHumansRNA MessengerChildHypoxiaGeneOligonucleotide Array Sequence AnalysisRegulation of gene expressionGene knockdownGene Expression ProfilingCell BiologyCell cycleHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseIn vitroGene Expression Regulation NeoplasticOxygenPhenotypeOncologyImmunologyCancer researchFemalemedicine.symptomNeoplasm TransplantationCancer Cell
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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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Mechanism of leptin expression in breast cancer cells: role of hypoxia-inducible factor-1α

2007

We reported previously that the obesity hormone leptin is overexpressed in breast cancer biopsies. Here, we investigated molecular mechanisms involved in this process, focusing on conditions that are associated with obesity, that is, hyperinsulinemia and induction of hypoxia. By using quantitative real-time PCR, immunofluorescent detection of proteins and enzyme-linked immunosorbent assays, we found that treatment of MCF-7 breast cancer cells with high doses of insulin or the hypoxia-mimetic agent CoCl2, or culturing the cells under hypoxic conditions significantly increased the expression of leptin mRNA and protein. Notably, the greatest leptin mRNA and protein expression were observed und…

Transcriptional ActivationCancer Researchmedicine.medical_specialtyActive Transport Cell NucleusBreast NeoplasmsBiologymedicine.disease_causeleptinbreast cancerInternal medicineCoactivatorGene expressionTumor Cells CulturedGeneticsmedicineHumansInsulinHIFp300-CBP Transcription FactorsPromoter Regions GeneticMolecular BiologyCell NucleusRegulation of gene expressionBinding SitesLeptin receptorLeptinPromoterCobaltHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaGene Expression Regulation NeoplasticEndocrinologyhyperinsulinemiaCarcinogenesisChromatin immunoprecipitationhormones hormone substitutes and hormone antagonistsProtein BindingOncogene
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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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Transcription factors involved in the expression of SLC28 genes in human liver parenchymal cells.

2007

Human nucleoside transporters are encoded by SLC28 (hCNTs) and SLC29 (hENTs) genes. These proteins mediate the uptake of anticancer and some antiviral drugs and are also suitable candidates to facilitate nucleoside-derived drug uptake into hepatocytes for detoxification. Despite the putative relevance of these genes in liver physiology, the human SLC28 and SLC29 expression pattern is not known and suitable cell models are not available. These issues have been addressed by examining NT expression in human liver and primary cultures of human hepatocytes. Moreover, the effect of specific liver enriched transcription factors (LETFs) in hCNTs expression has been analyzed. Human hepatocytes expre…

Transcriptional ActivationCellBiophysicsGene ExpressionMembrane Transport ProteinsEquilibrative nucleoside transporterTransporterCell BiologyBiologyBiochemistryPhenotypeCell biologymedicine.anatomical_structureGene expressionmedicineHepatocytesHumansMolecular BiologyGeneNucleosideTranscription factorCells CulturedTranscription FactorsBiochemical and biophysical research communications
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The HMGA1 protoncogene frequently deregulated in cancer is a transcriptional target of E2F1

2011

Reactivation of the HMGA1 protoncogene is very frequent in human cancer, but still very little is known on the molecular mechanisms leading to this event. Prompted by the finding of putative E2F binding sites in the human HMGA1 promoter and by the frequent deregulation of the RB/E2F1 pathway in human carcinogenesis, we investigated whether E2F1 might contribute to the regulation of HMGA1 gene expression. Here we report that E2F1 induces HMGA1 by interacting with a 193bp region of the HMGA1 promoter containing an E2F binding site surrounded by three putative Sp1 binding sites. Both gain and loss of function experiments indicate that Sp1 functionally interacts with E2F1 to promote HMGA1 expre…

Transcriptional ActivationChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternMolecular Sequence DataReal-Time Polymerase Chain ReactionRetinoblastoma ProteinSp1MiceAnimalsHumansPituitary NeoplasmsThyroid NeoplasmsHMGA1a ProteinPituitary NeoplasmRNA MessengerPromoter Regions GeneticCarcinogenesiThyroid NeoplasmHMGA1 promoterMice KnockoutBinding SitesBase SequenceAnimalReverse Transcriptase Polymerase Chain ReactionBinding SiteMutationMutagenesis Site-DirectedTranscriptionE2F1 Transcription FactorHumansp1; carcinogenesis; hmga1 promoter; transcription
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