Search results for "Sp1 transcription factor"

showing 10 items of 27 documents

Valproate and Short-Chain Fatty Acids Activate Transcription of the Human Vitamin D Receptor Gene through a Proximal GC-Rich DNA Region Containing Tw…

2022

The vitamin D receptor (VDR) mediates 1,25-dihydroxyvitamin D3 pleiotropic biological actions through transcription regulation of target genes. The expression levels of this ligand-activated nuclear receptor are regulated by multiple mechanisms both at transcriptional and post-transcriptional levels. Vitamin D3 is the natural VDR activator, but other molecules and signaling pathways have also been reported to regulate VDR expression and activity. In this study, we identify valproic acid (VPA) and natural short-chain fatty acids (SCFAs) as novel transcriptional activators of the human VDR (hVDR) gene. We further report a comprehensive characterization of VPA/SCFA-responsive elements in the 5…

BioquímicaBiologiaVDR induction; human VDR promoter; valproic acid; SCFA; Sp1.Binding SitesNutrition and DieteticsSp1 Transcription FactorValproic AcidDNAHumansReceptors Calcitriollipids (amino acids peptides and proteins)ChildPromoter Regions GeneticFood Science
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Functional analysis of the -2548G/A leptin gene polymorphism in breast cancer cells

2009

Leptin is overexpressed in human breast tumors and is produced by breast cancer cells in response to obesity-related stimuli. The leptin promoter polymorphism Lep-2548G/A can be associated with increased leptin secretion by adipocytes and elevated cancer risk. However, molecular mechanisms underlying the link between Lep-2548G/A and breast cancer have never been addressed. Lep-2548G/A is proximal to a binding site for the transcriptional factor Sp1. Furthermore nucleolin, a transcriptional repressor, can bind Sp1 or its consensus site. Consequently, we focused on the impact of Lep-2548G/A on Sp1- and nucleolin-dependent leptin transcription in breast cancer cells. The Lep-2548G/A was identi…

LeptinChromatin ImmunoprecipitationCancer Researchmedicine.medical_specialtyGenotypeSp1 Transcription FactorBlotting WesterneducationAdipokineBreast NeoplasmsBiologyBody Mass IndexBreast cancerInternal medicineTumor Cells CulturedmedicineHumansHypoglycemic AgentsInsulinObesityRNA MessengerPromoter Regions Genetichealth care economics and organizationsPolymorphism GeneticLeptin receptorReverse Transcriptase Polymerase Chain ReactionLeptinRNA-Binding ProteinsCancerPhosphoproteinsmedicine.diseaseEndocrinologyOncologyCancer researchImmunohistochemistryBreast diseaseNucleolinhormones hormone substitutes and hormone antagonistsInternational Journal of Cancer
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Identification of a gene-pathway associated with non-alcoholic steatohepatitis.

2007

Background/Aims We have integrated gene expression profiling of liver biopsies of NASH patients with liver samples of a mouse model of steatohepatitis (MAT1A-KO) to identify a gene-pathway associated with NASH. Methods Affymetrix U133 Plus 2.0 microarrays were used to evaluate nine patients with NASH, six patients with steatosis, and six control subjects; Affymetrix MOE430A microarrays were used to evaluate wild-type and MAT1A-KO mice at 15 days, 1, 3, 5 and 8 months after birth. Transcriptional profiles of patients with NASH and MAT1A-KO mice were compared with those of their proficient controls. Results We identified a gene-pathway associated with NASH, that accurately distinguishes betwe…

AdultMalePathologymedicine.medical_specialtySp1 Transcription FactorGene ExpressionHyperphosphorylationBiologyBioinformaticsdigestive systemSp1MiceGene-pathwayGene expressionmedicineAnimalsHumansPhosphorylationPromoter Regions GeneticGeneNon-alcoholic steatohepatitisMice KnockoutS-adenosylmethionineHepatologyMicroarray analysis techniquesGene Expression Profilingnutritional and metabolic diseasesMethionine AdenosyltransferaseMiddle AgedMicroarray Analysismedicine.diseasedigestive system diseasesFatty LiverGene expression profilingLiverFemaleSteatosisSteatohepatitisDNA microarray
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Insulin-dependent leptin expression in breast cancer cells.

2008

Abstract Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, and diabetes, seem to increase the risk of breast cancer. Here, we studied molecular mechanisms by which insulin activates the expression of leptin, an obesity hormone that has been shown to promote breast cancer progression in an autocrine or paracrine way. Using MDA-MB-231 breast cancer cells, we found that (a) insulin stimulated leptin mRNA and protein expression, which was associated with increased activation of the leptin gene promoter; (b) insulin increased nuclear accumulation of transcription factors hypoxia inducible factor (HIF)-1α and Sp1 and their loading on the leptin promoter;…

LeptinTranscriptional ActivationCancer Researchmedicine.medical_specialtySmall interfering RNAChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternFluorescent Antibody TechniqueBreast NeoplasmsEnzyme-Linked Immunosorbent AssayBiologyParacrine signallingPhosphatidylinositol 3-Kinasesbreast cancerInternal medicinemedicineHyperinsulinemiaTumor Cells CulturedHumansHypoglycemic AgentsInsulinRNA MessengerRNA Small InterferingAutocrine signallingLuciferasesPromoter Regions GeneticTranscription factorCell NucleusMitogen-Activated Protein Kinase 1Gene knockdownLeptin receptorMitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionLeptinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaEndocrinologyOncologyCancer researchFemalehormones hormone substitutes and hormone antagonistsCancer research
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How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights

2021

Osteoarthritis (OA) is a degenerative bone disease that involved micro and macro-environment of joints. To date, there are no radical curative treatments for OA and novel therapies are mandatory. Recent evidence suggests the role of miRNAs in OA progression. In our previous studies, we demonstrated the role of miR-31-5p and miR-33a families in different bone regeneration signaling. Here, we investigated the role of miR-31-5p and miR-33a-5p in OA progression. A different expression of miR-31-5p and miR-33a-5p into osteoblasts and chondrocytes isolated from joint tissues of OA patients classified in based on different Kellgren and Lawrence (KL) grading was highlighted

Male0301 basic medicineBone diseasechondrocytesOsteoarthritisCX43lcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5Cells CulturedSpectroscopymicroRNAosteoblastsGeneral MedicineMiddle AgedPrognosisComputer Science ApplicationsmicroRNAsmir-31030220 oncology & carcinogenesischondrocyteosteoblastFemalemedicine.symptomSignal TransductionAdultSp1 Transcription FactorInflammationBiologyArticleCatalysisInorganic Chemistry03 medical and health sciencesmicroRNAmedicineHumansPhysical and Theoretical ChemistryBone regenerationMolecular BiologyGeneLoss functionAgedOrganic Chemistrymedicine.diseaseSP1osteoarthritis030104 developmental biologyGene Expression Regulationlcsh:Biology (General)lcsh:QD1-999Connexin 43Cancer researchFollow-Up StudiesInternational Journal of Molecular Sciences
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Cloning and characterization of the promoter of Hugl-2, the human homologue of Drosophila lethal giant larvae (lgl) polarity gene.

2007

The human lgl gene, Hugl-2 (llgl2, Lgl2), codes for a cytoskeletal protein involved in regulating cell polarity. Here, we report the identification and functional characterization of the promoter region ( approximately 1.2kb) of the Hugl-2 gene. Luciferase expression assays show a high basal Hugl-2 promoter activity in different cell lines and primary human hepatocytes. Truncations of the promoter identified a GC-rich region important for this activity. Alignment of human and mouse genomic sequences demonstrate that this is an evolutionary conserved region fcontaining putative binding sites for several transcription factors including Elk-1 and Sp-1. Mithramycin A reduces Hugl-2 expression i…

Sp1 Transcription FactorMolecular Sequence DataBiophysicsDown-RegulationGenes InsectBiologyBiochemistryCell LineDownregulation and upregulationEpidermal growth factorCell polarityChlorocebus aethiopsAnimalsDrosophila ProteinsHumansLuciferaseCloning MolecularPromoter Regions GeneticMolecular BiologyGeneTranscription factorBase PairingBase SequenceEpidermal Growth FactorSequence Homology Amino AcidTumor Suppressor ProteinsCell PolarityPromoterCell BiologyMolecular biologyCytoskeletal ProteinsDrosophila melanogasterCell cultureCOS CellsSequence AlignmentBiochemical and biophysical research communications
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Resveratrol, a polyphenolic phytoalexin present in red wine, enhances expression and activity of endothelial nitric oxide synthase.

2002

Background— Estrogens can upregulate endothelial nitric oxide synthase (eNOS) in human endothelial cells by increasing eNOS promoter activity and enhancing the binding activity of the transcription factor Sp1. Resveratrol, a polyphenolic phytoalexin found in grapes and wine, has been reported to act as an agonist at the estrogen receptor. Therefore, we tested the effect of this putative phytoestrogen on eNOS expression in human endothelial cells. Methods and Results— Incubation of human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 cells with resveratrol for 24 to 72 hours upregulated eNOS mRNA expression in a time- and concentration-dependent manner (up to 2.8-fold)…

PolymersRNA StabilityElectrophoretic Mobility Shift AssayWineResveratrolUmbilical veinchemistry.chemical_compoundEnosStilbenesPromoter Regions GeneticCells Culturedchemistry.chemical_classificationbiologyPhytoalexinEstrogen Antagonistsfood and beveragesNitric Oxide Synthase Type IIIUp-RegulationNitric oxide synthasemedicine.anatomical_structureReceptors EstrogenEnzyme InductionCardiology and Cardiovascular MedicineSesquiterpenesmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIINuclease Protection AssaysEnzyme ActivatorsPhytoestrogensNitric OxidePhenolsPhytoalexinsPhysiology (medical)Internal medicinemedicineHumansEstrogens Non-SteroidalRNA MessengerFlavonoidsSp1 transcription factorPlant ExtractsTerpenesPolyphenolsbiology.organism_classificationMolecular biologyIsoflavonesEnzyme ActivationEndocrinologychemistryResveratrolbiology.proteinEndothelium VascularPlant PreparationsNitric Oxide SynthaseCirculation
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A novel SP-1 site in the human interleukin-1β promoter confers preferential transcriptional activity in keratinocytes

1996

To investigate the mechanisms of transcriptional activation of interleukin-1beta (IL-1beta) in non-monocytic cells, we constructed a series of reporter plasmids with the bacterial chloramphenicol acetyltransferase gene linked to various parts of the human IL-1beta promoter and performed transient transfection experiments. We identified a promoter segment that activates transcription most efficiently in keratinocytes. Electrophoretic mobility shift assays (EMSA) with a 43-mer oligonucleotide derived from the functionally identified cis-acting element revealed specific complexes. By competition analysis with transcription factor consensus sequence oligonucleotides and by immunosupershift, tra…

Cell NucleusKeratinocytesTranscriptional ActivationSp1 transcription factorTranscription GeneticSp1 Transcription FactorTumor Necrosis Factor-alphaImmunologyResponse elementBiologyMolecular biologyMonocytesChloramphenicol acetyltransferaseGenes ReporterTranscription (biology)MutationConsensus sequenceTranscriptional regulationHumansImmunology and AllergyPromoter Regions GeneticTranscription factorGeneCell Line TransformedInterleukin-1European Journal of Immunology
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11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma

2020

High-risk 11q deleted neuroblastomas typically display undifferentiated/poorly differentiated morphology. Neuroblastoma is thought to develop from Schwann cell precursors and undifferentiated neural crest (NC) derived cells. It is therefore vital to understand mechanisms involved in the block of differentiation. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in maintenance of undifferentiated NC-derived progenitors via repression of DLG2, a tumor suppressor in neuroblastoma. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors become chromaffin cells of the adrenal gland. We …

0301 basic medicineTranscription GeneticCarcinogenesisChromaffin CellsRetinoic acidlaw.inventionNeuroblastomachemistry.chemical_compound0302 clinical medicinelawNerve Growth FactorMedicine and Health Sciencesretinoic acidAnaplastic Lymphoma Kinaselcsh:QH301-705.5NeuronsMice Inbred BALB CNeural crestCell DifferentiationPrognosisCandidate Tumor Suppressor GeneDLG2Up-RegulationCell biologyGene Expression Regulation NeoplasticERKPhenotypeTreatment Outcomemedicine.anatomical_structureFemaleChromosome Deletiontumor suppressorMAP Kinase Signaling SystemSp1 Transcription FactorSchwann cellGenetics and Molecular BiologyTretinoinBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAdrenergic AgentsCell Line TumorNeuroblastomamedicineAnimalsHumansProgenitor cellGenePsychological repressionCell ProliferationChromosomes Human Pair 11Tumor Suppressor Proteinsmedicine.disease030104 developmental biologyALKlcsh:Biology (General)chemistryTrk receptorGeneral BiochemistrySuppressorSchwann CellsGuanylate Kinases030217 neurology & neurosurgerySSRN Electronic Journal
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The designer cytokine hyper-interleukin-6 is a potent activator of STAT3-dependent gene transcription in vivo and in vitro.

1999

Interleukin-6 (IL-6) triggers pivotal pathways in vivo. The designer protein hyper-IL-6 (H-IL-6) fuses the soluble IL-6 receptor (sIL-6R) through an intermediate linker with IL-6. The intracellular pathways that are triggered by H-IL-6 are not defined yet. Therefore, we studied the molecular mechanisms leading to H-IL-6-dependent gene activation. H-IL-6 stimulates haptoglobin mRNA expression in HepG2 cells, which is transcriptionally mediated as assessed by run-off experiments. The increase in haptoglobin gene transcription correlates with higher nuclear translocation of tyrosine-phosphorylated STAT3 and its DNA binding. As H-IL-6 stimulates STAT3-dependent gene transcription, we compared t…

Therapeutic gene modulationSTAT3 Transcription FactorTranscriptional ActivationTranscription GeneticRecombinant Fusion ProteinsResponse elementE-boxBiologyTransfectionBiochemistryCell LineMiceSp3 transcription factorAntigens CDCytokine Receptor gp130E2F1AnimalsHumansRNA MessengerPhosphorylationMolecular BiologyCell NucleusATF3Sp1 transcription factorMice Inbred C3HMembrane GlycoproteinsHaptoglobinsInterleukin-6Liver receptor homolog-1Biological TransportCell BiologyDNAReceptors InterleukinMolecular biologyReceptors Interleukin-6DNA-Binding ProteinsGene Expression RegulationTrans-ActivatorsTyrosineThe Journal of biological chemistry
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