Search results for "E2F"

showing 10 items of 37 documents

Id2 leaves the chromatin of the E2F4-p130-controlled c-myc promoter during hepatocyte priming for liver regeneration

2006

The Id (inhibitor of DNA binding or inhibitor of differentiation) helix–loop–helix proteins are involved in the regulation of cell growth, differentiation and cancer. The fact that the molecular mechanisms of liver regeneration are not completely understood prompted us to study the fate of Id2 in proliferating liver. Id2 increases in liver regeneration after partial hepatectomy, following the early induction of its gene. Co-immunoprecipitation shows that Id2 forms a complex with E2F4, p130 and mSin3A in quiescent liver and all these components are present at the c-myc promoter as shown using ChIP (chromatin immunoprecipitation). Activation of c-myc during hepatocyte priming (G0–G1 transitio…

MalePriming (immunology)E2F4 Transcription FactorId2Cell cycleBiologyBiochemistryProto-Oncogene Proteins c-mycE2FmedicineAnimalsHistone deacetylaseRats WistarPromoter Regions GeneticE2FMolecular BiologyE2F4Inhibitor of Differentiation Protein 2Cell BiologyMolecular biologyChromatinLiver regenerationLiver RegenerationRatsSpecific Pathogen-Free OrganismsUp-RegulationChromatinC-mycmedicine.anatomical_structureGene Expression RegulationHepatocyteHepatocytesLiver regenerationHistone deacetylaseCarrier ProteinsChromatin immunoprecipitationResearch Article
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Adenoviral RB2/p130 gene transfer inhibits smooth muscle cell proliferation and prevents restenosis after angioplasty.

1999

Abstract —Smooth muscle cell (SMC) proliferation that results in neointima formation is implicated in the pathogenesis of atherosclerotic plaques and accounts for the high rates of restenosis that occur after percutaneous transluminal coronary angioplasty, a widespread treatment for coronary artery disease. Endothelial lesions trigger intense proliferative signals to the SMCs of the subintima, stimulating their reentry into the cell cycle from a resting G 0 state, resulting in neointima formation and vascular occlusion. Cellular proliferation is negatively controlled by growth-regulatory or tumor-suppressor genes, or both, such as the retinoblastoma gene family members ( RB/p105, p107, RB2…

NeointimaTranscriptional Activationmedicine.medical_specialtyPhysiologyadenovirus; cell cycle; gene therapy; p130; prb2; restenosisCellGenetic VectorsCell Cycle ProteinsPulmonary ArteryMuscle Smooth VascularAdenoviridaeCatheterizationPathogenesisRestenosisRecurrencemedicineAnimalsCarotid StenosisAngioplasty Balloon CoronaryGenes RetinoblastomaCells CulturedNeointimal hyperplasiaWound HealingRetinoblastoma-Like Protein p130business.industryCell growthGenetic transferCell CycleProteinsGenetic TherapyCell cyclemedicine.diseasePhosphoproteinsSurgeryE2F Transcription FactorsRatsDNA-Binding Proteinsmedicine.anatomical_structureCancer researchCardiology and Cardiovascular MedicinebusinessCarotid Artery InjuriesCarrier ProteinsTunica IntimaTranscription Factor DP1Cell DivisionRetinoblastoma-Binding Protein 1Transcription FactorsCirculation research
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Mouse embryonic stem cells are hypersensitive to apoptosis triggered by the DNA damage O(6)-methylguanine due to high E2F1 regulated mismatch repair.

2007

Exposure of stem cells to genotoxins may lead to embryonic lethality or teratogenic effects. This can be prevented by efficient DNA repair or by eliminating genetically damaged cells. Using undifferentiated mouse embryonic stem (ES) cells as a pluripotent model system, we compared ES cells with differentiated cells, with regard to apoptosis induction by alkylating agents forming the highly mutagenic and killing DNA adduct O(6)-methylguanine. Upon treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), ES cells undergo apoptosis at much higher frequency than differentiated cells, although they express a high level of the repair protein O(6)-methylguanine-DNA methyltransferase (MGMT). Apo…

Pluripotent Stem CellsMethylnitronitrosoguanidineDNA ComplementaryGuanineDNA damageDNA repairCellular differentiationApoptosisBiologyDNA Mismatch RepairModels BiologicalDNA AdductsMiceO(6)-Methylguanine-DNA MethyltransferaseDNA adductAnimalsMolecular BiologyEmbryonic Stem CellsSwiss 3T3 CellsBase SequenceCell DifferentiationCell BiologyDNA MethylationFibroblastsEmbryonic stem cellMolecular biologyDNA-Binding ProteinsMutS Homolog 2 ProteinDNA methylationDNA mismatch repairStem cellE2F1 Transcription FactorDNA DamageCell death and differentiation
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Galactosylated polyaspartamide copolymers for siRNA targeted delivery to hepatocellular carcinoma cells

2017

The limited efficacy of available treatments for hepatocellular carcinoma (HCC) requires the development of novel therapeutic approaches. We synthesized a novel cationic polymer based on α,β-poly-(N-2-hydroxyethyl)-D,L-aspartamide (PHEA) for drug delivery to HCC cells. The copolymer was synthesized by subsequent derivatization of PHEA with diethylene triamine (DETA) and with a polyethylene glycol (PEG) derivative bearing galactose (GAL) molecules, obtaining the cationic derivative PHEA-DETA-PEG-GAL. PHEA-DETA-PEG-GAL has suitable chemical-physical characteristics for a potential systemic use and can effectively deliver a siRNA (siE2F1) targeted against the transcription factor E2F1, a gen…

Polyplexes HCC siRNA E2F1 PHEA-DETA-PEG-GALCarcinoma HepatocellularPolymersPharmaceutical ScienceE2F1; HCC; PHEA-DETA-PEG-GAL; Polyplexes; siRNA.02 engineering and technologyPolyethylene glycol03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorPEG ratiomedicineHumansE2F1Gene silencingGene SilencingRNA Small InterferingHCCReceptorCell growthChemistryLiver NeoplasmssiRNA.021001 nanoscience & nanotechnologymedicine.diseaseMolecular biologyPHEA-DETA-PEG-GALPolyplexeE2F1030220 oncology & carcinogenesisHepatocellular carcinomasiRNADrug deliveryCancer researchPeptides0210 nano-technologyE2F1 Transcription FactorPolyplexes
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DNA damage-induced cell death by apoptosis

2006

Following the induction of DNA damage, a prominent route of cell inactivation is apoptosis. During the last ten years, specific DNA lesions that trigger apoptosis have been identified. These include O6-methylguanine, base N-alkylations, bulky DNA adducts, DNA cross-links and DNA double-strand breaks (DSBs). Repair of these lesions are important in preventing apoptosis. An exception is O6-methylguanine-thymine lesions, which require mismatch repair for triggering apoptosis. Apoptosis induced by many chemical genotoxins is the consequence of blockage of DNA replication, which leads to collapse of replication forks and DSB formation. These DSBs are thought to be crucial downstream apoptosis-tr…

Programmed cell deathDNA RepairDNA repairDNA damageApoptosisp38 Mitogen-Activated Protein KinasesAnimalsHumansE2F1Molecular BiologybiologyCaspase 2DNA replicationDNAProliferating cell nuclear antigenCaspasesbiology.proteinCancer researchMolecular MedicineDNA mismatch repairTumor Suppressor Protein p53biological phenomena cell phenomena and immunityProto-Oncogene Proteins c-aktAtaxia telangiectasia and Rad3 relatedDNA DamageMutagensSignal TransductionTrends in Molecular Medicine
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GAM/ZFp/ZNF512B is central to a gene sensor circuitry involving cell-cycle regulators, TGF beta effectors, Drosha and microRNAs with opposite oncogen…

2010

MicroRNAs (miRNAs) are small regulatory RNAs targeting multiple effectors of cell homeostasis and development, whose malfunctions are associated with major pathologies such as cancer. Herein we show that GAM/ZFp/ZNF512B works within an intricate gene regulatory network involving cell-cycle regulators, TGFβ effectors and oncogenic miRNAs of the miR-17-92 cluster. Thus, GAM impairs the transcriptional activation of the miR-17-92 promoter by c-Myc, downregulates miR-17-92 miRNAs differentially, and limits the activation of genes responsive to TGFβ canonical pathway. In contrast, TGFβ decreases GAM transcripts levels while differentially upregulating miR-17-92 miRNAs. In turn, miR-17, miR-20a a…

Ribonuclease IIITranscriptional ActivationRegulatorGene regulatory networkBiologyProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)Transforming Growth Factor betamicroRNAGeneticsE2F1HumansGene Regulatory NetworksDroshaFeedback PhysiologicalEffectorCell CycleTransforming growth factor betaCell cycleCell biologyMicroRNAsbiology.proteinCancer researchRNACarrier ProteinsE2F1 Transcription Factor
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Targeted delivery of siRNAs against hepatocellular carcinoma-related genes by a galactosylated polyaspartamide copolymer

2021

Given the lack of effective treatments for Hepatocellular carcinoma (HCC), the development of novel therapeutic approaches is very urgent. Here, siRNAs were delivered to HCC cells by a synthetic polymer containing α,β-poly-(N-2-hydroxyethyl)-D,L-aspartamide-(PHEA) derivatized with diethylene triamine (DETA) and bearing in the side chain galactose (GAL) linked via a polyethylene glycol (PEG) to obtain (PHEA-DETA-PEG-GAL, PDPG). The GAL residue allows the targeting to the asialo-glycoprotein receptor (ASGPR), overexpressed in HCC cells compared to normal hepatocytes. Uptake studies performed using a model siRNA or a siRNA targeted against the enhanced green fluorescence protein, demonstrated …

Small interfering RNACarcinoma HepatocellularPolymersHepatocellular carcinomaCellASGPR targeted delivery; E2F1; Eukaryotic elongation Factor 1A; Hepatocellular carcinoma; siRNAPharmaceutical Science02 engineering and technologyEukaryotic elongation Factor 1AMice03 medical and health sciencesIn vivomedicineAnimalsE2F1RNA Small InterferingReceptor030304 developmental biology0303 health sciencesChemistryLiver NeoplasmsASGPR targeted deliveryGalactose021001 nanoscience & nanotechnologymedicine.diseasedigestive system diseasesEukaryotic translation elongation factor 1 alpha 1In vitromedicine.anatomical_structureE2F1Settore CHIM/09 - Farmaceutico Tecnologico ApplicativoHepatocellular carcinomasiRNACancer research0210 nano-technology
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Synthesis and characterization of polyaspartamide copolymers obtained by ATRP for nucleic acid delivery

2014

Abstract Nucleic acid molecules such as small interfering RNAs (siRNAs) and plasmidic DNAs (pDNAs) have been shown to have the potential to be of therapeutic value in different human diseases. Their practical use is however compromised by the lack of appropriate release systems. Delivered as naked molecules, siRNAs/pDNAs are rapidly degraded by extracellular nucleases thus considerably reducing the amount of molecule which can reach the target cells. Additionally, the anionic charge of the phosphate groups present on the siRNAs/pDNAs backbone, disfavors the interaction with the negatively charged surface of the cell membrane. In this paper we describe the generation of a novel polymer able …

Small interfering RNACell SurvivalPharmaceutical ScienceATRPMethacrylateTransfectionsiRNA; deliveryPolymerizationchemistry.chemical_compoundMiceSiRNA delivery; DNA delivery; Polyaspartamide; ATRPCell Line TumorPolymer chemistryCopolymerAnimalsHumansRNA MessengerRNA Small Interferingchemistry.chemical_classificationAtom-transfer radical-polymerizationPolymerDNACombinatorial chemistryPolyaspartamideMonomerchemistryPolymerizationsiRNANucleic acidSiRNA deliveryMethacrylatesdeliveryPeptidesE2F1 Transcription FactorDNA deliveryPlasmids
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Cloning and functional analyses of the mouse tapasin promoter

2003

The expression of tapasin is critical for an optimized MHC class I assembly and stable MHC class I surface expression. Thus, impaired MHC class I antigen expression of tumors can be attributable to tapasin downregulation. In order to understand the molecular mechanisms of deficient tapasin expression, the mouse tapasin promoter region and its 5'-flanking sequences were characterized. The mouse tapasin promoter lacks the TATA box and its transcription is initiated at multiple sites within a 51-nucleotide stretch. Sequence analyses revealed transcription factor binding motifs for NF-kappaB, GATA, E2F, p300, AP1, SP1 and IRF-1/2. Detailed analysis of deletion mutants and elimination of transcr…

TATA boxMolecular Sequence DataImmunologyImmunoglobulinsAntiportersInterferon-gammaMiceTapasinMHC class IGeneticsAnimalsCloning MolecularPromoter Regions GeneticE2FTranscription factorBase SequencebiologyNF-kappa BMembrane Transport ProteinsPromoterDNASequence Analysis DNATransporter associated with antigen processingMolecular biologyAP-1 transcription factorGene Expression Regulationbiology.proteinTranscription Initiation SiteImmunogenetics
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Glutathione regulates telomerase activity in 3T3 fibroblasts.

2004

Changes in telomerase activity have been associated either with cancer, when activity is increased, or with cell cycle arrest when it is decreased. We report that glutathione, a physiological antioxidant present at high intracellular concentrations, regulates telomerase activity in cells in culture. Telomerase activity increases in 3T3 fibroblasts before exponential cell growth. The peak of telomerase activity takes place 24 h after plating and coincides with the maximum levels of glutathione in the cells. When cells are treated with buthionine sulfoximine, which decreases glutathione levels in cells, telomerase activity decreases by 60%, and cell growth is delayed. Glutathione depletion in…

TelomeraseAntioxidantCell cycle checkpointTime FactorsCell divisionmedicine.medical_treatmentBlotting WesternImmunoblottingE2F4 Transcription FactorBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundMicemedicineAnimalsButhionine sulfoximineColoring AgentsMolecular BiologyButhionine SulfoximineTelomeraseInhibitor of Differentiation Protein 2Cell growthCell CycleCell BiologyGlutathione3T3 CellsTrypan BlueCell cycleFibroblastsFlow CytometryMolecular biologyGlutathioneDNA-Binding ProteinsRepressor ProteinschemistryOxidation-ReductionCell DivisionTranscription FactorsThe Journal of biological chemistry
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