Search results for "E2F1 Transcription Factor"

showing 10 items of 11 documents

Regulation of E2F1 Transcription Factor by Ubiquitin Conjugation

2017

IF 3.226; International audience; Ubiquitination is a post-translational modification that defines the cellular fate of intracellular proteins. It can modify their stability, their activity, their subcellular location, and even their interacting pattern. This modification is a reversible event whose implementation is easy and fast. It contributes to the rapid adaptation of the cells to physiological intracellular variations and to intracellular or environmental stresses. E2F1 (E2 promoter binding factor 1) transcription factor is a potent cell cycle regulator. It displays contradictory functions able to regulate both cell proliferation and cell death. Its expression and activity are tightly…

0301 basic medicineProgrammed cell deathReviewubiquitinationCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciencesUbiquitinAnimalsHumansE2F1Physical and Theoretical Chemistry[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologylcsh:QH301-705.5Molecular BiologyTranscription factorSpectroscopybiologyCell growthOrganic ChemistryE2F1 Transcription FactorGeneral MedicineCell cycleComputer Science ApplicationsCell biology030104 developmental biologyE2F1lcsh:Biology (General)lcsh:QD1-999biology.proteinDNA damagecell cycleE2F1 Transcription FactorIntracellularInternational Journal of Molecular Sciences
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E2F1 interacts with BCL-xL and regulates its subcellular localization dynamics to trigger cell death

2018

International audience; E2F1 is the main pro-apoptotic effector of the pRB-regulated tumor suppressor pathway by promoting the transcription of various pro-apoptotic proteins. We report here that E2F1 partly localizes to mitochondria, where it favors mitochondrial outer membrane permeabilization. E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death. We thus identify a new, non-BH3-binding regulator of BCL-xL localization dynamics that influences its anti-apoptotic activity.

0301 basic medicineProgrammed cell deathTranscription Geneticbcl-X ProteinRegulatorBcl-xL[SDV.CAN]Life Sciences [q-bio]/CancerBCL-xL mobilityMitochondrionBiochemistrylaw.invention[ SDV.CAN ] Life Sciences [q-bio]/CancerE2F1 Subject Category Autophagy & Cell Death03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerlawBCL-2 familyCell Line TumorGeneticsJournal ArticleHumansE2F1Molecular BiologyCell DeathbiologyManchester Cancer Research CentreEffectorChemistryResearchInstitutes_Networks_Beacons/mcrcScientific ReportsapoptosisSubcellular localizationMitochondriaCell biologyProtein Transportbcl-2 Homologous Antagonist-Killer Protein030104 developmental biologyGene Expression RegulationProto-Oncogene Proteins c-bcl-2biology.proteinSuppressorbiological phenomena cell phenomena and immunityExtracellular SpaceE2F1 Transcription FactorProtein Binding
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Development of a simple, biocompatible and cost-effective Inulin-Diethylenetriamine based siRNA delivery system

2015

Small interfering RNAs (siRNAs) have the potential to be of therapeutic value for many human diseases. So far, however, a serious obstacle to their therapeutic use is represented by the absence of appropriate delivery systems able to protect them from degradation and to allow an efficient cellular uptake. In this work we developed a siRNA delivery system based on inulin (Inu), an abundant and natural polysaccharide. Inu was functionalized via the conjugation with diethylenetriamine (DETA) residues to form the complex Inu-DETA. We studied the size, surface charge and the shape of the Inu-DETA/siRNA complexes; additionally, the cytotoxicity, the silencing efficacy and the cell uptake-mechanis…

3003Small interfering RNAJHH6CellPharmaceutical ScienceEndocytosisCell LineIn vivoCell Line TumormedicinePolyaminesGene silencingHumansMicropinocytosisRNA Small InterferingCytotoxicityChemistry16HBEInulinEndocytosisDiethylenetriamine (DETA)Cell biologyInu-DETA copolymermedicine.anatomical_structureBiochemistryCytoplasmSettore CHIM/09 - Farmaceutico Tecnologico ApplicativosiRNA16HBE; Diethylenetriamine (DETA); Inu-DETA copolymer; Inulin; JHH6; siRNA; 3003E2F1 Transcription Factor
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Low doses of paclitaxel potently induce apoptosis in human retinoblastoma Y79 cells by up-regulating E2F1.

2008

Paclitaxel (PTX) is an anticancer drug currently in phase II clinical trials. This study shows for the first time that low doses of PTX (5 nM) potently induce apoptosis in human retinoblastoma Y79 cells. The effect of PTX is accompanied by a potent induction of E2F1 which appears to play a critical role in the effects induced by PTX. PTX induced a dose- and time-dependent effect, with G2/M arrest, cyclines A, E and B1 accumulation and a marked modification in the status of Cdc2-cyclin B1 complex, the major player of the G2/M checkpoint. Apoptosis followed G2/M arrest. An early and prolonged increase in p53 expression with its stabilization by phosphorylation and acetylation and its nuclear …

Cyclin-Dependent Kinase Inhibitor p21G2 Phaseendocrine systemCancer ResearchProgrammed cell deathPaclitaxelApoptosisBiologyretinoblastoma apoptosis paclitaxelp14arfSettore BIO/10 - BiochimicaCell Line TumorE2F1HumansFragmentation (cell biology)PhosphorylationMembrane Potential MitochondrialRetinoblastomaCell cycleAntineoplastic Agents PhytogenicUp-RegulationGene Expression Regulation NeoplasticOncologyApoptosisCancer researchPhosphorylationApoptosomeTumor Suppressor Protein p53Cell DivisionE2F1 Transcription FactorInternational journal of oncology
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Benzo[a]pyrene represses DNA repair through altered E2F1/E2F4 function marking an early event in DNA damage-induced cellular senescence

2020

AbstractTranscriptional regulation of DNA repair is of outmost importance for the restoration of DNA integrity upon genotoxic stress. Here we report that the potent environmental carcinogen benzo[a]pyrene (B[a]P) activates a cellular DNA damage response resulting in transcriptional repression of mismatch repair (MMR) genes (MSH2, MSH6, EXO1) and of RAD51, the central homologous recombination repair (HR) component, ultimately leading to downregulation of MMR and HR. B[a]P-induced gene repression is caused by abrogated E2F1 signalling. This occurs through proteasomal degradation of E2F1 in G2-arrested cells and downregulation of E2F1 mRNA expression in G1-arrested cells. Repression of E2F1-me…

Cyclin-Dependent Kinase Inhibitor p21SenescenceAcademicSubjects/SCI00010DNA repairDNA damageRAD51E2F4 Transcription FactorBiologyDNA Mismatch Repair03 medical and health sciences0302 clinical medicineCell Line TumorBenzo(a)pyreneGeneticsHumansCellular SenescenceCell Line Transformed030304 developmental biology0303 health sciencesGene regulation Chromatin and EpigeneticsRecombinational DNA RepairEpithelial CellsKv Channel-Interacting ProteinsCell Cycle CheckpointsDNAFibroblastsCell biologyDNA-Binding ProteinsRepressor ProteinsMSH6DNA Repair EnzymesExodeoxyribonucleasesMutS Homolog 2 ProteinGamma RaysMSH2030220 oncology & carcinogenesisCarcinogensMCF-7 CellsDNA mismatch repairRad51 RecombinaseCell agingE2F1 Transcription FactorDNA DamageSignal TransductionNucleic Acids 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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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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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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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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