Search results for "E2F"

showing 10 items of 37 documents

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
researchProduct

Differentiative pathway activated by 3-aminobenzamide, an inhibitor of PARP, in human osteosarcoma MG-63 cells

2004

AbstractThis study describes the molecular mechanism by which treatment with 3-AB, a potent inhibitor of PARP, allows human osteosarcoma MG-63 cells to restrict growth and enter differentiation. Our findings show that in MG-63 cells, aberrant gene expression keeps Rb protein constitutively inactivated through hyperphosphorylation and this promotes uncontrolled proliferation of the cells. After 3-AB-treatment, the poly(ADP-ribosyl)ation of nuclear proteins markedly decreases and this results in an increase in both the hypophosphorylated active form of Rb and pRb/E2F complexes. These effects are accompanied by G1 arrest, downregulation of gene products required for proliferation (cyclin D1, β…

Blotting WesternBiophysicsHyperphosphorylationCell Cycle ProteinsPoly(ADP-ribose) Polymerase InhibitorsCell cycleRetinoblastoma ProteinBiochemistryPARPRb proteinCyclin D1Downregulation and upregulationStructural BiologyCell Line TumorGene expressionGeneticsHumansImmunoprecipitationOsteopontinEnzyme InhibitorsPhosphorylationE2FMolecular BiologyDNA PrimersAdenosine Diphosphate RiboseOsteosarcomaBase SequencebiologyReverse Transcriptase Polymerase Chain ReactionG1 PhaseCell DifferentiationCell BiologyCell cycleFlow Cytometry3-ABE2F Transcription FactorsChromatinDNA-Binding ProteinsGene Expression RegulationDifferentiationBenzamidesbiology.proteinCancer researchTranscription FactorsFEBS Letters
researchProduct

Artemisinin–Second Career as Anticancer Drug?

2015

Artemisinin represents a showcase example not only for the activity of medicinal herbs deriving from traditional chinese medicine, but for phytotherapy in general. Its isolation from Sweet Wormwood (qinhao, Artemisia annua L.) represents the starting point for an unprecedent success story in the treatment of malaria worldwide. Beyond the therapeutic value against Plasmodium parasites, it turned out in recent years that the bioactivity of artemisinin is not restricted to malaria. We and others found that this sesquiterpenoid also exerts profound anticancer activity in vitro and in vivo. Artemisinin-type drugs exert multi-factorial cellular and molecular actions in cancer cells. Ferrous iron …

lcsh:R5-920biologyChemistryKinaseKinase insert domain receptorPharmacologyArtemisia annuaMalariaQinhaosuComplementary and alternative medicineCyclin-dependent kinaseGSK-3parasitic diseasesbiology.proteinCancer researchE2F1ChemotherapyArtemisininProtein kinase Alcsh:Medicine (General)Protein kinase BTyrosine kinaseCancerPhytotherapyWorld Journal of Traditional Chinese Medicine
researchProduct

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
researchProduct

RB1 in cancer: Different mechanisms of RB1 inactivation and alterations of pRb pathway in tumorigenesis

2013

Loss of RB1 gene is considered either a causal or an accelerating event in retinoblastoma. A variety of mechanisms inactivates RB1 gene, including intragenic mutations, loss of expression by methylation and chromosomal deletions, with effects which are species-and cell type-specific. RB1 deletion can even lead to aneuploidy thus greatly increasing cancer risk. The RB1gene is part of a larger gene family that includes RBL1 and RBL2, each of the three encoding structurally related proteins indicated as pRb, p107, and p130, respectively. The great interest in these genes and proteins springs from their ability to slow down neoplastic growth. pRb can associate with various proteins by which it …

GeneticsPhysiologyRetinoblastomaClinical BiochemistryCancerCell BiologyBiologymedicine.diseasemedicine.disease_causeE2F Transcription Factor Familyeye diseasesCell biologyRetinoblastoma-like protein 1medicineGene familyGene silencingbiological phenomena cell phenomena and immunityE2FCarcinogenesisJournal of Cellular Physiology
researchProduct

Estudio de las alteraciones genéticas asociadas con la resistencia al tratamiento neoadjuvante de deprivación estrogénica en cáncer de mama

2021

With current standard of care adjuvant therapy, approximately 25-30% of women with high risk early stage HR+/HER2- breast cancer experience relapse. The preoperative platform offers an opportunity to interrogate mechanisms of drug resistance that, in turn, could inform the choice of adjuvant therapy. We report herein a study where we performed targeted DNA sequencing and whole transcriptome analysis on whole tumor sections from a cohort of 68 operable ER+ breast cancers treated with the aromatase inhibitor letrozole for a median of 7.2 months before surgery, and a with a median follow up of 5 years. We found that resistant tumors were enriched in clinically actionable mutation and showed an…

E2FUNESCO::CIENCIAS MÉDICAShormonoterapia neodayuvantecancer de mamaresistencia hormonal:CIENCIAS MÉDICAS [UNESCO]
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

p27Kip1 regulates alpha-synuclein expression

2018

Alpha-synuclein (α-SYN) is the main component of anomalous protein aggregates (Lewy bodies) that play a crucial role in several neurodegenerative diseases (synucleinopathies) like Parkinson’s disease and multiple system atrophy. However, the mechanisms involved in its transcriptional regulation are poorly understood. We investigated here the role of the cyclin-dependent kinase (Cdk) inhibitor and transcriptional regulator p27Kip1 (p27) in the regulation of α-SYN expression. We observed that selective deletion of p27 by CRISPR/Cas9 technology in neural cells resulted in increased levels of α-SYN. Knock-down of the member of the same family p21Cip1 (p21) also led to increased α-SYN levels, in…

0301 basic medicinep27Kip1[SDV]Life Sciences [q-bio]03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCyclin-dependent kinaseTranscriptional regulationalpha synucleinAlpha synucleinPsychological repressionE2F4Alpha-synucleinSynucleinopathiesbiologyPromoterEnzyme inhibitorsMolecular biologyExpressió gènica3. Good healthnervous system diseases030104 developmental biologyOncologychemistryInhibidors enzimàticsnervous systemE2F4biology.proteinGene expressionTranscription Factor E2F4transcriptionp21Cip1Transcription030217 neurology & neurosurgeryResearch Paper
researchProduct