Search results for "Proto-oncogene"

showing 10 items of 770 documents

Knockout of myeloid cell leukemia-1 induces liver damage and increases apoptosis susceptibility of murine hepatocytes

2008

Apoptosis, or programmed cell death, regulates tissue development and homeostasis in multi-cellular organisms. Extrinsic or intrinsic death signals activate pro-apoptotic pathways, resulting in the activation of caspases and finally in cell death. An important event during apoptosis process is the permeabilization of the outer mitochondrial membrane (OMM). Integrity of the OMM is regulated by the Bcl-2 protein family, which is divided into three groups: anti-apoptotic members Bcl-2, Bcl-xL and myeloid cell leukemia-1 (Mcl-1), pro-apoptotic multidomain members Bax and Bak, and pro-apoptotic BH3-only proteins. Mitochondrial activation is regulated by selective interactions of Bcl-2 proteins v…

Programmed cell deathGenotypeCellular differentiation610 Medicine & healthApoptosisBiologyPolymerase Chain ReactionArticleMiceimmune system diseases10049 Institute of Pathology and Molecular Pathologyhemic and lymphatic diseasesmedicineAnimalsAspartate AminotransferasesneoplasmsDNA PrimersHepatologyCaspase 3Alanine TransaminaseCell DifferentiationDNAFas receptorCell biologyMyeloid Cell Leukemia Sequence 1 ProteinHaematopoiesisGene Expression RegulationLiverProto-Oncogene Proteins c-bcl-2ApoptosisHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinRNA2721 HepatologyHepatocyte growth factorStem cellmedicine.drugHepatology
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Targeting Bcl-2 family proteins modulates the sensitivity of B-cell lymphoma to rituximab-induced apoptosis.

2008

The chimeric monoclonal antibody rituximab is the standard of care for patients with B-cell non-Hodgkin lymphoma (B-NHL). Rituximab mediates complementdependent cytotoxicity and antibodydependent cellular cytotoxicity of CD20-positive human B cells. In addition, rituximab sensitizes B-NHL cells to cytotoxic chemotherapy and has direct apoptotic and antiproliferative effects. Whereas expression of the CD20 antigen is a natural prerequisite for rituximab sensitivity, cell-autonomous factors determining the response of B-NHL to rituximab are less defined. To this end, we have studied rituximab-induced apoptosis in human B-NHL models. We find that rituximab directly triggers apoptosis via the m…

Programmed cell deathLymphoma B-CellImmunologyMedizinAntineoplastic AgentsApoptosisMice SCIDBiochemistryPiperazinesNitrophenolsAntibodies Monoclonal Murine-DerivedMicePhosphatidylinositol 3-Kinasesimmune system diseaseshemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansB-cell lymphomaCD20SulfonamidesbiologyBcl-2 familyBiphenyl CompoundsAntibodies MonoclonalCell BiologyHematologymedicine.diseaseAntigens CD20LymphomaGene Expression Regulation NeoplasticProto-Oncogene Proteins c-bcl-2Apoptosisbiology.proteinCancer researchMyeloid Cell Leukemia Sequence 1 ProteinRituximabSignal transductionRituximabNeoplasm Transplantationmedicine.drugSignal TransductionBlood
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Absence of correlation between oxysterol accumulation in lipid raft microdomains, calcium increase, and apoptosis induction on 158N murine oligodendr…

2013

There is some evidence that oxidized derivatives of cholesterol, 7-ketocholesterol (7KC) and 7β-hydroxycholesterol (7βOHC), are increased in the plasma of patients with neurodegenerative diseases associated with demyelinization of the central nervous system (CNS). It was therefore of interest to investigate the effects of these oxysterols on oligodendrocytes, the myelin-forming cells in the CNS. To this end, 158N murine oligodendrocytes were treated with 7KC or 7βOHC inducing an apoptotic mode of cell death characterized by condensation/fragmentation of the nuclei, dephosphorylation of Akt and GSK3, mitochondrial depolarization involving Mcl-1, and caspase-3 activation. In contrast, under t…

Programmed cell deathOxysterolCell Survivalalpha-TocopherolApoptosisBiologyBiochemistryCell Linechemistry.chemical_compoundGlycogen Synthase Kinase 3MiceMembrane MicrodomainsAnimalsFragmentation (cell biology)Protein kinase BLipid raftKetocholesterolsCell ProliferationPharmacologyDepolarizationHydroxycholesterolsCell biologyOligodendrogliaSterolschemistryProto-Oncogene Proteins c-bcl-2ApoptosisIonomycinMyeloid Cell Leukemia Sequence 1 Proteinlipids (amino acids peptides and proteins)CalciumProto-Oncogene Proteins c-aktBiochemical pharmacology
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Phospholipidosis and down-regulation of the PI3-K/PDK-1/Akt signalling pathway are vitamin E inhibitable events associated with 7-ketocholesterol-ind…

2007

International audience; Among the oxysterols accumulating in atherosclerotic plaque, 7-ketocholesterol (7KC) is a potent apoptotic inducer, which favours myelin figure formation and polar lipid accumulation. This investigation performed on U937 cells consisted in characterizing the myelin figure formation process; determining the effects of 7KC on the PI3-K/PDK-1/Akt signalling pathway; evaluating the activities of vitamin E (Vit-E) (α-tocopherol) on the formation of myelin figures and the PI3-K/PDK-1/Akt signalling pathway and assessing the effects of PI3-K inhibitors (LY-294002, 3-methyladenine) on the activity of Vit-E on cell death and polar lipid accumulation. The ultrastructural and b…

Programmed cell deathOxysterolEndocrinology Diabetes and MetabolismClinical BiochemistryDown-RegulationApoptosisPyrimidinones[SDV.BC]Life Sciences [q-bio]/Cellular BiologyProtein Serine-Threonine KinasesBiochemistryDephosphorylationPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineMicroscopy Electron TransmissionOxazinesHumansVitamin EKetocholesterolsMolecular BiologyProtein kinase BPhospholipids030304 developmental biologyPhospholipidosis0303 health sciencesNutrition and DieteticsPhosphoinositide 3-kinasebiologyChemistryPyruvate Dehydrogenase Acetyl-Transferring KinaseU937 CellsProtein phosphatase 2Cell biology030220 oncology & carcinogenesisbiology.proteinBenzimidazolesSignal transductionProto-Oncogene Proteins c-aktSignal TransductionThe Journal of Nutritional Biochemistry
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Hepatocyte-specific deletion of the antiapoptotic protein myeloid cell leukemia-1 triggers proliferation and hepatocarcinogenesis in mice

2010

Regulation of hepatocellular apoptosis is crucial for liver homeostasis. Increased sensitivity of hepatocytes toward apoptosis results in chronic liver injury, whereas apoptosis resistance is linked to hepatocarcinogenesis and nonresponsiveness to therapy-induced cell death. Recently, we have demonstrated an essential role of the antiapoptotic Bcl-2 family member Myeloid cell leukemia-1 (Mcl-1) in hepatocyte survival. In mice lacking Mcl-1 specifically in hepatocytes (Mcl-1Δhep), spontaneous apoptosis caused severe liver damage. Here, we demonstrate that chronically increased apoptosis of hepatocytes coincides with strong hepatocyte proliferation resulting in hepatocellular carcinoma (HCC).…

Programmed cell deathPathologymedicine.medical_specialty10208 Institute of NeuropathologyApoptosis610 Medicine & health10071 Functional Genomics Center ZurichBiologyArticleMiceLiver Neoplasms Experimental10049 Institute of Pathology and Molecular PathologySurvivinmedicineAnimalsneoplasmsCell ProliferationChromosome AberrationsMice KnockoutHepatologyCell growthLiver cellmedicine.diseaseMyeloid Cell Leukemia Sequence 1 ProteinLeukemiamedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisHepatocyteHepatocytesCancer researchMyeloid Cell Leukemia Sequence 1 Protein570 Life sciences; biology2721 HepatologyU7 Systems Biology / Functional GenomicsHepatology
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Dexamethasone treatment of naïve organ of Corti explants alters the expression pattern of apoptosis-related genes.

2009

Dexamethasone treatment of organ of Corti explants challenged with an ototoxic level of an inflammatory cytokine modulates NFkappaB signaling and the expression levels of both pro-and anti-apoptosis-related genes. It is not known if naïve organ of Corti explants will respond in a similar manner to treatment with a corticosteroid. This study examines the response of naïve organ of Corti explants to treatment with dexamethasone.Three-day-old rat organ of Corti explants were cultured for 1, 2, or 4 days. Four-day in vitro cultures were fixed, stained with FITC-phalloidin and hair cells were counted. ELISA was performed on 2-day cultures to determine the levels of phosphorylated nuclear factor …

Programmed cell deathPathologymedicine.medical_specialtyTime Factorsmedicine.medical_treatmentAnti-Inflammatory Agentsbcl-X ProteinGene ExpressionApoptosisCell CountEnzyme-Linked Immunosorbent AssayBiologyDexamethasoneStatistics NonparametricAndrologyRats Sprague-DawleyOrgan Culture TechniquesGene expressionmedicineAnimalsInner earPhosphorylationMolecular BiologyOrgan of CortiDexamethasonebcl-2-Associated X ProteinAnalysis of VarianceReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceNF-kappa BRatsCytokinemedicine.anatomical_structureAnimals NewbornProto-Oncogene Proteins c-bcl-2Organ of CortiApoptosisReceptors Tumor Necrosis Factor Type Isense organsNeurology (clinical)Hair cellDevelopmental Biologymedicine.drugBrain research
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µ-Calpain conversion of antiapoptotic Bfl-1 (BCL2A1) into a prodeath factor reveals two distinct alpha-helices inducing mitochondria-mediated apoptos…

2011

Anti-apoptotic Bfl-1 and pro-apoptotic Bax, two members of the Bcl-2 family sharing a similar structural fold, are classically viewed as antagonist regulators of apoptosis. However, both proteins were reported to be death inducers following cleavage by the cysteine protease µ-calpain. Here we demonstrate that calpain-mediated cleavage of full-length Bfl-1 induces the release of C-terminal membrane active α-helices that are responsible for its conversion into a pro-apoptotic factor. A careful comparison of the different membrane-active regions present in the Bfl-1 truncated fragments with homologous domains of Bax show that helix α5, but not α6, of Bfl-1 induces cell death and cytochrome c r…

Programmed cell deathProtein StructureCancer Treatmentlcsh:MedicineApoptosisMitochondrionCleavage (embryo)BiochemistryProtein Structure SecondaryMinor Histocompatibility AntigensMiceCell Line TumorMolecular Cell BiologyAnimalsHumanslcsh:ScienceProtein InteractionsBiologyMultidisciplinaryMicroscopy ConfocalbiologyCell DeathCalpainCytochrome clcsh:RCytochromes cProteinsCalpainCysteine proteaseCell biologyMitochondriaProto-Oncogene Proteins c-bcl-2OncologyApoptosisbiology.proteinMedicinelcsh:QElectrophoresis Polyacrylamide GelGlobular ProteinsBCL2-related protein A1Research ArticlePloS one
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Combined inhibition of Bcl-2 and NFκB synergistically induces cell death in cutaneous T-cell lymphoma.

2019

Abstract Therapeutic options for cutaneous T-cell lymphoma (CTCL) are limited and curative treatment regimens are not available. Thus, new targeted and well-tolerated therapeutic approaches are urgently needed. In this respect, we have recently shown that dimethyl fumerate (DMF) inhibits NF-κB acting as a survival factor in CTCL. Similarly, inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) has been shown to induce cell death in CTCL especially when combined with histone deacetylase inhibitors. Therefore, we hypothesized that inhibition of Bcl-2 should potentiate NF-κB inhibition in a novel combination treatment of CTCL. We show that, in vitro, the Bcl-2 inhibitors ABT-199 an…

Programmed cell deathT cellImmunologyAntineoplastic AgentsApoptosisBiochemistryMicehemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansRNA Small InterferingCell ProliferationNeoplasm StagingCell DeathDose-Response Relationship Drugbusiness.industryCutaneous T-cell lymphomaNF-kappa BDrug SynergismCell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysLymphomaLymphoma T-Cell CutaneousHistone Deacetylase InhibitorsDisease Models Animalmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCancer researchRNA InterferenceHistone deacetylaseSignal transductionbusinessProtein BindingBlood
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α-Tocopherol impairs 7-ketocholesterol-induced caspase-3-dependent apoptosis involving GSK-3 activation and Mcl-1 degradation on 158N murine oligoden…

2011

Abstract In important and severe neurodegenerative pathologies, 7-ketocholesterol, mainly resulting from cholesterol autoxidation, may contribute to dys- or demyelination processes. On various cell types, 7-ketocholesterol has often been shown to induce a complex mode of cell death by apoptosis associated with phospholipidosis. On 158N murine oligodendrocytes treated with 7-ketocholesterol (20 μg/mL corresponding to 50 μM, 24–48 h), the induction of a mode of cell death by apoptosis characterised by the occurrence of cells with condensed and/or fragmented nuclei, caspase activation (including caspase-3) and internucleosomal DNA fragmentation was observed. It was associated with a loss of tr…

Programmed cell deathTime FactorsCell Survivalalpha-TocopherolApoptosisCaspase 3BiochemistryDephosphorylationGlycogen Synthase Kinase 3MiceMembrane MicrodomainsGSK-3AnimalsKetocholesterolsMolecular BiologyProtein kinase BCell ProliferationMembrane Potential MitochondrialPhospholipidosisGlycogen Synthase Kinase 3 betaCaspase 3ChemistryOrganic ChemistryCytochromes cCell BiologyCell biologyEnzyme ActivationOligodendrogliaProtein TransportProto-Oncogene Proteins c-bcl-2ApoptosisMyeloid Cell Leukemia Sequence 1 ProteinDNA fragmentationChemistry and Physics of Lipids
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Effect of ultraviolet light, methyl methanesulfonate and ionizing radiation on the genotoxic response and apoptosis of mouse fibroblasts lacking c-Fo…

2001

c-Fos and p53 are DNA damage-inducible proteins that are involved in gene regulation, cell cycle checkpoint control and cell proliferation following exposure to genotoxic agents. To investigate comparatively the role of c-Fos and p53 in the maintenance of genomic stability and the induction of apoptosis, we generated mouse fibroblast cell lines from knockout mice deficient for either c-fos (fos -/-) or p53 (p53-/-) or for both gene products (fosp53-/-). The sensitivity of these established cell lines was compared with the corresponding wild-type cells as to the cytotoxic, clastogenic and apoptosis-inducing effects of ultraviolet (UV-C) light and methyl methanesulfonate (MMS). Additionally, …

Programmed cell deathTime FactorsCell cycle checkpointCell SurvivalUltraviolet RaysHealth Toxicology and MutagenesisBlotting WesternApoptosisBiologyToxicologyPolymerase Chain ReactionCell LineMiceNecrosischemistry.chemical_compoundRadiation IonizingGeneticsUltraviolet lightAnimalsCytotoxic T cellCells CulturedGenetics (clinical)Chromosome AberrationsMice KnockoutCell growthDose-Response Relationship RadiationFibroblastsBlotting NorthernMethyl MethanesulfonateMolecular biologyMethyl methanesulfonatechemistryApoptosisCell cultureTumor Suppressor Protein p53Proto-Oncogene Proteins c-fosDNA DamageMutagensMutagenesis
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