Search results for "Apoptosi"

showing 10 items of 1846 documents

Autophagy and apoptosis regolate survival of mesoangioblast stem cells subjected to oxidative stress

2012

Autophagy apoptosis mesoangioblasts oxidative stressSettore BIO/06 - Anatomia Comparata E Citologia
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Overexpression of Bcl-3 inhibits the development of marginal zone B cells.

2013

The transcription factor Bcl-3 functions as a proto-oncogene via regulation of cell proliferation and apoptosis. Bcl-3 is an atypical member of the IκB family and plays a central role in the immune response through interactions with the NF-κB subunits p50 and p52. To investigate the impact of Bcl-3 on B-cell maturation and regulation, we generated mice that overexpress Bcl-3 specifically in B cells. Interestingly, these mice lack marginal zone B cells and exhibit a significant reduction in the number of B-1 B cells. Further, B cells from these mice are impaired in their proliferative capacity. Our data demonstrate that the overexpression of the transcription factor Bcl-3 inhibits germinal c…

B-LymphocytesCell growthImmunologyGerminal centerGene ExpressionNF-κBBiologyMarginal zoneGerminal CenterMolecular biologyCell biologychemistry.chemical_compoundMiceImmune systemchemistryApoptosisB-Cell Lymphoma 3 ProteinProto-Oncogene ProteinsMarginal zone B-cellImmunology and AllergyAnimalsTranscription factorCell ProliferationTranscription FactorsEuropean journal of immunology
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Protein quality control during aging involves recruitment of the macroautophagy pathway by BAG3.

2009

The Hsc/Hsp70 co-chaperones of the BAG (Bcl-2-associated athanogene) protein family are modulators of protein quality control. We examined the specific roles of BAG1 and BAG3 in protein degradation during the aging process. We show that BAG1 and BAG3 regulate proteasomal and macroautophagic pathways, respectively, for the degradation of polyubiquitinated proteins. Moreover, using models of cellular aging, we find that a switch from BAG1 to BAG3 determines that aged cells use more intensively the macroautophagic system for turnover of polyubiquitinated proteins. This increased macroautophagic flux is regulated by BAG3 in concert with the ubiquitin-binding protein p62/SQSTM1. The BAG3/BAG1 ra…

BAG domainProteasome Endopeptidase ComplexProtein familyProtein degradationBAG3ubiquitinationGeneral Biochemistry Genetics and Molecular BiologyBAG1ArticleRats Sprague-DawleyMiceUbiquitinMicroscopy Electron TransmissionAutophagyAnimalsHumansSQSTM1Molecular BiologyCellular SenescenceAdaptor Proteins Signal TransducingBAG1General Immunology and MicrobiologybiologyGeneral Neurosciencep62ImmunohistochemistryCell biologyRatsDNA-Binding ProteinsproteasomeProteasomeBiochemistrybiology.proteinApoptosis Regulatory ProteinsFlux (metabolism)Transcription FactorsThe EMBO journal
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Toward the development of metal-based synthetic nucleases: DNA binding and oxidative DNA cleavage of a mixed copper(II) complex with N-(9H-purin-6-yl…

2009

Abstract The complex [Cu(N9-ABS)(phen) 2 ]·3.6H 2 O, H 2 N9-ABS  = N -(9 H -purin-6-yl)benzenesulfonamide and phen = 1,10-phenanthroline, has been synthesized and then characterized with the aid of X-ray diffraction, analytical, and spectroscopic techniques. The geometry of Cu(II) is distorted square pyramidal with the equatorial positions occupied by three N atoms from two phenantroline molecules and one N atom from the adenine ring of the sulfonamide ligand. The interaction of the complex with DNA was studied by means of viscosity measurements and fluorescence spectroscopy. The results pointed to a classic intercalation of the complex between the DNA base pairs. The complex was found to b…

Base pairStereochemistryIntercalation (chemistry)Antineoplastic AgentsApoptosisCleavage (embryo)BiochemistryJurkat cellsInorganic ChemistryJurkat Cellschemistry.chemical_compoundOrganometallic CompoundsHumansDNA CleavageCytotoxicitySulfonamidesChemistryDNASquare pyramidal molecular geometryProto-Oncogene Proteins c-bcl-2ApoptosisCaco-2 CellsTumor Suppressor Protein p53CopperDNAPhenanthrolinesJournal of Inorganic Biochemistry
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Pharmacophore modeling e screening in silico di nuovi inibitori della proteina antiapoptotica Bcl-xl

2008

Bcl-xlpharmacophore modelingin silico screeningapoptosiSettore CHIM/08 - Chimica Farmaceutica
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Islet Beta-Cell Apoptosis Triggered in Vivo by Interleukin-1 Is Not Related to the Inducible Nitric Oxide Synthase Pathway: Evidence for Mitochondria…

2003

Beta-cell Apoptosis
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Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ?accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. "Regulated cell death" (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to…

Biochemical Manifestations of Cell DeathISCHEMIA-REPERFUSION INJURYApoptosisReviewTransduction (genetics)0302 clinical medicineCASPASE INHIBITION SWITCHESAnimals; Humans; Terminology as Topic; Apoptosis; Signal Transduction610 Medicine & healthCaspaseTUMOR-NECROSIS-FACTOR0303 health sciencesSettore BIO/17biologySettore BIO/11NeurodegenerationSettore BIO/13APOPTOSIS3. Good healthMedicina Básicacell death030220 oncology & carcinogenesiscell death; Morphologic Aspects of Cell Death; Biochemical Manifestations of Cell DeathSignal transductionDOMAIN-LIKE PROTEINIntracellularHumanSignal TransductionNecroptosiCYTOCHROME-C RELEASEOUTER-MEMBRANE PERMEABILIZATIONProgrammed cell deathCIENCIAS MÉDICAS Y DE LA SALUDSettore BIO/06Inmunología610 Medicine & healthCELL DEATHNOQ-VD-OPH03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEddc:570Terminology as TopicAPOPTOSIS-INDUCING FACTORMIXED LINEAGE KINASEmedicineAnimalsHumansAnimals; Humans; Terminology as Topic; Apoptosis; Signal Transduction; Molecular Biology; Cell BiologyMorphologic Aspects of Cell DeathSettore BIO/10Molecular Biology030304 developmental biologyAnimalCell growthApoptosiBiology and Life SciencesCell Biologymedicine.diseaseMITOCHONDRIAL PERMEABILITY TRANSITIONApoptosisImmunologybiology.proteinNeuroscienceCell death and differentiation
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Inhibition of liver trans-sulphuration pathway by propargylglycine mimics gene expression changes found in the mammary gland of weaned lactating rats…

2003

In the lactatingmammary gland, weaning produces mitochondrial cytochrome c release and nuclear DNA fragmentation, as determined by gel electrophoresis. This is followed by a significant decrease in lactation. Weaning for 2 h produces an early induction of the tumour suppressor/transcription factor p53, whereas the oncoprotein c-Jun and c-Jun N-terminal kinase are elevated after 24 h of weaning when compared with controls. The expression of p21cip1 and p27kip1, cyclin-dependent kinase inhibitors, was significantly higher in weaned rats when compared with control lactating rats. All the changes mentioned above also happen in the lactatingmammary gland when propargylglycine, an inhibitor of th…

BiochemistryAcetylcysteinechemistry.chemical_compoundLactationGene expressionGamma-glutamyltransferaseRegulation of gene expression:CIENCIAS DE LA VIDA::Bioquímica [UNESCO]biologyReverse Transcriptase Polymerase Chain ReactionCystathionine gamma-lyaseapoptosisgamma-Glutamyltransferaseglutathione (GSH)Glutathioneγ-cystathionasemedicine.anatomical_structureLiverAlkynesFemaleResearch Articlemedicine.drugmedicine.medical_specialtyGlycinel-cysteinelactationWeaningMammary Glands AnimalInternal medicinemedicineAnimalsLactationButhionine sulfoximineRats WistarButhionine SulfoximineMolecular BiologyDNA PrimersBase SequenceCystathionine gamma-LyaseUNESCO::CIENCIAS DE LA VIDA::BioquímicaCell BiologyGlutathioneAcetylcysteineRatsEndocrinologyGene Expression Regulationchemistrybiology.proteinSulfurBiochemical Journal
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Effects in cigarette smoke stimulated bronchial epithelial cells of a corticosteroid entrapped into nanostructured lipid carriers

2014

Background Nanomedicine studies have showed a great potential for drug delivery into the lung. In this manuscript nanostructured lipid carriers (NLC) containing Fluticasone propionate (FP) were prepared and their biocompatibility and effects in a human bronchial epithelial cell line (16-HBE) stimulated with cigarette smoke extracts (CSE) were tested. Results Biocompatibility studies showed that the NLC did not induce cell necrosis or apoptosis. Moreover, it was confirmed that CSE increased intracellular ROS production and TLR4 expression in bronchial epithelial cells and that FP-loaded NLC were more effective than free drug in modulating these processes. Finally, the nanoparticles increased…

BiocompatibilityCellBiomedical EngineeringMedicine (miscellaneous)Pharmaceutical ScienceApoptosisBronchiBioengineeringChronic obstructive pulmonary disease; Asthma; hronic obstructive pulmonary disease.PharmacologyFluticasone propionatemedicine.disease_causeApplied Microbiology and BiotechnologyNanostructured lipid carriers Corticosteroid Fluticasone propionate Cigarette smoke Airway epithelial cell Chronic obstructive pulmonary disease Asthmachemistry.chemical_compoundAirway epithelial cellmedicineHumansCorticosteroidCells CulturedFluticasoneDrug CarriersNanostructured lipid carriersbusiness.industryResearchChronic obstructive pulmonary diseaseSmokingCigarette smokeEpithelial CellsGlutathioneGlutathioneLipidsAsthmaNanostructuresToll-Like Receptor 4medicine.anatomical_structurechemistrySettore CHIM/09 - Farmaceutico Tecnologico ApplicativoApoptosisDrug deliveryFluticasoneMolecular MedicineReactive Oxygen SpeciesbusinessOxidative stressIntracellularmedicine.drugJournal of Nanobiotechnology
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N-acetyl-L-cysteine (NAC) inhibit mucin synthesis and pro-inflammatory mediators in alveolar type II epithelial cells infected with influenza virus A…

2011

64% of chronic obstructive pulmonary disease (COPD) exacerbations are caused by respiratory infections including influenza (strains A and B) and respiratory syncytial virus (RSV). They affect the airway epithelium increasing inflammatory and apoptosis events through mechanisms involving ROS generation, and induce the release of mucins from epithelial cells that are involved in the deterioration of the patient's health during the course of the disease. The antioxidant NAC has proved useful in the management of COPD reducing symptoms, exacerbations and accelerated lung function decline. It has been shown to inhibit influenza virus replication and to diminish the release of inflammatory and ap…

BiologyMucin 5ACmedicine.disease_causeVirus ReplicationBiochemistryp38 Mitogen-Activated Protein KinasesVirusCell LinePulmonary Disease Chronic ObstructivemedicineHumansInterleukin 8PhosphorylationPharmacologyA549 cellMucinNF-kappa BAcetylcysteineRespiratory Syncytial VirusesPulmonary AlveoliInfluenza B virusRespiratory syncytial virus (RSV)Viral replicationApoptosisInfluenza A virusImmunologyRespiratory epitheliumInflammation MediatorsBiochemical pharmacology
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