Search results for "Membrane permeabilization"

showing 8 items of 8 documents

Hidden complexity in membrane permeabilization behavior of antimicrobial polycations.

2021

A promising alternative to classical antibiotics are antimicrobial peptides and their synthetic mimics (smAMPs) that supposedly act directly on membranes. For a more successful design of smAMPs, we need to know how the type of interaction with the membrane determines the type of membrane perturbation. How this, in turn, transfers into selectivity and microbial killing activity is largely unknown. Here, we characterize the action of two smAMPs: MM:CO (a copolymer of hydrophobic cyclooctyl subunits and charged β-monomethyl-α-aminomethyl subunits) and the highly charged poly-NM (a homopolymer of α-aminomethyl subunits). By thorough characterization of vesicle leakage experiments, we elucidate …

0303 health sciencesMembrane permeabilizationChemistryVesicleKineticsAntimicrobial peptidesStatic ElectricityGeneral Physics and Astronomy010402 general chemistryAntimicrobialFluoresceins01 natural sciencesPermeability0104 chemical sciences03 medical and health sciencesMembraneGlycerophosphatesBiophysicsPhysical and Theoretical ChemistryHydrophobic and Hydrophilic InteractionsUnilamellar Liposomes030304 developmental biologyLeakage (electronics)Antimicrobial Cationic PeptidesProtein BindingPhysical chemistry chemical physics : PCCP
researchProduct

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
researchProduct

Release of canine parvovirus from endocytic vesicles

2003

Canine parvovirus (CPV) is a small nonenveloped virus with a single-stranded DNA genome. CPV enters cells by clathrin-mediated endocytosis and requires an acidic endosomal step for productive infection. Virion contains a potential nuclear localization signal as well as a phospholipase A(2) like domain in N-terminus of VP1. In this study we characterized the role of PLA(2) activity on CPV entry process. PLA(2) activity of CPV capsids was triggered in vitro by heat or acidic pH. PLA(2) inhibitors inhibited the viral proliferation suggesting that PLA(2) activity is needed for productive infection. The N-terminus of VP1 was exposed during the entry, suggesting that PLA(2) activity might have a …

Cell Membrane PermeabilityTransferrin receptorParvovirus CanineMembrane permeabilizationEndosomeanimal diseasesvirusesEndocytic cycleEntryBiologyEndocytosisPhospholipases AParvovirusAmiloridechemistry.chemical_compoundCapsidPhospholipase A2VirologyReceptors TransferrinmedicineAnimalsMonensinTransport VesiclesBrefeldin AVesicleBafilomycinDextransBrefeldin ALipid MetabolismEndocytosisAmilorideCell biologyEndocytic vesiclechemistryCatsCapsid ProteinsMacrolidesBafilomycin A1Lysosomesmedicine.drugVirology
researchProduct

Consensus guidelines for the detection of immunogenic cell death

2014

Apoptotic cells have long been considered as intrinsically tolerogenic or unable to elicit immune responses specific for dead cell-associated antigens. However, multiple stimuli can trigger a functionally peculiar type of apoptotic demise that does not go unnoticed by the adaptive arm of the immune system, which we named "immunogenic cell death" (ICD). ICD is preceded or accompanied by the emission of a series of immunostimulatory damage-associated molecular patterns (DAMPs) in a precise spatiotemporal configuration. Several anticancer agents that have been successfully employed in the clinic for decades, including various chemotherapeutics and radiotherapy, can elicit ICD. Moreover, defect…

HSV-1 herpes simplex virus type IΔψm mitochondrial transmembrane potentialmedicine.medical_treatmentDAMP damage-associated molecular patterndetectionFLT3LG fms-related tyrosine kinase 3 ligandReviewmember 3calreticulinEukaryotic translation initiation factor 2ARFP red fluorescent protein0302 clinical medicineMOMP mitochondrial outer membrane permeabilizationImmunology and AllergyGFP green fluorescent proteinHMGB10303 health scienceseducation.field_of_studyToll-like receptorBAK1 BCL2-antagonist/killer 1H2B histone 2Bendoplasmic reticulum stre3. Good healthBAX BCL2-associated X proteinXBP1 X-box binding protein 1cell deathOncologyPDIA3 protein disulfide isomerase family A030220 oncology & carcinogenesisendoplasmic reticulum stressImmunogenic cell deathHSP heat shock proteinimmunotherapyTLR Toll-like receptorautophagyATF6 activating transcription factor 6ImmunologyICD immunogenic cell deathEIF2A eukaryotic translation initiation factor 2AGuidelinesBiologyBCL2 B-cell CLL/lymphoma 2 proteinER endoplasmic reticulumPI propidium iodideATP release03 medical and health sciencesImmune systemimmunogenicmedicineIFN interferonAntigen-presenting celleducation030304 developmental biologyCALR calreticulinDamage-associated molecular patternImmunotherapyCTL cytotoxic T lymphocyteHMGB1 high mobility group box 1IL interleukinG3BP1 GTPase activating protein (SH3 domain) binding protein 1APC antigen-presenting cellCancer cellImmunologyDiOC6(3) 33′-dihexyloxacarbocyanine iodideDAPI 4′6-diamidino-2-phenylindoleOncoImmunology
researchProduct

Resealing of large transmembrane pores produced by streptolysin O in nucleated cells is accompanied by NF‐κB activation and downstream events

2001

Streptolysin O (SLO), archetype of a cholesterol-binding bacterial cytolysin, forms large pores in the plasma membrane of mammalian cells. We have recently reported that when a limited number of pores are generated in a cell, they can be sealed in a Ca++-dependent process. Here, we show that resealing is followed by the release of IL-6 and IL-8 from keratinocytes and from endothelial cells, both relevant targets for SLO attack. Production of cytokines by these cells was preceded by activation of transcription factor nuclear factor kappaB, which thus emerges as a common denominator of stress responses to various pore-forming agents, including alpha-toxin of Staphylococcus aureus and compleme…

KeratinocytesCell Membrane PermeabilityTime FactorsBiologyBiochemistryCell LineAdenosine TriphosphateBacterial ProteinsNucleated cellGeneticsHumansInterleukin 8Molecular BiologyMicrobial toxinsMembrane permeabilizationDose-Response Relationship Drugintegumentary systemInterleukin-6Interleukin-8NF-kappa BTransmembrane proteinCell biologyStreptolysinsStreptolysinEndothelium VascularNf κb activationBiotechnologyThe FASEB Journal
researchProduct

Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

2009

Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases. Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies. It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios. Thus far, dozens of methods have been proposed to quantify cell death-related parameters. However, no guid…

MESH: Cell DeathcytofluorometryMESH : Microscopy Fluorescenceved/biology.organism_classification_rank.speciesCellMESH: Flow CytometryMESH: Microscopy FluorescenceApoptosisfluorescence microscopyMESH: Eukaryotic CellsAnnexin Vnecrosis0302 clinical medicineEukaryotic Cells/cytologyMitochondrial membrane permeabilizationScanningMESH : ImmunoblottingGeneticsApoptosis; Cell Death; Eukaryotic Cells/cytology; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence0303 health sciencesMicroscopyMESH : Spectrometry FluorescenceMESH: ImmunoblottingCell DeathMESH: Guidelines as Topic//purl.org/becyt/ford/3.1 [https]Bioquímica y Biología MolecularFlow Cytometry3. Good healthTunelMedicina Básicamedicine.anatomical_structureEukaryotic Cellscaspases030220 oncology & carcinogenesis//purl.org/becyt/ford/3 [https]MESH: Spectrometry FluorescenceMESH : Microscopy Electron ScanningProgrammed cell deathautophagyCIENCIAS MÉDICAS Y DE LA SALUDMESH: Microscopy Electron ScanningMESH : Flow CytometrycaspaseImmunoblottingGuidelines as TopicComputational biologyBiologyElectronFluorescenceArticle03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyModel organismddc:612mitotic catastropheMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Guidelines as Topic030304 developmental biologycell death; Apoptosis; caspase; autophagy; Oxidative stress; fluorescence microscopyMESH: Humansved/biologySpectrometryInterpretation (philosophy)MESH: ApoptosisMESH : Eukaryotic CellsMESH : HumansApoptosis; Eukaryotic Cells; Flow Cytometry; Guidelines as Topic; Humans; Immunoblotting; Microscopy Electron Scanning; Microscopy Fluorescence; Spectrometry Fluorescence; Cell Death; Molecular Biology; Cell Biologyimmunofluorescence microscopyCell BiologySpectrometry FluorescenceMicroscopy FluorescenceOxidative stressMESH : Cell DeathCancer cellMicroscopy Electron ScanningMESH : Apoptosis
researchProduct

2NH and 3OH are crucial structural requirements in sphingomyelin for sticholysin II binding and pore formation in bilayer membranes.

2013

AbstractSticholysin II (StnII) is a pore-forming toxin from the sea anemone Stichodactyla heliantus which belongs to the large actinoporin family. The toxin binds to sphingomyelin (SM) containing membranes, and shows high binding specificity for this lipid. In this study, we have examined the role of the hydrogen bonding groups of the SM long-chain base (i.e., the 2NH and the 3OH) for StnII recognition. We prepared methylated SM-analogs which had reduced hydrogen bonding capability from 2NH and 3OH. Both surface plasmon resonance experiments, and isothermal titration calorimetry measurements indicated that StnII failed to bind to bilayers containing methylated SM-analogs, whereas clear bind…

Models MolecularPore Forming Cytotoxic ProteinsMembrane permeabilizationLipid BilayersBiophysicsCalorimetryta3111Biochemistrychemistry.chemical_compoundCnidarian VenomsAnimalsComputer SimulationLipid bilayerta116Binding selectivityUnilamellar LiposomesPhosphocholineBinding SitesMolecular StructureChemistryHydrogen bondVesicleta1182Isothermal titration calorimetryHydrogen BondingCell BiologySurface Plasmon ResonanceProtein Structure TertiarySphingomyelinsKineticsMembraneSea AnemonesBiochemistryMolecular dockingIsothermal titration calorimetryBiophysicsPhosphatidylcholinesSphingomyelinProtein BindingBiochimica et biophysica acta
researchProduct

Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis

2004

The tumor suppressor p53 exerts its anti-neoplastic activity primarily through the induction of apoptosis. We found that cytosolic localization of endogenous wild-type or trans-activation–deficient p53 was necessary and sufficient for apoptosis. p53 directly activated the proapoptotic Bcl-2protein Bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program. p53 also released both proapoptotic multidomain proteins and BH3-only proteins [Proapoptotic Bcl-2family proteins that share only the third Bcl-2homology domain (BH3)] that were sequestered by Bcl-xL. The transcription-independent activation of Bax by p53 occurred with similar kinetics and concentra…

Tumor suppressor geneProtein ConformationUltraviolet RaysWheat Germ AgglutininsRecombinant Fusion Proteinsbcl-X ProteinApoptosisEndogenyMitochondrionBiologyPermeabilityHomology (biology)law.inventionMiceCytosollawProto-Oncogene ProteinsMitochondrial membrane permeabilizationAnimalsHumansCells CulturedCell Line Transformedbcl-2-Associated X ProteinCell NucleusMultidisciplinaryCytochromes cIntracellular MembranesGenes p53MitochondriaCell biologyCytosolGene Expression RegulationProto-Oncogene Proteins c-bcl-2ApoptosisLiposomesMutationSuppressorTumor Suppressor Protein p53biological phenomena cell phenomena and immunityCarrier ProteinsBH3 Interacting Domain Death Agonist ProteinHeLa CellsScience
researchProduct