Search results for "Apoptosis ."

showing 10 items of 177 documents

Microarray analysis in sperm from fertile and infertile men without basic sperm analysis abnormalities reveals a significantly different transcriptom…

2007

Sperm analysis following World Health Organization guidelines is unable to explain the molecular causes of male infertility when basic sperm parameters are within a normal range and women do not present gynecologic pathology. Consequently, there is a need for accurate diagnostic tools in this area, and microarray technology emerges as promising. We present, for the first time, preliminary results of a comparison of sperm mRNA expression profiles between fertile and infertile men with normal semen parameters, discovering profound discrepancies between groups, with potential diagnostic and therapeutic possibilities.

InfertilityMaleSemenBiologyMale infertilityTranscriptomeAndrologyAntigens NeoplasmSemenmedicineHumansTrypsinRNA MessengerInfertility MaleOligonucleotide Array Sequence Analysisurogenital systemGynecologic pathologyGene Expression ProfilingObstetrics and GynecologyDNAgamma-Glutamyltransferasemedicine.diseaseSpermSpermatozoaGene expression profilingFertilityReproductive MedicineGene chip analysisTrypsinogenApoptosis Regulatory ProteinsFertility and sterility
researchProduct

Caspase-2 is an initiator caspase responsible for pore-forming toxin-mediated apoptosis

2012

Bacterial pathogens modulate host cell apoptosis to establish a successful infection. Pore-forming toxins (PFTs) secreted by pathogenic bacteria are major virulence factors and have been shown to induce various forms of cell death in infected cells. Here we demonstrate that the highly conserved caspase-2 is required for PFT-mediated apoptosis. Despite being the second mammalian caspase to be identified, the role of caspase-2 during apoptosis remains enigmatic. We show that caspase-2 functions as an initiator caspase during Staphylococcus aureus alpha-toxin- and Aeromonas aerolysin-mediated apoptosis in epithelial cells. Downregulation of caspase-2 leads to a strong inhibition of PFT-mediate…

Inhibitor of apoptosis domain0303 health sciencesProgrammed cell deathPore-forming toxinGeneral Immunology and MicrobiologybiologyNLRP1General Neuroscience030302 biochemistry & molecular biologyCaspase 2Molecular biologyGeneral Biochemistry Genetics and Molecular Biology3. Good healthCell biology03 medical and health sciencesDownregulation and upregulationApoptosisbiology.proteinMolecular BiologyCaspase030304 developmental biologyThe EMBO Journal
researchProduct

Novel isatin-derived molecules activate p53 via interference with Mdm2 to promote apoptosis

2018

International audience; The p53 protein is a key tumor suppressor in mammals. In response to various forms of genotoxic stress p53 stimulates expression of genes whose products induce cell cycle arrest and/or apoptosis. An E3-ubiquitin ligase, Mdm2 (mouse-double-minute 2) and its human ortholog Hdm2, physically interact with the amino-terminus of p53 to mediate its ubiquitin-mediated degradation via the proteasome. Thus, pharmacological inhibition of the p53-Mdm2 interaction leads to overall stabilization of p53 and stimulation of its anti-tumorigenic activity. In this study we characterize the biological effects of a novel class of non-genotoxic isatin Schiff and Mannich base derivatives (…

Isatin0301 basic medicineProgrammed cell deathCell cycle checkpointAntineoplastic AgentsApoptosis[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyPiperazinesHistonesMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNutlinCell Line TumorProto-Oncogene ProteinsAnimalsHumansMolecular Biologychemistry.chemical_classificationDNA ligaseIsatinImidazolesISMBDsProto-Oncogene Proteins c-mdm2Cell BiologyNutlinp53-activating moleculesCell biology030104 developmental biologychemistryProteasomeApoptosis030220 oncology & carcinogenesisbiology.proteinMdm2PumaTumor Suppressor Protein p53Apoptosis Regulatory Proteinsautomated microscopy system OperettaResearch PaperDevelopmental BiologyCell Cycle
researchProduct

cFLIPL Inhibits Tumor Necrosis Factor-related Apoptosis-inducing Ligand-mediated NF-κB Activation at the Death-inducing Signaling Complex in Human Ke…

2004

Human keratinocytes undergo apoptosis following treatment with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) via surface-expressed TRAIL receptors 1 and 2. In addition, TRAIL triggers nonapoptotic signaling pathways including activation of the transcription factor NF-kappaB, in particular when TRAIL-induced apoptosis is blocked. The intracellular protein cFLIP(L) interferes with TRAIL-induced apoptosis at the death-inducing signaling complex (DISC) in many cell types. To study the role of cFLIP(L) in TRAIL signaling, we established stable HaCaT keratinocyte cell lines expressing varying levels of cFLIP(L). Functional analysis revealed that relative cFLIP(L) levels correlat…

KeratinocytesCytoplasmReceptor complexCell SurvivalCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisCell SeparationBiologyCaspase 8Sensitivity and SpecificityBiochemistryProinflammatory cytokineTNF-Related Apoptosis-Inducing LigandRibonucleasesCell Line TumorHumansEnzyme InhibitorsMolecular BiologyTranscription factorSkinInflammationCaspase 8Membrane GlycoproteinsTumor Necrosis Factor-alphaIntracellular Signaling Peptides and ProteinsNF-kappa BCell BiologyFlow CytometryRecombinant ProteinsCell biologyRetroviridaeApoptosisCaspasesDeath-inducing signaling complexRNATumor necrosis factor alphaSignal transductionApoptosis Regulatory ProteinsPropidiumProtein BindingSignal TransductionJournal of Biological Chemistry
researchProduct

Cytotoxicity of botanicals and isolated phytochemicals from Araliopsis soyauxii Engl. (Rutaceae) towards a panel of human cancer cells.

2020

Abstract Ethnopharmacological relevance Araliopsis soyauxii Engl. (Rutaceae) is a Cameroonian medicinal plant traditionally used to treat lung diseases, malaria, and gonorrhea. It has been demonstrated that infectious disease contribute to about 20% of all human tumours. Aims of the study (1) To perform a phytochemical investigation of the dichloromethane-methanol 1:1 extracts of the bark (ASB), roots (ASR), and leaves (ASL) from Araliopsis soyauxii; (2) to evaluate the cytotoxicity of extracts and isolated compounds; (3) to determine the mode of induction of apoptosis of ASB and kihadanin B (12). Materials and methods Fourteen constituents of the crude extracts were isolated by column chro…

LimoninsPhytochemicalsApoptosisFlow cytometry03 medical and health sciencesInhibitory Concentration 500302 clinical medicineAnnexinNeoplasmsDrug DiscoverymedicineCytotoxic T cellBenzoxepinsHumansCytotoxicityRutaceae030304 developmental biologyPharmacologychemistry.chemical_classificationMembrane Potential Mitochondrial0303 health sciencesReactive oxygen speciesmedicine.diagnostic_testDose-Response Relationship DrugChemistryPlant ExtractsCell Cycle CheckpointsHep G2 CellsCell cycleHCT116 CellsMolecular biologyAntineoplastic Agents PhytogenicMitochondriaOxidative StressPhytochemicalApoptosis030220 oncology & carcinogenesisApoptosis Regulatory ProteinsReactive Oxygen SpeciesSignal TransductionJournal of ethnopharmacology
researchProduct

Ablation of c-FLIP in hepatocytes enhances death-receptor mediated apoptosis and toxic liver injury in vivo

2010

Background & Aims Apoptosis is crucially involved in acute and chronic liver injury, including viral, cholestatic, toxic, and metabolic liver disease. Additionally, dysregulation of apoptosis signaling pathways has been implicated in hepatocarcinogenesis. The most prominent members of the apoptosis-mediating tumor necrosis factor receptor superfamily are the TNF-R1 (CD120a) and the CD95 (Apo-1/Fas) receptor. Although extensively studied, the intracellular signaling events in hepatocytes are only incompletely understood. Methods To examine the role of the caspase-8 homolog cellular FLICE-inhibitory protein (c-FLIP) in liver injury, we generated mice with hepatocyte specific deletion of c-FLI…

LipopolysaccharidesProgrammed cell deathMAP Kinase Signaling SystemCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisGalactosamineBiologyCaspase 8MiceLiver diseaseConcanavalin AmedicineAnimalsfas ReceptorAnthracenesMice KnockoutLiver injuryHepatologyReceptors Death DomainFas receptormedicine.diseasemedicine.anatomical_structureApoptosisCaspasesHepatocyteDeath-inducing signaling complexHepatocytesCancer researchFemaleChemical and Drug Induced Liver InjuryJournal of Hepatology
researchProduct

Quaking and miR-155 interactions in inflammation and leukemogenesis.

2015

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas …

LipopolysaccharidesTime Factorsmedicine.medical_treatmentmedicine.disease_causeTransgenicMiceInnatePhosphorylationChronicB-LymphocytesLeukemiaRNA-Binding ProteinsU937 CellsLymphocyticCell biologyCytokineOncologyPhosphorylationCytokinesCLL; Glioblastoma; Inflammation; MiR-155; QKI; Animals; Apoptosis Regulatory Proteins; B-Lymphocytes; Case-Control Studies; Cytokines; Humans; Immunity Innate; Inflammation; Leukemia Lymphocytic Chronic B-Cell; Lipopolysaccharides; Macrophages; Mice; Mice Transgenic; MicroRNAs; Mitogen-Activated Protein Kinases; Phosphorylation; RAW 264.7 Cells; RNA-Binding Proteins; Signal Transduction; Time Factors; Transfection; U937 Cells; OncologySignal transductionMitogen-Activated Protein KinasesSignal Transductionp38 mitogen-activated protein kinasesOncology and CarcinogenesisMice TransgenicTransfectionNOmiR-155miR-155Downregulation and upregulationmicroRNAmedicineAnimalsHumansInflammationQKIbusiness.industryMacrophagesB-CellImmunityglioblastomaLeukemia Lymphocytic Chronic B-CellImmunity InnateMicroRNAsRAW 264.7 CellsCase-Control StudiesImmunologyCarcinogenesisbusinessApoptosis Regulatory ProteinsCLLPriority Research Paper
researchProduct

Increased hepatic fibrosis and JNK2-dependent liver injury in mice exhibiting hepatocyte-specific deletion of cFLIP.

2012

Chronic liver disease promotes hepatocellular injury involving apoptosis and triggers compensatory regeneration that leads to the activation of quiescent stellate cells in the liver. The deposition of extracellular matrix from activated myofibroblasts promotes hepatic fibrosis and the progression to cirrhosis with deleterious effects on liver physiology. The role of apoptosis signaling pathways in the development of fibrosis remains undefined. The aim of the current study was to determine the involvement of the caspase-8 homologue cellular FLICE-inhibitory protein (cFLIP) during the initiation and progression of fibrosis. Liver injury and fibrosis from carbon tetrachloride (CCl4) and thioa…

Liver CirrhosisMalePathologymedicine.medical_specialtyTime FactorsGenotypePhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBiologyThioacetamideChronic liver diseaseMicePhysiology (medical)medicineAnimalsMitogen-Activated Protein Kinase 9PhosphorylationExtracellular Signal-Regulated MAP KinasesCarbon TetrachlorideCompensatory regenerationLiver injuryMice KnockoutHepatologyCaspase 3Gastroenterologymedicine.diseaseCaspase 9Enzyme ActivationDisease Models Animalmedicine.anatomical_structurePhenotypeLiverApoptosisHepatocyteHepatic stellate cellCancer researchDisease ProgressionHepatocytesHepatocellular injuryChemical and Drug Induced Liver InjuryHepatic fibrosisSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
researchProduct

IAPs and cell migration.

2015

Inhibitors of apoptosis (IAPs) constitute a family of cell signaling regulators controlling several fundamental biological processes such as innate immunity, inflammation, cell death, cell proliferation, and cell differentiation. Increasing evidence from in vivo and in vitro studies indicate a function for IAPs in the modulation of invasive and migratory properties of cells. Here, we present and discuss the mechanisms whereby IAPs can control cell migration.

MAPK/ERK pathwayCell signalingProgrammed cell deathInnate immune systemCell growthCellular differentiationCell migrationCell BiologyBiologyCell biologyInhibitor of Apoptosis Proteinsbody regionsApoptosisCell MovementCancer researchCell AdhesionAnimalsHumansCytoskeletonDevelopmental BiologySignal TransductionSeminars in celldevelopmental biology
researchProduct

Divide and rule: The role of ubiquitination in inactivation of the ERK5-MAPK cascade

2014

Recently, we revealed that ubiquitination of MEKK2 and MEKK3 by inhibitor of apoptosis proteins (IAPs) directly disrupts MEK5/ERK5 interaction and subsequently attenuates ERK5 activation. In addition, loss of XIAP promotes human myogenic differentiation in an ERK5-dependent manner. These results reveal another layer of MAPK regulation and a novel role for XIAP in controlling myogenic differentiation.

MAPK/ERK pathwayInhibitor of apoptosis domainCancer ResearchAkt/PKB signaling pathwayChemistryMAPK cascadeInhibitor of apoptosisMAP2K7XIAPCell biologyCancer researchMolecular MedicineAuthor's ViewProtein kinase BMolecular & Cellular Oncology
researchProduct