Search results for "SIG"

showing 10 items of 19670 documents

BAX inhibitor-1 is a Ca(2+) channel critically important for immune cell function and survival.

2015

The endoplasmic reticulum (ER) serves as the major intracellular Ca(2+) store and has a role in the synthesis and folding of proteins. BAX (BCL2-associated X protein) inhibitor-1 (BI-1) is a Ca(2+) leak channel also implicated in the response against protein misfolding, thereby connecting the Ca(2+) store and protein-folding functions of the ER. We found that BI-1-deficient mice suffer from leukopenia and erythrocytosis, have an increased number of splenic marginal zone B cells and higher abundance and nuclear translocation of NF-κB (nuclear factor-κ light-chain enhancer of activated B cells) proteins, correlating with increased cytosolic and ER Ca(2+) levels. When put into culture, purifie…

0301 basic medicineProgrammed cell deathCytoplasmEncephalomyelitis Autoimmune ExperimentalCell SurvivalT-LymphocytesActive Transport Cell NucleusApoptosisBiologyEndoplasmic Reticulum03 medical and health sciencesAnimalsCalcium SignalingObesityMolecular BiologyCalcium signalingMice KnockoutOriginal PaperB-LymphocytesBAX inhibitor 1Endoplasmic reticulumNF-kappa BMembrane ProteinsCell BiologyLeukopeniaNFKB1Acquired immune systemCell biologyEnzyme ActivationMice Inbred C57BLCytosol030104 developmental biologyApoptosisCaspasesCalciumFemaleSpleen
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Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.

2017

The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF…

0301 basic medicineProgrammed cell deathLiver tumorCell SurvivalNecroptosisMice TransgenicBiologyChronic liver diseaseProinflammatory cytokine03 medical and health sciencesLiver diseaseMiceLiver Neoplasms ExperimentalmedicineAnimalsDiethylnitrosamineKinase activityTranscription Factor RelAGeneral Medicinemedicine.disease3. Good healthNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticReceptors Tumor Necrosis Factor Type IHepatocyteReceptor-Interacting Protein Serine-Threonine KinasesCancer researchHepatocytesSignal TransductionResearch ArticleThe Journal of clinical investigation
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Itinéraire d’un agent double

2016

Protein S-nitrosylation is now recognized as a ubiquitous regulatory mechanism. Like any post-translational modifications, S-nitrosylation is critical for the control of numerous cellular processes. It is now clear that S-nitrosylation is playing a double game, enhancing or inhibiting the tumor growth or the induction of cell death. Thanks to research aimed at demonstrating NO cytotoxic effects, new therapeutic strategies based on NO donor drugs have emerged. Although therapeutic NO donors can target a large number of proteins, the cellular mechanism is still not fully understood. This review reflects the current state of knowledge on S-nitrosylated proteins that take part of the oncogenic …

0301 basic medicineProgrammed cell deathMechanism (biology)Cell growthGeneral MedicineBiologyGeneral Biochemistry Genetics and Molecular Biology3. Good healthNo donorsCellular mechanism03 medical and health sciences030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisCytotoxic T cellTumor growthSignal transductionNeurosciencemédecine/sciences
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Taking up the cudgels for the traditional reactive oxygen and nitrogen species detection assays and their use in the cardiovascular system

2017

Reactive oxygen and nitrogen species (RONS such as H2O2, nitric oxide) confer redox regulation of essential cellular functions (e.g. differentiation, proliferation, migration, apoptosis), initiate and catalyze adaptive stress responses. In contrast, excessive formation of RONS caused by impaired break-down by cellular antioxidant systems and/or insufficient repair of the resulting oxidative damage of biomolecules may lead to appreciable impairment of cellular function and in the worst case to cell death, organ dysfunction and severe disease phenotypes of the entire organism. Therefore, the knowledge of the severity of oxidative stress and tissue specific localization is of great biological …

0301 basic medicineProgrammed cell deathRedox signalingClinical BiochemistrySevere diseaseReview ArticleBiologymedicine.disease_causeCardiovascular SystemBiochemistry03 medical and health sciencesPhysiology (medical)medicineDihydroethidium oxidative fluorescence microtopographyAnimalsHumanslcsh:QH301-705.5Organismchemistry.chemical_classificationlcsh:R5-920Reactive oxygen speciesFluorescence and chemiluminescence-based assaysOrganic ChemistrySpecies detectionNADPH OxidasesPhenotypeReactive Nitrogen SpeciesOxidative Stress030104 developmental biologylcsh:Biology (General)chemistryBiochemistryL-012-enhanced chemiluminescenceLuminescent MeasurementsLucigenin-enhanced chemiluminescencelcsh:Medicine (General)Reactive Oxygen SpeciesNeuroscienceOxidation-ReductionFunction (biology)Oxidative stressFree Radical Biology and Medicine
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Ferroptosis and Its Potential Role in Human Diseases

2020

Ferroptosis is a novel regulated cell death pattern discovered when studying the mechanism of erastin-killing RAS mutant tumor cells in 2012. It is an iron-dependent programmed cell death pathway mainly caused by an increased redox imbalance but with distinct biological and morphology characteristics when compared to other known cell death patterns. Ferroptosis is associated with various diseases including acute kidney injury, cancer, and cardiovascular, neurodegenerative, and hepatic diseases. Moreover, activation or inhibition of ferroptosis using a variety of ferroptosis initiators and inhibitors can modulate disease progression in animal models. In this review, we provide a comprehensiv…

0301 basic medicineProgrammed cell deathReviewdegenerative diseasesBiologyHepatic Diseases03 medical and health sciences0302 clinical medicineRegulated cell deathmedicinePharmacology (medical)Pharmacologyreactive oxygen speciesMechanism (biology)Ferroptosislcsh:RM1-950Disease progressionCancermedicine.diseaseferroptosissignaling pathwayslcsh:Therapeutics. Pharmacology030104 developmental biologypharmacology design030220 oncology & carcinogenesisCancer researchSignal transductionFrontiers in Pharmacology
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The endoplasmic reticulum unfolded protein response in neurodegenerative disorders and its potential therapeutic significance

2017

In eukaryotic cells, the endoplasmic reticulum (ER) is the cell compartment involved in secretory protein translocation and quality control of secretory protein folding. Different conditions can alter ER function, resulting in the accumulation of unfolded or misfolded proteins within the ER lumen. Such a condition, known as ER stress, elicits an integrated adaptive response known as the unfolded protein response (UPR) that aims to restore proteostasis within the secretory pathway. Conversely, in prolonged cell stress or insufficient adaptive response, UPR signaling causes cell death. ER dysfunctions are involved and contribute to neuronal degeneration in several human diseases, including Al…

0301 basic medicineProgrammed cell deathTherapeutic targetReviewBiologytherapeutic targetsNeurodegenerative diseaselcsh:RC321-571Unfolded protein response03 medical and health sciencesCellular and Molecular NeuroscienceProtein misfolding disordermedicineneurodegenerative diseasesprotein misfolding disorderslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologySecretory pathwayEndoplasmic reticulumNeurodegenerationmedicine.diseaseCell biology030104 developmental biologyProteostasisSecretory proteinUnfolded protein responseER streSignal transductionER stressNeuroscience
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Fold formation at the compartment boundary of Drosophila wing requires Yki signaling to suppress JNK dependent apoptosis

2016

AbstractCompartment boundaries prevent cell populations of different lineage from intermingling. In many cases, compartment boundaries are associated with morphological folds. However, in the Drosophila wing imaginal disc, fold formation at the anterior/posterior (A/P) compartment boundary is suppressed, probably as a prerequisite for the formation of a flat wing surface. Fold suppression depends on optomotor-blind (omb). Omb mutant animals develop a deep apical fold at the A/P boundary of the larval wing disc and an A/P cleft in the adult wing. A/P fold formation is controlled by different signaling pathways. Jun N-terminal kinase (JNK) and Yorkie (Yki) signaling are activated in cells alo…

0301 basic medicineProgrammed cell deathanimal structuresMAP Kinase Kinase 4CellMutantApoptosisBiologyArticle03 medical and health sciences0302 clinical medicinemedicineAnimalsDrosophila ProteinsWings AnimalBody PatterningMultidisciplinaryWingKinaseGene Expression Regulation DevelopmentalNuclear ProteinsYAP-Signaling ProteinsAnatomyCell biologyImaginal discDrosophila melanogaster030104 developmental biologymedicine.anatomical_structureImaginal DiscsApoptosisTrans-ActivatorsSignal transduction030217 neurology & neurosurgerySignal TransductionScientific Reports
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Sicilian Litchi Fruit Extracts Induce Autophagy versus Apoptosis Switch in Human Colon Cancer Cells

2018

Litchi chinensis Sonnerat is a tropical tree whose fruits contain significant amounts of bioactive polyphenols. Litchi cultivation has recently spread in Sicily where the climate conditions are particularly favorable for this crop. Recent findings have shown that Litchi extracts display anti-tumor and pro-apoptotic effects in vitro, but the precise underlying mechanisms have not been fully elucidated. In this study, we report for the first time the effects of Sicilian litchi fruit extracts on colon cancer cells. The results indicated that litchi exocarp, mesocarp and endocarp fractions reduce the viability and clonogenic growth of HT29 cells. These effects were due to cell cycle arrest in t…

0301 basic medicineProgrammed cell deathautophagyCell cycle checkpointAtg1Apoptosislcsh:TX341-641Litchi chinensisArticle03 medical and health sciencesHT29 Cells0302 clinical medicineLitchiSettore BIO/10 - BiochimicaHumansClonogenic assaySicilyNutrition and DieteticsPlant ExtractsChemistryKinaseAutophagyPolyphenolsLitchi chinensiCell Cycle CheckpointsAntineoplastic Agents PhytogenicCell biology030104 developmental biologycolon cancerApoptosisFruit030220 oncology & carcinogenesisColonic Neoplasmsanti-tumor activityCaco-2 Cells<i>Litchi chinensis</i>HT29 Cellslcsh:Nutrition. Foods and food supplyPhytotherapySignal TransductionFood ScienceNutrients
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Regulation of Autophagic Signaling by Mechanical Loading and Inflammation in Human PDL Fibroblasts

2020

Autophagy (cellular self-consumption) is a crucial adaptation mechanism during cellular stress conditions. This study aimed to examine how this important process is regulated in human periodontal ligament (PDL) fibroblasts by mechanical and inflammatory stress conditions and whether the mammalian target of rapamycin (mTOR) signaling pathway is involved. Autophagy was quantified by flow cytometry. Qualitative protein phosphorylation profiling of the mTOR pathway was carried out. Effects of mTOR regulation were assessed by quantification of important synthesis product collagen 1, cell proliferation and cell death with real-time PCR and flow cytometry. Autophagy as a response to mechanical or …

0301 basic medicineProgrammed cell deathautophagyInflammationCatalysisArticlelcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicineinflammatory conditionsmedicineHumansProtein phosphorylationPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyPI3K/AKT/mTOR pathwayCells CulturedInflammationCell DeathCell growthChemistryOrganic ChemistryAutophagymechanical stress030206 dentistryGeneral MedicineFibroblastsComputer Science ApplicationsCell biologyorthodontic tooth movement030104 developmental biologylcsh:Biology (General)lcsh:QD1-999mammalian target of rapamycin (mTOR) signaling pathwayPhosphorylationStress Mechanicalmedicine.symptomSignal transductionSignal TransductionInternational Journal of Molecular Sciences
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Extracellular histones disarrange vasoactive mediators reléase through COX-NOS interaction in human endothelial cells

2017

Abstract Extracellular histones are mediators of inflammation, tissue injury and organ dysfunction. Interactions between circulating histones and vascular endothelial cells are key events in histone‐mediated pathologies. Our aim was to investigate the implication of extracellular histones in the production of the major vasoactive compounds released by human endothelial cells (HUVECs), prostanoids and nitric oxide (NO). HUVEC exposed to increasing concentrations of histones (0.001 to 100 μg/ml) for 4 hrs induced prostacyclin (PGI2) production in a dose‐dependent manner and decreased thromboxane A2 (TXA2) release at 100 μg/ml. Extracellular histones raised cyclooxygenase‐2 (COX‐2) and prostac…

0301 basic medicineProstacyclinHistoneschemistry.chemical_compoundThromboxane A2Cytochrome P-450 Enzyme SystemSuperoxidesEnosvascular mediatorsGenètica humanabiologySuperoxideendothelial cellsIntramolecular OxidoreductasesEndothelial stem cellMolecular MedicineOriginal ArticleThromboxane-A SynthaseSignal Transductionmedicine.drugmedicine.medical_specialtyNitric Oxide Synthase Type IIIPrimary Cell CultureNitric OxideProstacyclin synthaseNitric oxideCyclic N-OxidesThromboxane A203 medical and health sciencesInternal medicineHuman Umbilical Vein Endothelial CellsmedicineExtracellularHumansRNA MessengerprostanoidsDose-Response Relationship DrugOriginal ArticlesCell Biologybiology.organism_classificationEpoprostenolÒxid nítric030104 developmental biologyEndocrinologyGene Expression RegulationchemistryCelecoxibCyclooxygenase 2Cyclooxygenase 1biology.proteinSpin LabelsProteïnesextracellular histones
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