Search results for "Gram"

showing 10 items of 9069 documents

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1

2021

Contains fulltext : 232759.pdf (Publisher’s version ) (Closed access) In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to…

0301 basic medicineProgrammed cell deathSettore BIO/06AutophagosomeAutolysosome[SDV]Life Sciences [q-bio]lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Autophagy-Related ProteinsReviewComputational biology[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologySettore MED/0403 medical and health sciencesstressChaperone-mediated autophagyddc:570AutophagyLC3AnimalsHumanscancerSettore BIO/10Autophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSet (psychology)Molecular Biologyvacuole.phagophore030102 biochemistry & molecular biologyvacuolebusiness.industryInterpretation (philosophy)AutophagyAutophagosomesneurodegenerationCell BiologyfluxMulticellular organismmacroautophagy030104 developmental biologyKnowledge baselysosomeAutophagosome; LC3; cancer; flux; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleBiological AssayLysosomesbusinessBiomarkers[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Anticancer activity of biogenerated silver nanoparticles: an integrated proteomic investigation

2018

Silver nanoparticles (AgNPs), embedded into a specific polysaccharide (EPS), were biogenerated by Klebsiella oxytoca DSM 29614 under aerobic (AgNPs-EPSaer) and anaerobic conditions (AgNPs-EPSanaer). Both AgNPs-EPS matrices were tested by MTT assay for cytotoxic activity against human breast (SKBR3 and 8701-BC) and colon (HT-29, HCT 116 and Caco-2) cancer cell lines, revealing AgNPs-EPSaer as the most active, in terms of IC50, with a more pronounced efficacy against breast cancer cell lines. Therefore, colony forming capability, morphological changes, generation of reactive oxygen species (ROS), induction of apoptosis and autophagy, inhibition of migratory and invasive capabilities and prote…

0301 basic medicineProgrammed cell deathSettore BIO/11 - Biologia MolecolareMitochondrionmedicine.disease_causeSettore BIO/19 - Microbiologia Generale03 medical and health sciencesproteomicsbreast cancer cellmedicineMTT assaySettore BIO/06 - Anatomia Comparata E Citologiabacteriachemistry.chemical_classificationAnticancer activity; Bacteria; Breast cancer cells; Proteomics; Silver nanoparticles (AgNPs); OncologyReactive oxygen speciesBreast cancer cellsChemistryAutophagysilver nanoparticles (AgNPs)Cell biology030104 developmental biologyanticancer activitysilver nanoparticles (AgNPs); bacteria; breast cancer cells; anticancer activity; proteomicsOncologyApoptosisSKBR3Oxidative stressResearch Paper
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Pekinenin E Inhibits the Growth of Hepatocellular Carcinoma by Promoting Endoplasmic Reticulum Stress Mediated Cell Death.

2017

Hepatocellular carcinoma (HCC) is a malignant primary liver cancer with poor prognosis. In the present study, we report that pekinenin E (PE), a casbane diterpenoid derived from the roots of Euphorbia pekinensis, has a strong antitumor activity against human HCC cells both in vitro and in vivo. PE suppressed the growth of human HCC cells Hep G2 and SMMC-7721. In addition, PE-mediated endoplasmic reticulum (ER) stress caused increasing expressions of C/EBP homologous protein (CHOP), leading to apoptosis in HCC cells both in vitro and in vivo. Inhibition of ER stress with CHOP small interfering RNA or 4-phenyl-butyric acid partially reversed PE-induced cell death. Furthermore, PE induced S ce…

0301 basic medicineProgrammed cell deathSmall interfering RNAPathologymedicine.medical_specialtyCell cycle checkpointCHOP03 medical and health sciencesmedicinePharmacology (medical)Original ResearchPharmacologybusiness.industryEndoplasmic reticulumlcsh:RM1-950apoptosisdigestive system diseasesHep G2030104 developmental biologylcsh:Therapeutics. PharmacologyApoptosishepatocarcinomacell cycle arrestUnfolded protein responseCancer researchbusinessER stresspekinenin EFrontiers 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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The HMGB1 protein induces a metabolic type of tumour cell death by blocking aerobic respiration

2016

The high-mobility group box 1 (HMGB1) protein has a central role in immunological antitumour defense. Here we show that natural killer cell-derived HMGB1 directly eliminates cancer cells by triggering metabolic cell death. HMGB1 allosterically inhibits the tetrameric pyruvate kinase isoform M2, thus blocking glucose-driven aerobic respiration. This results in a rapid metabolic shift forcing cells to rely solely on glycolysis for the maintenance of energy production. Cancer cells can acquire resistance to HMGB1 by increasing glycolysis using the dimeric form of PKM2, and employing glutaminolysis. Consistently, we observe an increase in the expression of a key enzyme of glutaminolysis, malic …

0301 basic medicineProgrammed cell deathThyroid HormonesCellular respirationScienceCell RespirationMalic enzymeGeneral Physics and Astronomychemical and pharmacologic phenomenaPKM2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesCell Line TumorHumansGlycolysisHMGB1 ProteinMultidisciplinaryGlutaminolysisCell DeathQMembrane ProteinsGeneral ChemistryCell biology030104 developmental biologyGlucoseCancer cellColonic NeoplasmsCarrier ProteinsGlycolysisPyruvate kinaseNature Communications
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E2F1 interacts with BCL-xL and regulates its subcellular localization dynamics to trigger cell death

2018

International audience; E2F1 is the main pro-apoptotic effector of the pRB-regulated tumor suppressor pathway by promoting the transcription of various pro-apoptotic proteins. We report here that E2F1 partly localizes to mitochondria, where it favors mitochondrial outer membrane permeabilization. E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death. We thus identify a new, non-BH3-binding regulator of BCL-xL localization dynamics that influences its anti-apoptotic activity.

0301 basic medicineProgrammed cell deathTranscription Geneticbcl-X ProteinRegulatorBcl-xL[SDV.CAN]Life Sciences [q-bio]/CancerBCL-xL mobilityMitochondrionBiochemistrylaw.invention[ SDV.CAN ] Life Sciences [q-bio]/CancerE2F1 Subject Category Autophagy & Cell Death03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerlawBCL-2 familyCell Line TumorGeneticsJournal ArticleHumansE2F1Molecular BiologyCell DeathbiologyManchester Cancer Research CentreEffectorChemistryResearchInstitutes_Networks_Beacons/mcrcScientific ReportsapoptosisSubcellular localizationMitochondriaCell biologyProtein Transportbcl-2 Homologous Antagonist-Killer Protein030104 developmental biologyGene Expression RegulationProto-Oncogene Proteins c-bcl-2biology.proteinSuppressorbiological phenomena cell phenomena and immunityExtracellular SpaceE2F1 Transcription FactorProtein Binding
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The dissociation of the Hsp60/pro-Caspase-3 complex by bis(pyridyl)oxadiazole copper complex (CubipyOXA) leads to cell death in NCI-H292 cancer cells

2017

Abstract Cell survival and proliferation are central to carcinogenesis, involving various mechanisms among which those that impede apoptosis are important. In this, the role of the molecular chaperone Hsp60 is unclear since it has been reported that it can be both, pro- or anti-apoptotic. A solution to this riddle is crucial to the development of anti-cancer therapies targeting Hsp60. We addressed this question using a tumor cell line, NCI-H292, and [Cu(3,5-bis(2′-pyridyl)-1,2,4-oxadiazole) 2 (H 2 O) 2 ](ClO 4 ) 2 , CubipyOXA , a copper-containing compound with cytotoxic properties. We treated cells with various doses of the compound and measured cell viability; apoptosis indicators; and le…

0301 basic medicineProgrammed cell deathanimal structuresApoptosischemical and pharmacologic phenomenaCaspase 3medicine.disease_causecomplex mixturesBiochemistryMitochondrial ProteinsHsp60/pC3 complexInorganic Chemistry03 medical and health sciences0302 clinical medicineCoordination ComplexesCell Line TumorNeoplasmsCubipyOXAmedicineHumansCytotoxic T cellViability assayCancerOxadiazolesCaspase 3ChemistryfungiApoptosiChaperonin 60Hsp60Neoplasm ProteinsCell biology030104 developmental biologyApoptosisPro-caspase-3 (pC3)Multiprotein Complexes030220 oncology & carcinogenesisCancer cellHSP60Apoptosis; Cancer; CubipyOXA; Hsp60; Hsp60/pC3 complex; Pro-caspase-3 (pC3); Biochemistry; Inorganic ChemistryCarcinogenesisCopper
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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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