Search results for " Biochemistry"

showing 10 items of 5648 documents

Glutathione in metastases: From mechanisms to clinical applications.

2016

Metastatic spread, not primary tumors, is the leading cause of cancer death. Glutathione (γ-glutamyl-cysteinyl-glycine, GSH) is particularly relevant in cancer cells as it is involved in regulating carcinogenic mechanisms, growth and dissemination, and multidrug and radiation resistance. Upon interaction of metastatic cells with the vascular endothelium, a high percentage of metastatic cells with high GSH levels survive the combined nitrosative and oxidative stresses elicited by the vascular endothelium. GSH release from different organs, mainly the liver, and its interorgan transport through the blood circulation to metastatic foci, promote their growth. This review focuses on the relation…

0301 basic medicineProgrammed cell deathClinical BiochemistryCancer therapyOxidative phosphorylationBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineMetastatic cellNeoplasmsmedicineAnimalsHumansNeoplasm MetastasisCarcinogenBiochemistry (medical)CancerGlutathionemedicine.diseaseGlutathione030104 developmental biologychemistry030220 oncology & carcinogenesisCancer cellImmunologyCancer researchCritical reviews in clinical laboratory sciences
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Metabolic Imaging in Multicellular Spheroids of Oncogene-transfected Fibroblasts

2000

Four rat embryo fibroblast (REF) cell lines with defined oncogenic transformation were used to study the relationship between tumorigenic conversion, metabolism, and development of cell death in a 3D spheroid system. Rat1 (spontaneously immortalized) and M1 ( myc-transfected) fibroblasts represent early nontumorigenic transformation stages, whereas Rat1-T1 (T24Ha- ras-transfected Rat1) and MR1 ( myc/T24Ha- ras-co-transfected REF) cells express a highly tumorigenic phenotype. Localized ATP, glucose, and lactate concentrations in spheroid median sections were determined by imaging bioluminescence. ATP concentrations were low in the nonproliferating Rat1 aggregates despite sufficient oxygen an…

0301 basic medicineProgrammed cell deathHistologyGenes mycApoptosisBiology030218 nuclear medicine & medical imaging03 medical and health sciencesAdenosine Triphosphate0302 clinical medicineSpheroids CellularImage Processing Computer-AssistedmedicineAnimalsFrozen SectionsLactic AcidFibroblastCell Line Transformed030102 biochemistry & molecular biologyOncogeneSpheroidEmbryoTransfectionMetabolismMolecular biologyRats Inbred F344RatsCell biologyGenes rasGlucosemedicine.anatomical_structureCell cultureLuminescent Measurementsembryonic structuresAnatomyCell DivisionJournal of Histochemistry & Cytochemistry
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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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Viral Bcl2s' transmembrane domain interact with host Bcl2 proteins to control cellular apoptosis

2020

© The Author(s) 2020.

0301 basic medicineProgrammed cell deathScienceProtein domainGeneral Physics and AstronomyApoptosisBiologyVirus-host interactionsArticleGeneral Biochemistry Genetics and Molecular BiologyFluorescenceCell Line03 medical and health sciences0302 clinical medicineProtein Domainsimmune system diseaseshemic and lymphatic diseasesmedicineHumansAmino Acid SequenceAuthor CorrectionPeptide sequenceneoplasmsMultidisciplinaryVirus–host interactionsQCell MembraneGeneral ChemistryViral proteinsmedicine.diseaseControl cellLymphomaCell biologyVirusTransmembrane domain030104 developmental biologyProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisDoxorubicin030220 oncology & carcinogenesisbiological phenomena cell phenomena and immunityProtein MultimerizationHydrophobic and Hydrophilic InteractionsProteïnesProtein Binding
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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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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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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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Suicidal Erythrocyte Death in Metabolic Syndrome.

2021

Eryptosis is a coordinated, programmed cell death culminating with the disposal of cells without disruption of the cell membrane and the release of endocellular oxidative and pro-inflammatory milieu. While providing a convenient form of death for erythrocytes, dysregulated eryptosis may result in a series of detrimental and harmful pathological consequences highly related to the endothelial dysfunction (ED). Metabolic syndrome (MetS) is described as a cluster of cardiometabolic factors (hyperglycemia, dyslipidemia, hypertension and obesity) that increases the risk of cardiovascular complications such as those related to diabetes and atherosclerosis. In the light of the crucial role exerted …

0301 basic medicineProgrammed cell deathobesityhypertensionPhysiologyClinical BiochemistryReview030204 cardiovascular system & hematologyBioinformaticsmedicine.disease_causeBiochemistrymetabolic syndromeendothelial dysfunction03 medical and health sciences0302 clinical medicineDiabetes mellituseryptosisvascular damagemedicineoxidative stressEndothelial dysfunctionMolecular BiologyPathologicaldiabetesbusiness.industrylcsh:RM1-950dyslipidemiaCell Biologymedicine.diseaseObesitylcsh:Therapeutics. Pharmacology030104 developmental biologyMetabolic syndromeatherosclerosisbusinessDyslipidemiaOxidative stressAntioxidants (Basel, Switzerland)
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The C-terminal region of human plasma fetuin-B is dispensable for the raised-elephant-trunk mechanism of inhibition of astacin metallopeptidases

2019

© The Author(s) 2019.

0301 basic medicineProteasesProtein Conformationlcsh:MedicineAstacoideaCrystallography X-RayCleavage (embryo)Protein Structure SecondaryArticleMice03 medical and health sciencesScissile bondHydrolaseAnimalsHumansAmino Acid Sequencelcsh:ScienceProtein secondary structureX-ray crystallographyBinding SitesMultidisciplinary030102 biochemistry & molecular biologyChemistrylcsh:RMetalloendopeptidasesProteasesFetuinFetuin-BCell biologyZincFertility030104 developmental biologyProteolysisMetalloproteaseslcsh:QAstacinLinkerScientific Reports
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