Search results for "Cytochromes c"

showing 10 items of 46 documents

Large Spatial Scale of the Phenotype-Environment Color Matching in Two Cryptic Species of African Desert Jerboas (Dipodidae: Jaculus)

2014

We tested the camouflage hypothesis, or the linkage between animal (Saharan rodent) and habitat coloration, on the largest geographical scale yet conducted. We aimed to determine whether phenotypic variation is explained by micro-habitat variation and/or genetic polymorphism to determine 1) the strength of linkage between fur color and local substrate color, and 2) the divergence in fur coloration between two genetic clades, representing cryptic species, throughout the complete range of the African desert jerboas (Jaculus jaculus). We used a combination of museum and field-collected specimens, remote sensing tools, satellite and digital photography and molecular genetic and phylogenetic met…

0106 biological sciencesRange (biology)Skin Pigmentation01 natural sciencesDipodidaeJaculus jaculusGeoinformaticsPhylogeny0303 health sciencesMultidisciplinaryRemote Sensing ImageryPhylogenetic treeEcologyGeographyPigmentationQRCytochromes cBiological EvolutionPhenotypeSympatric speciationMedicineResearch ArticleSpecies complexComputer and Information SciencesScienceZoologyRodentiaBiologyEnvironment010603 evolutionary biology03 medical and health sciencesGenetic variationAnimalsSelection Genetic030304 developmental biologyEvolutionary BiologySpatial AnalysisPolymorphism GeneticEcology and Environmental SciencesBiology and Life SciencesGenetic Variation15. Life on landbiology.organism_classificationGenetic divergenceHaplotypesEvolutionary EcologyRemote Sensing TechnologyEarth Sciencesta1181HairPlos One
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Betulinic acid induces a novel cell death pathway that depends on cardiolipin modification

2016

Cancer is associated with strong changes in lipid metabolism. For instance, normal cells take up fatty acids (FAs) from the circulation, while tumour cells generate their own and become dependent on de novo FA synthesis, which could provide a vulnerability to target tumour cells. Betulinic acid (BetA) is a natural compound that selectively kills tumour cells through an ill-defined mechanism that is independent of BAX and BAK, but depends on mitochondrial permeability transition-pore opening. Here we unravel this pathway and show that BetA inhibits the activity of steroyl-CoA-desaturase (SCD-1). This enzyme is overexpressed in tumour cells and critically important for cells that utilize de n…

0301 basic medicineCancer ResearchProgrammed cell deathCardiolipinsMitochondrionCell Line03 medical and health scienceschemistry.chemical_compoundSDG 3 - Good Health and Well-beingBetulinic acidGeneticsCardiolipinHumansBetulinic AcidCytotoxicityMolecular BiologyCell DeathbiologyCytochrome cFatty AcidsCytochromes cLipid metabolismAntineoplastic Agents PhytogenicTriterpenesMitochondriaCell biology030104 developmental biologyBiochemistrychemistryCancer cellbiology.protein/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingPentacyclic TriterpenesStearoyl-CoA Desaturase
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Role of Circulating miRNAs as Biomarkers in Idiopathic Pulmonary Arterial Hypertension: Possible Relevance of miR-23a

2015

Idiopathic pulmonary hypertension (IPAH) is a rare disease characterized by a progressive increase in pulmonary vascular resistance leading to heart failure. MicroRNAs (miRNAs) are small noncoding RNAs that control the expression of genes, including some involved in the progression of IPAH, as studied in animals and lung tissue. These molecules circulate freely in the blood and their expression is associated with the progression of different vascular pathologies. Here, we studied the expression profile of circulating miRNAs in 12 well-characterized IPAH patients using microarrays. We found significant changes in 61 miRNAs, of which the expression of miR23a was correlated with the patients’ …

AdultMaleAgingArticle SubjectNF-E2-Related Factor 2Idiopathic Pulmonary HypertensionBiologyBiochemistryPulmonary function testingmicroRNAmedicineGene silencingHumansFamilial Primary Pulmonary Hypertensionlcsh:QH573-671Cells CulturedAgedlcsh:CytologySuperoxide DismutaseGene Expression ProfilingCytochromes cCell BiologyGeneral MedicineMiddle Agedmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaGene expression profilingMicroRNAsmedicine.anatomical_structureHeart failureImmunologyVascular resistanceBiomarker (medicine)FemaleBiomarkersHeme Oxygenase-1Research ArticleTranscription FactorsOxidative Medicine and Cellular Longevity
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PGC-1α Induction in Pulmonary Arterial Hypertension

2012

Idiopathic Pulmonary arterial hypertension (IPAH) is characterized by the obstructive remodelling of pulmonary arteries, and a progressive elevation in pulmonary arterial pressure (PAP) with subsequent right-sided heart failure and dead. Hypoxia induces the expression of peroxisome proliferator activated receptorγcoactivator-1α(PGC-1α) which regulates oxidative metabolism and mitochondrial biogenesis. We have analysed the expression of PGC-1α, cytochrome C (CYTC), superoxide dismutase (SOD), the total antioxidant status (TAS) and the activity of glutathione peroxidase (GPX) in blood samples of IPAH patients. Expression of PGC-1αwas detected in IPAH patients but not in healthy volunteers. Th…

AdultMaleAgingmedicine.medical_specialtyArticle SubjectHypertension PulmonaryPeroxisome proliferator-activated receptorBiologyBiochemistrySuperoxide dismutaseChloridesInternal medicinemedicineHumansFamilial Primary Pulmonary Hypertensionlcsh:QH573-671Heat-Shock ProteinsAgedchemistry.chemical_classificationGlutathione Peroxidaselcsh:CytologySuperoxide DismutaseGlutathione peroxidaseAge FactorsCytochromes cCell BiologyGeneral MedicineHypoxia (medical)Middle Agedmedicine.diseasePulmonary hypertensionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaEndocrinologymedicine.anatomical_structurechemistryMitochondrial biogenesisHeart failurebiology.proteinVascular resistanceFemaleVascular Resistancemedicine.symptomTranscription FactorsResearch ArticleOxidative Medicine and Cellular Longevity
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Spectroelectrochemistry of cytochrome c and azurin immobilized in nanoporous antimony-doped tin oxide

2011

Stable immobilization of two redox proteins, cytochrome c and azurin, in a thin film of highly mesoporous antimony-doped tin oxide is demonstrated via UV-vis spectroscopic and electrochemical investigation.

AntimonyMaterials scienceInorganic chemistrychemistry.chemical_elementElectrochemistryRedoxCatalysisNanoporesAntimonyAzurinMaterials ChemistrybiologyNanoporousCytochrome ctechnology industry and agricultureMetals and AlloysCytochromes cTin CompoundsElectrochemical TechniquesGeneral Chemistryequipment and suppliesTin oxideSurfaces Coatings and FilmsElectronic Optical and Magnetic MaterialsImmobilized ProteinschemistryCeramics and Compositesbiology.proteinSpectrophotometry UltravioletAdsorptionAzurinMesoporous materialChemical Communications
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Revisiting the thiosemicarbazonecopper(II) reaction with glutathione. Activity against colorectal carcinoma cell lines.

2018

Thiosemicarbazones (TSCs), and their copper derivatives, have been extensively studied mainly due to the potential applications as antitumor compounds. A part of the biological activity of the TSC-CuII complexes rests on their reactivity against cell reductants, as glutathione (GSH). The present paper describes the structure of the [Cu(PTSC)(ONO2)]n compound (1) (HPTSC =pyridine-2-carbaldehyde thiosemicarbazone) and its spectroscopic and magnetic properties. ESI studies performed on the reaction of GSH with 1 and the analogous [{Cu (PTSC*)(ONO2)}2] derivative (2, HPTSC* =pyridine-2-carbaldehyde 4N-methylthiosemicarbazone) show the absence of peaks related with TSC-Cu-GSH species. However GS…

Aparato digestivo-EnfermedadesThiosemicarbazonesSpectrometry Mass Electrospray IonizationColorectal cancerColon carcinoma010402 general chemistryCrystallography X-RayThiosemicarbazone01 natural sciencesBiochemistryInorganic Chemistrychemistry.chemical_compoundColon carcinomaCell Line TumorSpectroscopy Fourier Transform InfraredmedicineHumansMolecular magnetismDigestive organs-DiseasesMolecular Structure010405 organic chemistryChemistryMyoglobinCytochromes cGlutathioneChemistry Inorganicmedicine.diseaseMolecular biologyGlutathioneQuímica inorgánica0104 chemical sciencesCell cultureDrug Screening Assays AntitumorColorectal NeoplasmsCopperJournal of inorganic biochemistry
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Bax-derived membrane-active peptides act as potent and direct inducers of apoptosis in cancer cells.

2011

SUMMARYAlthough many cancer cells are primed for apoptosis, they usually develop resistance to cell death at multiple levels. Permeabilization of the outer mitochondrial membrane, which is mediated by proapoptotic Bcl-2 family members like Bax, is considered as a point-of-no-return for initiating apoptotic cell death. This crucial role has placed Bcl-2 family proteins as recurrent targets for anticancer drug development. Here, we propose and demonstrate a new concept based on using minimal active version of Bax to induce cell death independently of endogenous Bcl-2 proteins. We show that membrane-active segments of Bax can directly induce the release of mitochondria-residing apoptogenic fac…

ApoptosisMitochondrionMiceMESH: Protein Structure Tertiary0302 clinical medicineNeoplasmsgeneticsMESH: AnimalsMESH: Neoplasmsbcl-2-Associated X Protein0303 health sciencesbiologyMESH: PeptidesCytochrome capoptosisCytochromes cMESH: Cytochromes cproapoptotic BaxCell biologyMitochondriadrug therapymitochondria030220 oncology & carcinogenesisBacterial outer membraneProgrammed cell deathMESH: Cell Line TumorMESH: MitochondriaAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancerpore-forming peptideschemistryArticle03 medical and health sciencesBcl-2-associated X proteinBcl-2 familyCell Line TumorAnimalsHumansMESH: bcl-2-Associated X ProteinMESH: Mice030304 developmental biologyMESH: HumansMESH: ApoptosisBcl-2 familyCell BiologyProtein Structure Tertiaryanticancer agentantivascular therapyApoptosisdrug effectsCancer cellbiology.proteinMESH: Antineoplastic AgentspharmacologyphysiopathologyPeptidesmetabolism
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Isoprenylhydroquinone glucoside: a new non-antioxidant inhibitor of peroxynitrite-mediated tyrosine nitration

2004

Abstract Three hydroquinone glucosides and four caffeoylquinic esters were examined for their effect on tyrosine nitration, as well as on the oxidation of dihydrorhodamine (DHR) 123 and cytochrome c 2+ induced by peroxynitrite. All these phenolics, which had previously been characterized as the active principles of the plant Phagnalon rupestre , were fairly active in preventing the oxidation of DHR 123, though inefficient in the cytochrome c test. While their antioxidant potency is associated with the presence of a caffeoyl moiety, not so an obvious chemical character was correlated to a greater activity against nitration of tyrosine. Here, the highest potency corresponded to 2-isoprenylhyd…

Cancer ResearchAntioxidantCytochromePhysiologymedicine.medical_treatmentClinical BiochemistryAsteraceaeBiochemistrychemistry.chemical_compoundGlucosidesGlucosidePeroxynitrous AcidNitrationmedicineTyrosineNitratesMolecular StructurebiologyHydroquinoneRhodaminesCytochrome cCytochromes cHydroquinoneschemistryBiochemistrybiology.proteinTyrosineOxidation-ReductionPeroxynitriteNitric Oxide
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Smac induces cytochrome c release and apoptosis independently from Bax/Bcl-xL in a strictly caspase-3-dependent manner in human carcinoma cells

2004

The mitochondrial apoptosis pathway mediates cell death through the release of various pro-apoptotic factors including cytochrome c and Smac, the second mitochondrial activator of caspases, into the cytosol. Smac was shown previously to inhibit IAP proteins and to facilitate initiation of the caspase cascade upon cytochrome c release. To investigate Smac function during apoptosis and to explore Smac as an experimental cancer therapeutic, we constructed an expression system based on a single adenoviral vector containing Smac under control of the Tet-off system supplied in cis. Conditional expression of Smac induced apoptosis in human HCT116 and DU145 carcinoma cells regardless of the loss of…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsBcl-xLCaspase 3Cysteine Proteinase InhibitorsAdenoviridaeMitochondrial ProteinsBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedGeneticsHumansMolecular BiologyCaspasebcl-2-Associated X ProteinCaspase-9biologyCaspase 3Cytochrome cCarcinomaIntracellular Signaling Peptides and ProteinsCytochromes cCaspase InhibitorsCaspase 9Cell biologyEnzyme ActivationProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesMutationbiology.proteinCancer researchbiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsCarrier ProteinsOligopeptidesProtein Processing Post-TranslationalOncogene
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Pharmacologic activation of p53 elicits Bax-dependent apoptosis in the absence of transcription

2003

AbstractRecent efforts to develop pharmacologic agents that restore function to mutant forms of p53 hold significant promise in cancer therapy. Here, we examine the effects of such pharmacologic activation of p53 function using a small molecule, PRIMA-1, and a model system employing a p53 protein fused to a mutant steroid binding domain of the murine estrogen receptor (p53ERtam) that renders it responsive only in the presence of 4-hydroxytamoxifen. In either case, p53 activation triggered apoptosis that was not inhibited by the presence of macromolecular synthesis inhibitors. This p53-induced, transcription-independent apoptosis is Bax dependent, proceeds in the absence of a nucleus, and in…

Cancer ResearchTranscription GeneticRecombinant Fusion ProteinsMutantEstrogen receptorApoptosis03 medical and health sciencesMice0302 clinical medicineBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedAnimalsHumansCloning MolecularReceptorCells Cultured030304 developmental biologybcl-2-Associated X ProteinCell NucleusProtein Synthesis Inhibitors0303 health sciencesAza CompoundsbiologyCytochrome cCytochromes cCell BiologyFibroblastsBridged Bicyclo Compounds Heterocyclic3. Good healthCell biologyTransport proteinMitochondriaProtein TransportTamoxifenProto-Oncogene Proteins c-bcl-2Receptors EstrogenOncologyApoptosis030220 oncology & carcinogenesisMutationbiology.proteinTumor Suppressor Protein p53Binding domainCancer Cell
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