Search results for "Mitochondrial Protein"

showing 10 items of 89 documents

Kinetic studies on protoporphyrinogen oxidase inhibition by diphenyl ether herbicides

1991

Diphenyl ethers (DPEs) and related herbicides are powerful inhibitors of protoporphyrinogen oxidase, an enzyme involved in the biosynthesis of haems and chlorophylls. The inhibition kinetics of protoporphyrinogen oxidase of various origins by four DPEs, (methyl)-5-[2-chloro-4-(trifluoromethyl)phenoxy]-2-nitrobenzoic acid (acifluorfen and its methyl ester, acifluorfen-methyl), methyl-5-[2-chloro-4-(trifluoromethyl) phenoxy]-2-chlorobenzoate (LS 820340) and methyl-5-[2-chloro-5-(trifluoromethyl)phenoxy]-2-nitrobenzoic acid (RH 5348), were studied. The inhibitions of the enzymes from maize (Zea mays) mitochondrial and etiochloroplastic membranes and mouse liver mitochondrial membranes were com…

0106 biological sciencesOxidoreductases Acting on CH-CH Group DonorsStereochemistry[SDV]Life Sciences [q-bio]Carboxylic acidMitochondria LiverEtherSaccharomyces cerevisiaeAcifluorfen01 natural sciencesBiochemistryMitochondrial ProteinsMiceStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compoundMALHERBOLOGIEPhenolsAnimalsProtoporphyrinogen OxidaseMolecular BiologyComputingMilieux_MISCELLANEOUS030304 developmental biologychemistry.chemical_classification0303 health sciencesTrifluoromethylFlavoproteinsHerbicidesDiphenyl etherIntracellular MembranesCell BiologyPlantsMitochondriaProtoporphyrinogen IX[SDV] Life Sciences [q-bio]KineticsEnzymechemistryProtoporphyrinogen oxidaseOxidoreductasesEthersResearch Article010606 plant biology & botanyBiochemical Journal
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Quantitative patterns of Hsps in tubular adenoma compared with normal and tumor tissues reveal the value of Hsp10 and Hsp60 in early diagnosis of lar…

2016

Large bowel carcinogenesis involves accumulation of genetic alterations leading to transformation of normal mucosa into dysplasia and, lastly, adenocarcinoma. It is pertinent to elucidate the molecular changes occurring in the pre-neoplastic lesions to facilitate early diagnosis and treatment. Heat shock proteins (Hsps), many of which are molecular chaperones, are implicated in carcinogenesis, and their variations with tumor progression encourage their study as biomarkers. There are many reports on Hsps and cancer but none to our knowledge on their systematic quantification in pre-neoplastic lesions of the large bowel. We performed immunohistochemical determinations of Hsp10, Hsp60, Hsp70, …

0301 basic medicineAdenomaMaleDysplasiaPathologymedicine.medical_specialtyColorectal cancerColonLarge bowelChaperoneBiologyAdenocarcinomamedicine.disease_causeBiochemistryMitochondrial Proteins03 medical and health sciencesBiomarker; Chaperone; Dysplasia; Hsps; Large bowel; Tubular adenoma; Biochemistry; Cell Biology0302 clinical medicineTubular adenomaHeat shock proteinmedicineBiomarkers TumorChaperonin 10HspHumansIntestinal MucosaEarly Detection of CancerAgedTubular adenomaAged 80 and overLamina propriaOriginal PaperBiomarkerCell BiologyChaperonin 60Middle Agedmedicine.disease030104 developmental biologymedicine.anatomical_structureDysplasiaTumor progression030220 oncology & carcinogenesisCase-Control StudiesImmunologyAdenocarcinomaFemaleCarcinogenesisColorectal Neoplasms
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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Mitophagy in human astrocytes treated with the antiretroviral drug Efavirenz: Lack of evidence or evidence of the lack

2019

Efavirenz (EFV), a first generation non-nucleoside analogue reverse transcriptase inhibitor widely employed in combination antiretroviral therapy regimens over the last 20 years, has been associated with a wide range of neuropsychiatric effects and has also been linked with HIV-associated neurocognitive disorder (HAND). EFV has been reported to alter mitochondrial dysfunction and bioenergetics in different cell types, including astrocytes. Here, we analyzed whether this mitochondrial effect is associated with alterations in autophagy and, more specifically, mitophagy. U251-MG cells were exposed to EFV (10 and 25 μM; 24 h) and the effect was compared with that of CCCP - an uncoupler of the m…

0301 basic medicineCyclopropanesCell typeThapsigarginEfavirenz030106 microbiologyMitochondrial DegradationBiologyMitochondrionPharmacologyMitochondrial Proteins03 medical and health scienceschemistry.chemical_compoundCitologíaVirologyCell Line TumorMitophagymedicineAutophagyHumansPharmacologyReverse-transcriptase inhibitorBiología celularAutophagyAutophagosomesMitophagyBenzoxazinesMitochondriaAntiretroviral030104 developmental biologychemistryAnti-Retroviral AgentsAlkynesAstrocytesReverse Transcriptase InhibitorsEfavirenzVirologíamedicine.drug
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Mitochondrial BAX Determines the Predisposition to Apoptosis in Human AML

2017

Abstract Purpose: Cell-to-cell variability in apoptosis signaling contributes to heterogenic responses to cytotoxic stress in clinically heterogeneous neoplasia, such as acute myeloid leukemia (AML). The BCL-2 proteins BAX and BAK can commit mammalian cells to apoptosis and are inhibited by retrotranslocation from the mitochondria into the cytosol. The subcellular localization of BAX and BAK could determine the cellular predisposition to apoptotic death. Experimental Design: The relative localization of BAX and BAK was determined by fractionation of AML cell lines and patient samples of a test cohort and a validation cohort. Results: This study shows that relative BAX localization determine…

0301 basic medicineCytoplasmCancer ResearchApoptosisKaplan-Meier EstimateBiologyMitochondrionMitochondrial Proteins03 medical and health sciencesCell Line Tumorhemic and lymphatic diseasesmedicineHumansCytotoxic T cellLeukocytosisRetrospective Studiesbcl-2-Associated X ProteinMyeloid leukemiaCancerRetrospective cohort studymedicine.diseaseMitochondriaProtein TransportLeukemiabcl-2 Homologous Antagonist-Killer Protein030104 developmental biologyOncologyLeukemia MyeloidApoptosisAcute DiseaseImmunologyCancer researchmedicine.symptomHeLa CellsClinical Cancer Research
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CD1A-positive cells and HSP60 (HSPD1) levels in keratoacanthoma and squamous cell carcinoma.

2015

CD1a is involved in presentation to the immune system of lipid antigen derived from tumor cells with subsequent T cell activation. Hsp60 is a molecular chaperone implicated in carcinogenesis by, for instance, modulating the immune reaction against the tumor. We have previously postulated a synergism between CD1a and Hsp60 as a key factor in the activation of an effective antitumor immune response in squamous epithelia. Keratoacantomas (KAs) are benign tumors that however can transform into squamous cell carcinomas (SCCs), but the reasons for this malignization are unknown. In a previous study, we found that CD1a-positive cells are significantly more numerous in KA than in SCC. In this study…

0301 basic medicineKeratoacanthomaCellmedicine.disease_causeBiochemistryAntigens CD10302 clinical medicineSquamous cell carcinomaAged 80 and overintegumentary systemPrognostic evaluationMiddle AgedHsp60ImmunohistochemistryKeratoacanthomamedicine.anatomical_structure030220 oncology & carcinogenesisCarcinoma Squamous CellImmunohistochemistryHSP60AdultT cellDifferential diagnosichemical and pharmacologic phenomenaCD1aBiologySettore MED/08 - Anatomia PatologicaDiagnosis DifferentialMitochondrial Proteins03 medical and health sciencesYoung AdultKeratoacantomaImmune systemmedicineBiomarkers TumorHumansAgedRetrospective StudiesOriginal PaperSettore BIO/16 - Anatomia UmanaCD1a; Differential diagnosis; Hsp60; Immunohistochemistry; Keratoacantoma; Prognostic evaluation; Squamous cell carcinoma; Treatment; Biochemistry; Cell BiologyfungiCell BiologyChaperonin 60medicine.diseaseTreatmentstomatognathic diseases030104 developmental biologyCancer researchDifferential diagnosisCarcinogenesisCell stresschaperones
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Effects of Ranolazine on Astrocytes and Neurons in Primary Culture.

2016

Ranolazine (Rn) is an antianginal agent used for the treatment of chronic angina pectoris when angina is not adequately controlled by other drugs. Rn also acts in the central nervous system and it has been proposed for the treatment of pain and epileptic disorders. Under the hypothesis that ranolazine could act as a neuroprotective drug, we studied its effects on astrocytes and neurons in primary culture. We incubated rat astrocytes and neurons in primary cultures for 24 hours with Rn (10-7, 10-6 and 10-5 M). Cell viability and proliferation were measured using trypan blue exclusion assay, MTT conversion assay and LDH release assay. Apoptosis was determined by Caspase 3 activity assay. The …

0301 basic medicineMacroglial CellsPhysiologyInterleukin-1betaProtein ExpressionCell Culture Techniqueslcsh:MedicineApoptosisPharmacologyPathology and Laboratory Medicine0302 clinical medicineRanolazineAnimal CellsImmune PhysiologyMedicine and Health SciencesEnzyme assaysColorimetric assaysEnzyme-Linked Immunoassayslcsh:ScienceBioassays and physiological analysisImmune ResponseNeuronsInnate Immune SystemMultidisciplinaryMTT assayCell DeathCaspase 3medicine.anatomical_structureCell ProcessesCytokinesTumor necrosis factor alphaCellular TypesAstrocyteResearch ArticleProgrammed cell deathCell SurvivalImmunologyCaspase 3Glial CellsBiologyGene Expression Regulation EnzymologicMitochondrial Proteins03 medical and health sciencesSigns and SymptomsmedicineGene Expression and Vector TechniquesAnimalsMTT assayViability assayMolecular Biology TechniquesImmunoassaysMolecular BiologyInflammationMolecular Biology Assays and Analysis TechniquesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RBiology and Life SciencesCell BiologyMolecular DevelopmentRatsPPAR gammaResearch and analysis methodsOxidative Stress030104 developmental biologyCell cultureApoptosisAstrocytesImmune SystemBiochemical analysisImmunologic Techniqueslcsh:QFisiologia humanaApoptosis Regulatory ProteinsCarrier Proteins030217 neurology & neurosurgeryDevelopmental BiologyPloS one
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The Effect of a Novel c.820C>T (Arg274Trp) Mutation in the Mitofusin 2 Gene on Fibroblast Metabolism and Clinical Manifestation in a Patient

2017

Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal peripheral neuropathy caused by mutations in the mitofusin 2 gene (MFN2). Mitofusin 2 is a GTPase protein present in the outer mitochondrial membrane and responsible for regulation of mitochondrial network architecture via the fusion of mitochondria. As that fusion process is known to be strongly dependent on the GTPase activity of mitofusin 2, it is postulated that the MFN2 mutation within the GTPase domain may lead to impaired GTPase activity, and in turn to mitochondrial dysfunction. The work described here has therefore sought to verify the effects of MFN2 mutation within its GTPase domain on mitochondrial and e…

0301 basic medicineMaleHydrolasesMutantMFN2lcsh:MedicineGTPaseMitochondrionmedicine.disease_causeEndoplasmic ReticulumBiochemistryGTP Phosphohydrolases0302 clinical medicineMental RetardationAnimal CellsCharcot-Marie-Tooth DiseaseMedicine and Health SciencesMissense mutationlcsh:ScienceEnergy-Producing OrganellesCells CulturedConnective Tissue CellsGeneticsMutationMultidisciplinarySecretory PathwayOrganic CompoundsMonosaccharidesTryptophanMitochondrial DNACell biologyMitochondriaEnzymesNucleic acidsChemistryNeurologyConnective TissueCell ProcessesPhysical SciencesCellular Structures and OrganellesCellular TypesAnatomyResearch ArticleForms of DNACarbohydratesMutation MissenseBiologyBioenergeticsArgininePolymorphism Single NucleotideMitochondrial Proteins03 medical and health sciencesMitofusin-2Young AdultmedicineGeneticsHumansEndoplasmic reticulumlcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsCell BiologyDNAFibroblastsGuanosine Triphosphatase030104 developmental biologyBiological TissueGlucoseAmino Acid SubstitutionCase-Control StudiesMutationEnzymologylcsh:Q030217 neurology & neurosurgeryPLoS ONE
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Sex-based differences after a single bout of exercise on PGC1α isoforms in skeletal muscle: A pilot study

2020

To date, there are limited and incomplete data on possible sex-based differences in fiber-types of skeletal muscle and their response to physical exercise. Adult healthy male and female mice completed a single bout of endurance exercise to examine the sex-based differences of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α), heat shock protein 60 (Hsp60), interleukin 6 (IL-6) expression, as well as the Myosin Heavy Chain (MHC) fiber-type distribution in soleus and extensor digitorum longus (EDL) muscles. Our results showed for the first time that in male soleus, a muscle rich of type IIa fibers, endurance exercise activates specifically genes involved in mito…

0301 basic medicineMalemedicine.medical_specialtyAlpha (ethology)interleukin 6Physical exerciseMotor ActivityBiochemistryMitochondrial Proteins03 medical and health sciencesMice0302 clinical medicineSex FactorsEndurance trainingphysical exerciseInternal medicineHeat shock proteinMyosinGeneticsmedicineAnimalsProtein Isoformsskeletal muscleInterleukin 6Muscle SkeletalMolecular BiologyMice Inbred BALB Cbiologybusiness.industryInterleukin-6Myosin Heavy ChainSkeletal muscleChaperonin 60musculoskeletal systemPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha030104 developmental biologyEndocrinologymedicine.anatomical_structureMitochondrial biogenesisbiology.proteinFemalebusiness030217 neurology & neurosurgeryheat shock protein 60Biotechnology
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