Search results for "Phosphor"

showing 10 items of 1952 documents

Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax.

2018

Experimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro-survival and anti-apoptotic roles through molecule phosphorylated extracellular signal-regulated kinase1/2 (p-ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p-ERK1/2 and pro-apoptotic molecule Bax. In this study, the rat-derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the ca…

0301 basic medicinePhysiologyCell SurvivalEndogenyApoptosisCell LineSmall hairpin RNA03 medical and health sciences0302 clinical medicinePhysiology (medical)ExtracellularmedicineGene silencingAnimalsMyocytes CardiacGene SilencingGuanine Nucleotide-Releasing Factor 2Cell Proliferationbcl-2-Associated X ProteinPharmacologyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Cell growthChemistryHypoxia (medical)PhosphoproteinsCell biologyRats030104 developmental biologyApoptosis030220 oncology & carcinogenesisPhosphorylationmedicine.symptomClinical and experimental pharmacologyphysiology
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MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation

2017

Summary Most patients with advanced triple-negative breast cancer (TNBC) develop drug resistance. MYC and MCL1 are frequently co-amplified in drug-resistant TNBC after neoadjuvant chemotherapy. Herein, we demonstrate that MYC and MCL1 cooperate in the maintenance of chemotherapy-resistant cancer stem cells (CSCs) in TNBC. MYC and MCL1 increased mitochondrial oxidative phosphorylation (mtOXPHOS) and the generation of reactive oxygen species (ROS), processes involved in maintenance of CSCs. A mutant of MCL1 that cannot localize in mitochondria reduced mtOXPHOS, ROS levels, and drug-resistant CSCs without affecting the anti-apoptotic function of MCL1. Increased levels of ROS, a by-product of a…

0301 basic medicinePhysiologyMice NudeTriple Negative Breast NeoplasmsOxidative phosphorylationTumor initiationMitochondrionBiologyOxidative PhosphorylationArticleProto-Oncogene Proteins c-myc03 medical and health sciencesCancer stem cellCell Line TumorAnimalsHumansMCL1Molecular BiologyTriple-negative breast cancerchemistry.chemical_classificationReactive oxygen speciesCell BiologyMitochondria030104 developmental biologychemistryDrug Resistance NeoplasmNeoplastic Stem CellsCancer researchMyeloid Cell Leukemia Sequence 1 ProteinFemaleStem cellReactive Oxygen SpeciesCell Metabolism
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The Intracellular Cleavage Product of the NG2 Proteoglycan Modulates Translation and Cell-Cycle Kinetics via Effects on mTORC1/FMRP Signaling

2018

The NG2 proteoglycan is expressed by oligodendrocyte precursor cells (OPCs) and is abundantly expressed by tumors such as melanoma and glioblastoma. Functions of NG2 include an influence on proliferation, migration and neuromodulation. Similar to other type-1 membrane proteins, NG2 undergoes proteolysis, generating a large ectodomain, a C-terminal fragment (CTF) and an intracellular domain (ICD) via sequential action of α- and γ-secretases which is enhanced by neuronal activity. Functional roles of NG2 have so far been shown for the full-length protein, the released ectodomain and CTF, but not for the ICD. In this study, we characterized the role of the NG2 ICD in OPC and Human Embryonic Ki…

0301 basic medicinePopulationP70-S6 Kinase 1mTORC1γ-secretaselcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceNG2educationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryPI3K/AKT/mTOR pathwayOriginal Researcheducation.field_of_studyChemistryICDHEK 293 cellsTranslation (biology)S6K1Cell biologystomatognathic diseases030104 developmental biologyEctodomainnervous systemeEF2mTORPhosphorylationFMRPOPCNeuroscienceFrontiers in Cellular Neuroscience
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Transcriptomic study of the toxic mechanism triggered by beauvericin in Jurkat cells

2018

Beauvericin (BEA), an ionophoric cyclic hexadepsipeptide mycotoxin, is able to increase oxidative stress by altering membrane ion permeability and uncoupling oxidative phosphorylation. A toxicogenomic study was performed to investigate gene expression changes triggered by BEA exposure (1.5, 3 and 5 mu M; 24 h) in Jurkat cells through RNA-sequencing and differential gene expression analysis. Perturbed gene expression was observed in a concentration dependent manner, with 43 differentially expressed genes (DEGs) overlapped in the three studied concentrations. Gene ontology (GO) analysis showed several biological processes related to electron transport chain, oxidative phosphorylation, and cel…

0301 basic medicineProgrammed cell deathCYTOCHROME-C RELEASEBCL-2 FAMILYCell Membrane PermeabilityRespiratory chainCell Culture TechniquesCASPASE-3 ACTIVATIONApoptosisOxidative phosphorylationCHO-K1 CELLSToxicologyJurkat cellsOxidative PhosphorylationElectron Transport03 medical and health sciencesJurkat CellsFUSARIUM MYCOTOXINSImmunotoxicologyDepsipeptidesHumansREAL-TIME PCROXIDATIVE STRESSTranscriptomicsCaspaseINDUCED APOPTOSISLEUKEMIA-CELLS030102 biochemistry & molecular biologybiologyDose-Response Relationship DrugChemistryJurkatGene Expression ProfilingBcl-2 familyDEATHGeneral MedicineBeauvericinToxicogenomicsCell biologyGene expression profiling030104 developmental biologyMitochondrial respiratory chainGene Ontologybiology.proteinRNA-seqTranscriptomeToxicology Letters
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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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Peroxisome proliferator-activated receptor-γ coactivator-1α mediates neuroprotection against excitotoxic brain injury in transgenic mice: role of mit…

2016

Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is a transcriptional coactivator involved in the regulation of mitochondrial biogenesis and cell defense. The functions of PGC-1α in physiology of brain mitochondria are, however, not fully understood. To address this we have studied wild-type and transgenic mice with a two-fold overexpression of PGC-1α in brain neurons. Data showed that the relative number and basal respiration of brain mitochondria were increased in PGC-1α transgenic mice compared with wild-type mitochondria. These changes occurred concomitantly with altered levels of proteins involved in oxidative phosphorylation (OXPHOS) as studied by proteomi…

0301 basic medicineProgrammed cell deathKainic acidTransgenebcl-X ProteinPeroxisome proliferator-activated receptorBiologyInhibitor of apoptosisSettore BIO/09 - FisiologiaNeuroprotectionOxidative PhosphorylationInhibitor of Apoptosis ProteinsMice03 medical and health scienceschemistry.chemical_compoundXIAP0302 clinical medicineBrain InjurieInhibitor of Apoptosis ProteinAnimalsCA1 Region HippocampalCells CulturedNeuronschemistry.chemical_classificationNeuroscience (all)Kainic AcidCell DeathAnimalNeuron survivalGeneral NeuroscienceProteomicXIAP; Kainic acid; Mitochondria; Neuron survival; PGC-1α; Proteomics; Animals; Brain Injuries; CA1 Region Hippocampal; Cell Death; Cells Cultured; Inhibitor of Apoptosis Proteins; Kainic Acid; Mice; Mitochondria; Neurons; Oxidative Phosphorylation; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Proto-Oncogene Proteins c-bcl-2; bcl-X Protein; Neuroscience (all)NeuronPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaCell biologyXIAP030104 developmental biologyProto-Oncogene Proteins c-bcl-2chemistryMitochondrial biogenesisBrain InjuriesImmunologyPGC-1α030217 neurology & neurosurgeryEuropean Journal of Neuroscience
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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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Phosphorylation and proteasome recognition of the mRNA- binding protein Cth2 facilitates yeast adaptation to iron deficiency

2018

Iron is an indispensable micronutrient for all eukaryotic organisms due to its participation as a redox cofactor in many metabolic pathways. Iron imbalance leads to the most frequent human nutritional deficiency in the world. Adaptation to iron limitation requires a global reorganization of the cellular metabolism directed to prioritize iron utilization for essential processes. In response to iron scarcity, the conserved Saccharomyces cerevisiae mRNA-binding protein Cth2, which belongs to the tristetraprolin family of tandem zinc finger proteins, coordinates a global remodeling of the cellular metabolism by promoting the degradation of multiple mRNAs encoding highly iron-consuming proteins.…

0301 basic medicineProteasome Endopeptidase ComplexSaccharomyces cerevisiae ProteinsIronPosttranslational regulationSaccharomyces cerevisiaeMrna bindingMicrobiology03 medical and health sciencesProtein stabilityTristetraprolinGene Expression Regulation FungalVirologyPolitical scienceProtein stabilitySerineRNA MessengerPhosphorylationIron deficiencyAdaptation PhysiologicalQR1-502Yeast030104 developmental biologyMutagenesisChristian ministryProtein Processing Post-TranslationalHumanities
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Oxidative post‐translational modifications in histones

2019

Epigenetic regulation is attracting much attention because it explains many of the effects that the external environment induces in organisms. Changes in the cellular redox status and even more specifically in its nuclear redox compartment is one of these examples. Redox changes can induce modulation of the epigenetic regulation in cells. Here we present a few cases where reactive oxygen or nitrogen species induces epigenetic marks in histones. Posttranslational modification of these proteins like histone nitrosylation, carbonylation, or glutathionylation together with other mechanisms not reviewed here are the cornerstones of redox-related epigenetic regulation. We currently face a new fie…

0301 basic medicineProtein CarbonylationClinical BiochemistryOxidative phosphorylationmedicine.disease_causeBiochemistryEpigenesis GeneticHistonesProtein CarbonylationMice03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansEpigeneticsEpigenesisSulfur CompoundsbiologyChemistryNitrosylationGeneral MedicineGlutathioneReactive Nitrogen SpeciesCell biologyOxidative Stress030104 developmental biologyHistone030220 oncology & carcinogenesisbiology.proteinMolecular MedicineSignal transductionReactive Oxygen SpeciesOxidation-ReductionProtein Processing Post-TranslationalOxidative stressNitroso CompoundsSignal TransductionBioFactors
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Insights into the inhibited form of the redox-sensitive SufE-like sulfur acceptor CsdE

2017

17 p.-8 fig.

0301 basic medicineProtein ConformationDimerlcsh:MedicineMolecular DynamicsCrystallography X-RayPhysical ChemistryBiochemistryDEAD-box RNA HelicasesMolecular dynamicschemistry.chemical_compoundComputational ChemistryNucleophileBiochemical Simulationslcsh:ScienceMultidisciplinaryCrystallographyChemistryOrganic CompoundsPhysicsEscherichia coli ProteinsCondensed Matter Physics3. Good healthPhysical sciencesChemistryCarbon-Sulfur LyasesBiochemistryCrystal StructureResearch ArticleChemical ElementsProtein subunitChemical physicschemistry.chemical_elementOxidative phosphorylationMolecular Dynamics Simulation03 medical and health sciencesThiolsEscherichia coliSolid State PhysicsProtein Interaction Domains and MotifsChemical BondingOrganic Chemistrylcsh:RChemical CompoundsBiology and Life SciencesComputational BiologyDimers (Chemical physics)Hydrogen BondingCell BiologySulfurAcceptorRedox sensitiveOxidative Stress030104 developmental biologyBiophysicslcsh:QProtein MultimerizationSulfur
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