Search results for "Trx"

showing 10 items of 12 documents

Thioredoxin (Trxo1) interacts with proliferating cell nuclear antigen (PCNA) and its overexpression affects the growth of tobacco cell culture.

2017

Thioredoxins (Trxs), key components of cellular redox regulation, act by controlling the redox status of many target proteins, and have been shown to play an essential role in cell survival and growth. The presence of a Trx system in the nucleus has received little attention in plants, and the nuclear targets of plant Trxs have not been conclusively identified. Thus, very little is known about the function of Trxs in this cellular compartment. Previously, we studied the intracellular localization of PsTrxo1 and confirmed its presence in mitochondria and, interestingly, in the nucleus under standard growth conditions. In investigating the nuclear function of PsTrxo1 we identified proliferati…

0106 biological sciences0301 basic medicineTFs transcription factorsOverexpressionBiologíaBiFC bimolecular fluorescence complementationClinical BiochemistryCell Culture TechniquesTobacco BY-2 cells01 natural sciencesBiochemistryTBY-2 tobacco bright yellow-2DTT 14-dithiothreitolBimolecular fluorescence complementationThioredoxinsGene Expression Regulation PlantTrx thioredoxinlcsh:QH301-705.5GFP green fluorescent proteinlcsh:R5-920biologyProliferating cell nuclear antigen (PCNA)Cell cycleGlutathione3. Good healthCell biologyMitochondriaNTR NADPH thioredoxin reductaseProtein TransportDEM diethyl maleateRT-qPCR Reverse transcription quantitative polymerase chain reactionThioredoxinlcsh:Medicine (General)Oxidation-ReductionAMS 4-acetamido-4-maleimidylstilbene-22-disulfonic acidResearch PaperPCNA proliferating cell nuclear antigenOex overexpressingCell cycleNucleusThioredoxin o103 medical and health sciencesROS reactive oxygen speciesDownregulation and upregulationProliferating Cell Nuclear AntigenTobaccoDAPI 46-diamidine-2-phenylindolmCBM monochlorobimaneCellular compartmentCell NucleusCell growthOrganic ChemistryBotánicaPeasMolecular biologyYFP yellow fluorescent proteinProliferating cell nuclear antigenTBS Tris-buffered salineOD optical density030104 developmental biologylcsh:Biology (General)Cell cultureRNA reactive nitrogen speciesbiology.proteinPrx peroxiredoxinBSA bovine serum albumin010606 plant biology & botanyRedox biology
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Alternative lengthening of telomeres (ALT) influences survival in soft tissue sarcomas: a systematic review with meta-analysis

2019

Background Alternative lengthening of telomeres (ALT) is a telomerase-independent mechanism used by a broad range of neoplasms to maintain telomere length, permitting uncontrolled replication during their progression. ALT has been described in different types of sarcoma, but a comprehensive analysis of its clinical significance is still lacking. Therefore, we provide here the first meta-analysis on this topic. Methods We searched SCOPUS and PubMed through July 2018 to identify all studies that investigated the prognostic role of ALT in sarcomas. We considered the risk of death (risk ratio, RR) calculated as the number of death vs. total participants during follow-up in ALT+ versus ALT- pati…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyMultivariate analysisMesenchymalSurvivalALTlcsh:RC254-282digestive systemRisk Assessmentnot known03 medical and health sciences0302 clinical medicineSurgical oncologyInternal medicineGeneticsmedicineHumansClinical significanceALT; ATR; ATRX; Mesenchymal; Prognosis; Sarcoma; SurvivalProportional Hazards Modelsbusiness.industryHazard ratioSoft tissueTelomere HomeostasisSarcomaMiddle AgedTelomeremedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisSurvival Analysisdigestive system diseases3. Good health030104 developmental biologyATRATRXOncology030220 oncology & carcinogenesisRelative riskMeta-analysisSarcomabusinessResearch ArticleBMC Cancer
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Changes in sprint performance and sagittal plane kinematics after heavy resisted sprint training in professional soccer players

2019

Background Sprint performance is an essential skill to target within soccer, which can be likely achieved with a variety of methods, including different on-field training options. One such method could be heavy resisted sprint training. However, the effects of such overload on sprint performance and the related kinetic changes are unknown in a professional setting. Another unknown factor is whether violating kinematic specificity via heavy resistance will lead to changes in unloaded sprinting kinematics. We investigated whether heavy resisted sled training (HS) affects sprint performance, kinetics, sagittal plane kinematics, and spatiotemporal parameters in professional male soccer players.…

Anatomy and Physiologycoordinationkoordinaatio (motoriikka)bepress|Life Sciences|KinesiologyeducationProfessional sportVelocity-based trainingstrength trainingSportRxiv|Sport and Exercise Science|Strength and ConditioningSprintingnopeusvoimaprofessional sportKinesiologypikajuoksuResistance trainingharjoitusvastesprintingjalkapalloilijatSportRxiv|Sport and Exercise ScienceCoordinationbiomekaniikkavoimaharjoitteluStrength trainingresistance traininghuman activitiesvelocity-based training
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Resveratrol reduces oxidative stress and cell death and increases mitochondrial antioxidants and XIAP in PC6.3-cells.

2010

Resveratrol, a polyphenol derived e.g. from red grapes, has been shown to mediate several positive biological actions such as protection of cells against oxidative stress. It can also influence cell signaling, but the mechanisms behind its antioxidant properties are largely unknown. Here we show that RSV reduces oxidative stress and enhances cell survival in PC6.3 cells depending on the concentration. In these cells, RSV increased the levels of antioxidants, SOD2 and TRX2, and of X chromosome-linked inhibitor of apoptosis protein. RSV also activated NFκB signaling as shown using luciferase reporter constructs. These findings show that RSV regulates oxidative stress and mitochondrial antioxi…

Cell signalingProgrammed cell deathBlotting WesternSOD2Settore BIO/11 - Biologia MolecolareApoptosisX-Linked Inhibitor of Apoptosis ProteinMitochondrionBiologyResveratrolmedicine.disease_causeInhibitor of apoptosisSettore BIO/09 - FisiologiaPolymerase Chain ReactionAntioxidantsCell LineMitochondrial Proteins03 medical and health scienceschemistry.chemical_compoundXIAP0302 clinical medicineThioredoxinsStilbenesmedicineTRX2Humans030304 developmental biologyNeurons0303 health sciencesSuperoxide DismutaseGeneral Neurosciencefood and beveragesROSSOD23. Good healthXIAPCell biologyMitochondriaOxidative StressBiochemistrychemistryResveratrolSettore BIO/14 - FarmacologiaOxidative stre030217 neurology & neurosurgeryOxidative stressNFκBNeuroscience letters
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Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

2015

Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed …

Genome instabilityRedox signalingRNA UntranslatedEpigenetic regulation of neurogenesisDNA RepairHuR mRNA-binding protein in the 3′-untranslated regionClinical BiochemistryHDAC histone deacetylaseReview ArticleAP-1 activator protein 1BiochemistryApe-1 apurinic/apyrimidinic endonuclease 1GPx-1 glutathione peroxidase-1Epigenesis GeneticHistonesTrx thioredoxinPHD prolylhydroxylaseBER base excision repairlcsh:QH301-705.5HO-1 heme oxygenase-1EpigenomicsGeneticsRegulation of gene expressionNox member of the NADPH oxidase familylcsh:R5-920JmjC Jumonji C domain-containing histone demethylasesHIF-1α hypoxia inducible factor-1α5-hmC 5-hydroxymethylcytosineddc:Cell biologyMMP matrix metalloproteinaseGrx glutaredoxinGAPDH glyceraldehyde-3-phosphate dehydrogenaseNrf2 nuclear factor erythroid related factor 2DNA methylationEpigeneticslcsh:Medicine (General)Oxidation-ReductionSignal Transduction5-mC 5-methylcytosineDNA repairDNA damageNF-κB nuclear factor-κBBiologyGenomic InstabilityRNS reactive nitrogen speciesROS reactive oxygen speciesNER nucleotide excision repairSOD superoxide dismutaseOxyR transcription factor (hydrogen peroxide-inducible genes activator)HumansEpigeneticsOrganic ChemistryPETN pentaerithrityl tetranitrateGene regulationOxidative StressDNMT DNA methyltransferaseGene Expression Regulationlcsh:Biology (General)AREs AU-rich elementsHAT histone acetyltransferaseKeap1 kelch-like ECH-associated protein 1BiomarkersCOPD chronic obstructive pulmonary disorderDNA DamageRedox Biology
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Corticotroph aggressive pituitary tumours and carcinomas frequently harbour ATRX mutations

2021

Abstract Context Aggressive pituitary tumors (APTs) are characterized by unusually rapid growth and lack of response to standard treatment. About 1% to 2% develop metastases being classified as pituitary carcinomas (PCs). For unknown reasons, the corticotroph tumors are overrepresented among APTs and PCs. Mutations in the alpha thalassemia/mental retardation syndrome X-linked (ATRX) gene, regulating chromatin remodeling and telomere maintenance, have been implicated in the development of several cancer types, including neuroendocrine tumors. Objective To study ATRX protein expression and mutational status of the ATRX gene in APTs and PCs. Design We investigated ATRX protein expression by us…

Male0301 basic medicineEndocrinology Diabetes and MetabolismClinical Biochemistrypituitary adenomapituitary carcinomaBiochemistryPATHWAYCohort Studies0302 clinical medicineEndocrinologyGene FrequencyTELOMERESCorticotrophsClinical Laboratory MedicineGenomicsMiddle AgedCushing’s diseaseEUROPEAN-SOCIETY3. Good healthEuropeKlinisk laboratoriemedicinACTH-Secreting Pituitary Adenoma030220 oncology & carcinogenesisDAXX/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingCushing's diseaseFemaleATRX (alpha thalassemia/mental retardation syndrome X-linked); aggressive PitNETs; pituitary carcinoma; pituitary adenoma; Cushings diseaseAcademicSubjects/MED00250EXPRESSIONAdenomaAdultX-linked Nuclear Proteinmedicine.medical_specialtyGENESAdolescentATRX (alpha thalassemia/mental retardation syndrome X-linked)3122 CancersNonsense mutationContext (language use)CLASSIFICATIONYoung Adult03 medical and health sciencesDeath-associated protein 6SDG 3 - Good Health and Well-beingPituitary adenomaInternal medicineADENOMASmedicineHumansGenetic Predisposition to DiseaseNeoplasm InvasivenessPituitary NeoplasmsClinical Research ArticlesATRXAgedCancer och onkologiaggressive PitNETsbusiness.industryCarcinomaBiochemistry (medical)Pituitary tumorsCancerAMPLIFICATIONNeuroendocrinologymedicine.disease030104 developmental biologyEndocrinologyPituitary3121 General medicine internal medicine and other clinical medicineCancer and OncologyMutationPituitary carcinomaCancer researchbusinessATRX (alpha thalassemia/mental retardation syndrome X-linked); Cushing’s disease; aggressive PitNETs; pituitary adenoma; pituitary carcinoma
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Neuroblastoma after Childhood: Prognostic Relevance of Segmental Chromosome Aberrations, ATRX Protein Status, and Immune Cell Infiltration

2014

AbstractNeuroblastoma (NB) is a common malignancy in children but rarely occurs during adolescence or adulthood. This subgroup is characterized by an indolent disease course, almost uniformly fatal, yet little is known about the biologic characteristics. The aim of this study was to identify differential features regarding DNA copy number alterations, α-thalassemia/mental retardation syndrome X-linked (ATRX) protein expression, and the presence of tumor-associated inflammatory cells. Thirty-one NB patients older than 10 years who were included in the Spanish NB Registry were considered for the current study; seven young and middle-aged adult patients (range 18-60 years) formed part of the c…

MaleCancer ResearchHet heterogeneousGene ExpressionNeuroblastomaImmunophenotypingRegistriesYoung adultNeoplasm MetastasisMLPA multiplex ligation probe amplificationChildIn Situ Hybridization FluorescenceNuclear ProteinsMiddle AgedAYA adolescent and young adultsPrognosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNCA numerical chromosome aberrationImmunohistochemistryFemaleSCA segmental chromosome aberrationIHC immunohistochemistryNB neuroblastomaAdultX-linked Nuclear ProteinAdolescentaSNP single nucleotide polymorphism arrayBiologyMalignancyChromosome aberrationPolymorphism Single Nucleotidelcsh:RC254-282ArticleImmunophenotypingYoung AdultLymphocytes Tumor-InfiltratingNeuroblastomacnLOH copy-neutral loss of heterozygositymedicineHumansHom homogeneousATRXNeoplasm StagingChromosome AberrationsDNA Helicasesmedicine.diseaseSpainMNNA MYCN not amplifiedCancer researchFSCA focal segmental chromosome aberrationCD8MNA MYCN amplifiedNeoplasia
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Monitoring training and recovery responses with heart rate measures during standardized warm-up in elite badminton players.

2020

\(\bf Purpose\) To investigate short-term training and recovery-related effects on heart rate during a standardized submaximal running test. \(\bf Methods\) Ten elite badminton players (7 females and 3 males) were monitored during a 12-week training period in preparation for the World Championships. Exercise heart rate (HRex) and perceived exertion were measured in response to a 5-min submaximal shuttle-run test during the morning session warm-up. This test was repeatedly performed on Mondays after 1–2 days of pronounced recovery (‘recovered’ state; reference condition) and on Fridays following 4 consecutive days of training (‘strained’ state). In addition, the serum concentration of creati…

MalePhysiologySocial SciencesSports SciencesRunningExercise PhysiologyHeart RateMedicine and Health SciencesUreaPsychologyPublic and Occupational Healthddc:796GeneralLiterature_REFERENCE(e.g.dictionariesencyclopediasglossaries)Creatine Kinasebepress|Life Sciences|PhysiologyOrganic CompoundsQRLife SciencesKinesiologySports ScienceChemistrySportRxiv|Sport and Exercise SciencePhysical SciencesSportRxiv|Sport and Exercise Science|Sport and Exercise PhysiologyMedicineFemaleathleteplayerPhysical Conditioning HumanResearch ArticleSportsAdultWarm-Up ExerciseSciencebepress|Life Sciences|KinesiologyPhysical ExertionCardiologyAthletic PerformancerecoveryYoung AdultHumansSportRxiv|Sport and Exercise Science|Strength and ConditioningSports and Exercise MedicineExerciseBehaviorBiological LocomotionOrganic ChemistryChemical CompoundsBiology and Life SciencesPhysical ActivityExercise ScienceCreatinemonitoringPhysical FitnessFOS: Biological sciencesRecreationfatigueindividual responsePloS one
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Mitochondrial dynamics in type 2 diabetes: Pathophysiological implications

2017

Mitochondria play a key role in maintaining cellular metabolic homeostasis. These organelles have a high plasticity and are involved in dynamic processes such as mitochondrial fusion and fission, mitophagy and mitochondrial biogenesis. Type 2 diabetes is characterised by mitochondrial dysfunction, high production of reactive oxygen species (ROS) and low levels of ATP. Mitochondrial fusion is modulated by different proteins, including mitofusin-1 (MFN1), mitofusin-2 (MFN2) and optic atrophy (OPA-1), while fission is controlled by mitochondrial fission 1 (FIS1), dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF). PARKIN and (PTEN)-induced putative kinase 1 (PINK1) partici…

MiD51 mitochondrial dynamics proteins of 51 kDaΔΨm mitochondrial membrane potential0301 basic medicineMitochondrial fission factorClinical BiochemistryMitochondrial DegradationMFN2Review ArticleTXNIP thioredoxin interacting proteinMitochondrial DynamicsBiochemistryAdenosine TriphosphateGRP78 78 kDa glucose-regulated proteinMFF mitochondrial fission factorMFN2 mitofusin 2TRX2 thioredoxin 2Redox biologylcsh:QH301-705.5NF-κB nuclear factor kappa Blcsh:R5-920MitophagyType 2 diabetesDRP1 dynamin-related protein 1FIS1 fission protein 1BNIP3 BCL2/adenovirus E1B 19 kDa interacting protein 3MitochondriaOPA1 optic atrophy 1SIRT1/3 sirtuin 1/3Biochemistrymitochondrial fusionTGF-β1 transforming growth factor-β1Mitochondrial fissionOMM outer mitochondrial membranelcsh:Medicine (General)MiD49 mitochondrial dynamics proteins of 49Nox 4 NADPH oxidase-4IMM inner mitochondrial membraneFIS1ATF6 activating transcription factor 6PINK1mTOR mammalian target of rapamycinCHOP C/EBP homologous proteinBiologymdivi-1 mitochondrial division inhibitor-1Mitochondrial Proteins03 medical and health sciencesROS reactive oxygen speciessXBP1 spliced X-box binding protein 1UCP-1 uncoupling protein-1MFN1 mitofusin 1SOD superoxide dismutaseLC3 1 A/1B-light chain 3HumansPINK1 (PTEN)-induced putative kinase 1S3 15-OxospiramilactoneOrganic ChemistrymtDNA mitochondrial DNAAMPK AMP-activated protein kinase030104 developmental biologyDiabetes Mellitus Type 2Mitochondrial biogenesislcsh:Biology (General)Oxidative stressp38 MAPK p38 mitogen-activated protein kinasep62/SQSTM1 ubiquitin and sequestosome-1Reactive Oxygen SpeciesRedox Biology
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Age-dependent regulation of antioxidant genes by p38α MAPK in the liver

2018

p38α is a redox sensitive MAPK activated by pro-inflammatory cytokines and environmental, genotoxic and endoplasmic reticulum stresses. The aim of this work was to assess whether p38α controls the antioxidant defense in the liver, and if so, to elucidate the mechanism(s) involved and the age-related changes. For this purpose, we used liver-specific p38α-deficient mice at two different ages: young-mice (4 months-old) and old-mice (24 months-old). The liver of young p38α knock-out mice exhibited a decrease in GSH levels and an increase in GSSG/GSH ratio and malondialdehyde levels. However, old mice deficient in p38α had higher hepatic GSH levels and lower GSSG/GSH ratio than young p38α knock-…

ROS Reactive oxygen species;RSK1 Ribosomal S6 kinase10301 basic medicineMAPK/ERK pathwayAgingHPLC High-performance liquid chromatographyAntioxidantmedicine.medical_treatmentTBP TATA-binding proteinClinical BiochemistryDEN Diethyl nitrosamine;MKP-1 MAPK phosphatase-1IκB kinaseGCLc Glutamate cysteine ligase catalytic subunitp38 Mitogen-Activated Protein KinasesG6PDH Glucose-6-phosphate dehydrogenaseBiochemistryAntioxidantsMicechemistry.chemical_compoundSuperoxide Dismutase-1Akt Protein kinase B0302 clinical medicineNrf2 Nuclear factor erythroid 2-related factor-2IL InterleukinSOD1 Cu/Zn-superoxide dismutaselcsh:QH301-705.5Mice KnockoutMK2 MAP-activated protein kinase 2;PGC-1α Peroxisome proliferator-activated receptor gamma coactivator 1-alphachemistry.chemical_classificationlcsh:R5-920Trx ThioredoxinGlutathione DisulfideTNF-α Tumor necrosis factor-alphabiologyLPS Lipopolysaccharide;GSSG Oxidized glutathione;MEF Mouse embryonic fibroblastsNF-kappa BGstm1 Glutathione S-transferase mu 1CatalaseEndoplasmic Reticulum StressGlutathioneLiverGSH Reduced glutathione;Catalase030220 oncology & carcinogenesisJNK c-Jun N-terminal kinaselcsh:Medicine (General)Research Papermedicine.medical_specialtyNF-E2-Related Factor 2Glutamate-Cysteine LigaseMKK MAPK kinaseAP-1 Activator protein-1IKK IƙB KinaseGene Expression Regulation EnzymologicSuperoxide dismutase03 medical and health sciencesInternal medicineGlutamate cysteine ligaseEGFR Epidermal growth factor receptormedicineAnimalsNuclear factor ƙBAnd catalaseChIP Chromatin immunoprecipitation;Protein kinase BNF-ƙB Nuclear factor kappa BSuperoxide DismutaseSuperoxide dismutase 1Superoxide dismutase 2Organic ChemistryGlutathioneASK1 Apoptosis signal-regulating kinase 1ATF2 activating transcription factor 2;030104 developmental biologyEndocrinologyEnzymeHsp Heat shock proteinlcsh:Biology (General)chemistrybiology.proteinSOD2 Mn-superoxide dismutaseMAPK mitogen activated protein kinaseNEM N-ethyl maleimide;Redox Biology
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