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MINORITY PREDOCTORAL FELLOWSHIP PROGRAM

MINORITY PREDOCTORAL FELLOWSHIP PROGRAM
少数族裔博士前奖学金计划
批准号:
7295970
负责人:
JOHN Tyson MCDONALD
金额:
$3.01万
依托单位国家:
美国
项目类别:
财政年份:
2006
资助国家:
美国
项目状态:
已结题
起止时间:
2006-09-30 至 2009-09-29
关键词:
Activation AnalysisAnimal ModelAntioxidantsBiologicalBiological AssayCell CycleCell Cycle ProgressionCell SurvivalCell physiologyCellsCessation of lifeChemicalsChemopreventive AgentChinese Hamster Ovary CellComplementary DNAConditionDU145DoseDyesEnvironmentEnzymesEquilibriumEventExclusionExposure toExtracellular Signal Regulated KinasesFellowship ProgramFlow CytometryFluorescence-Activated Cell SortingFutureGene ExpressionGene ProteinsGenetic TranscriptionGlutathioneGoalsGrowthHandHumanImmunoblottingIn Situ Nick-End LabelingIndiumInflammationIonizing radiationJUN geneKnock-outLiverLuciferasesLuminescent MeasurementsManganese Superoxide DismutaseMethodsMinorityMitogen-Activated Protein KinasesModelingMonitorMusN-terminalNAD(P)H dehydrogenase (quinone) 1, humanNF-E2-related factor 2NF-kappa BNamesNormal tissue morphologyNuclearNumbersOxidation-ReductionOxidative StressPC3 cell linePathway interactionsPhasePhosphatidylinositolsProtein DephosphorylationProtein OverexpressionProteinsRNA InterferenceRadiationRadiation ToleranceRadioprotectionReactive Oxygen SpeciesResponse ElementsReverse Transcriptase Polymerase Chain ReactionRoleSignal PathwaySignal TransductionSmall Interfering RNAStaining methodStainsSuperoxidesTechniquesTestingTimeTranscription Factor AP-1TransfectionTrypan BlueTumor VolumeWestern BlottingWorkcatalasecell growthcopper zinc superoxide dismutasecytotoxicglutathione peroxidaseheme oxygenase-1improvedin vivoinsightirradiationluminescencelymphoblastmitogen-activated protein kinase p38pre-doctoralprotein expressionprotein kinase C kinaserepairedresearch studyresponsescaffoldtranscription factortumortumor growthvector

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DESCRIPTION (provided by applicant): At present, there is a lack in the understanding of how antioxidants impact radioprotection. The cellular redox balance is maintained through a number of antioxidant enzymes such as heme oxygenase 1, superoxide dimutase, catalase, and glutathione. Oxidative stress and ionizing radiation activate transcriptional factors such as AP-1, NF-kB, and NRF-2 and PI-3K, PKC, and MAPK signaling cascades resulting in the induction of cellular antioxidants. Exploring the effects of ionizing radiation on antioxidant expression at the cellular level is essential before these pathways can be used to enhance radioprotection. We hypothesize that there is a hierarchal response to oxidative stress, inflammation, and cellular death in response to radiation dose. In addition to characterizing the antioxidant expression, we will explore the potential of modifying these redox responses in terms of their radioprotective effects. This project aims to improve the understanding of antioxidants in response to ionizing radiation and will clarify the importance of these mechanisms for radioprotection.
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