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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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中文摘要
翻译
描述(由申请人提供):目前,对抗氧化剂如何影响辐射防护的理解缺乏。细胞氧化还原平衡是通过一些抗氧化酶维持的,如血红素加氧酶1、超氧化物歧化酶、过氧化氢酶和谷胱甘肽。氧化应激和电离辐射激活转录因子,如AP-1、NF-kB、NRF-2和PI-3K、PKC和MAPK信号级联,导致细胞抗氧化剂的诱导。探索电离辐射对细胞水平抗氧化表达的影响是必要的,然后这些途径可以用来增强辐射防护。我们假设辐射剂量对氧化应激、炎症和细胞死亡有层次反应。除了表征抗氧化表达外,我们还将探索在其辐射防护作用方面修改这些氧化还原反应的潜力。该项目旨在提高对抗氧化剂在电离辐射反应中的认识,并将阐明这些机制对辐射防护的重要性。
英文摘要
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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