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: UNIVERSITY OF CALIFORNIA LOS ANGELES
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-09-30 至 2009-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7295970
• 关键词: Activation Analysis; Animal Model; Antioxidants; Biological; Biological Assay; Cell Cycle; Cell Cycle Progression; Cell Survival; Cell physiology; Cells; Cessation of life; Chemicals; Chemopreventive Agent; Chinese Hamster Ovary Cell; Complementary DNA; Condition; DU145; Dose; Dyes; Environment; Enzymes; Equilibrium; Event; Exclusion; Exposure to; Extracellular Signal Regulated Kinases; Fellowship Program; Flow Cytometry; Fluorescence-Activated Cell Sorting; Future; Gene Expression; Gene Proteins; Genetic Transcription; Glutathione; Goals; Growth; Hand; Human; Immunoblotting; In Situ Nick-End Labeling; Indium; Inflammation; Ionizing radiation; JUN gene; Knock-out; Liver; Luciferases; Luminescent Measurements; Manganese Superoxide Dismutase; Methods; Minority; Mitogen-Activated Protein Kinases; Modeling; Monitor; Mus; N-terminal; NAD(P)H dehydrogenase (quinone) 1, human; NF-E2-related factor 2; NF-kappa B; Names; Normal tissue morphology; Nuclear; Numbers; Oxidation-Reduction; Oxidative Stress; PC3 cell line; Pathway interactions; Phase; Phosphatidylinositols; Protein Dephosphorylation; Protein Overexpression; Proteins; RNA Interference; Radiation; Radiation Tolerance; Radioprotection; Reactive Oxygen Species; Response Elements; Reverse Transcriptase Polymerase Chain Reaction; Role; Signal Pathway; Signal Transduction; Small Interfering RNA; Staining method; Stains; Superoxides; Techniques; Testing; Time; Transcription Factor AP-1; Transfection; Trypan Blue; Tumor Volume; Western Blotting; Work; catalase; cell growth; copper zinc superoxide dismutase; cytotoxic; glutathione peroxidase; heme oxygenase-1; improved; in vivo; insight; irradiation; luminescence; lymphoblast; mitogen-activated protein kinase p38; pre-doctoral; protein expression; protein kinase C kinase; repaired; research study; response; scaffold; transcription factor; tumor; tumor growth; vector

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.

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。