MINORITY PREDOCTORAL FELLOWSHIP PROGRAM

少数族裔博士前奖学金计划

基本信息

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
项目类别：
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

项目摘要

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.

描述（由申请人提供）：目前，人们对抗氧化剂如何影响辐射防护缺乏了解。细胞氧化还原平衡通过多种抗氧化酶来维持，例如血红素加氧酶 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 和 NRF-2 以及 PI-3K、PKC 和 MAPK 信号级联，从而诱导细胞抗氧化剂。在利用这些途径增强辐射防护之前，探索电离辐射对细胞水平抗氧化剂表达的影响至关重要。我们假设辐射剂量对氧化应激、炎症和细胞死亡存在分层反应。除了表征抗氧化剂表达之外，我们还将探索改变这些氧化还原反应的辐射防护作用的潜力。该项目旨在提高对抗氧化剂响应电离辐射的理解，并将阐明这些辐射防护机制的重要性。