Ephrin A receptor tyrosine kinases in preventing axonal regeneration

Ephrin A 受体酪氨酸激酶预防轴突再生

• 批准号: 6667572
• 负责人: JORGE David MIRANDA
• 金额: $ 24.81万
• 依托单位: UNIVERSITY OF PUERTO RICO MED SCIENCES
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-09-01 至 2003-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6667572
• 关键词: chimeric proteins; cooperative study; growth inhibitors; laboratory rat; membrane proteins; nervous system regeneration; protein localization; protein tyrosine kinase; receptor binding; receptor expression; spinal cord injury

The goal of this study is to investigate the role of Eph A receptor protein tyrosine kinases (RPTK) and their ligands (ephrins) in producing a non- permissive environment for axonal regeneration after spinal cord injury (SCI). Molecular biology, protein biochemistry, neuroimaging tracing strategies and behavioral assays will be used in conjunction with injured rats at the T10 level to analyze the expression of these proteins. The first aim will focus on the spatial and temporal expression of Eph A and ephrin A, mRNAs and proteins, after spinal after Central Nervous System (CNS) lesion at the nuclei and amino acid level. The expression pattern will moderate spinal cord contusion, In the second aim, we will determine the possible role of Eph A RPTK and ephrins as repulsive molecular cues that restrict axonal regeneration and functional recovery after SCI. For this study, fusion proteins expressing the amino terminus of the Eph A RPTKs or ephrins A will be temporal and spatial expression of individual Eph A RPTKs and ephrins, both on the regenerating fibers and in the local environment, may lead to novel therapeutic strategies to enhanced regeneration and functional recovery after SCI.

本研究的目的是探讨Eph A受体蛋白酪氨酸激酶（RPTK）及其配体（ephrins）在脊髓损伤（SCI）后产生轴突再生的非许可环境中的作用。结合损伤大鼠T10水平的分子生物学、蛋白质生物化学、神经影像学追踪策略和行为分析，分析这些蛋白的表达。第一个目的是研究Eph A和ephrin A、mrna和蛋白在脊髓后中枢神经系统（CNS）损伤后在细胞核和氨基酸水平上的时空表达。在第二个目标中，我们将确定Eph A RPTK和ephrin作为限制脊髓损伤后轴突再生和功能恢复的排斥分子线索的可能作用。在本研究中，表达Eph A RPTKs或ephrins A的氨基末端的融合蛋白将是个体Eph A RPTKs和ephrins的时空表达，无论是在再生纤维上还是在局部环境中，都可能导致新的治疗策略，以增强脊髓损伤后的再生和功能恢复。