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.

本研究的目的是研究Eph A受体蛋白酪氨酸激酶（RPTK）及其配体（ephrin）在脊髓损伤（SCI）后轴突再生的非许可环境中的作用。分子生物学、蛋白质生物化学、神经影像学示踪策略和行为学测定将在T10水平上与损伤大鼠结合使用，以分析这些蛋白质的表达。第一个目的将集中在空间和时间的表达Eph A和ephrin A，mRNA和蛋白质，脊髓后中枢神经系统（CNS）损伤后，在核和氨基酸水平。在第二个目标中，我们将确定Eph A RPTK和ephrins作为排斥性分子线索限制SCI后轴突再生和功能恢复的可能作用。对于本研究，表达Eph A RPTKs或肝配蛋白A的氨基末端的融合蛋白将是单个Eph A RPTKs和肝配蛋白在再生纤维上和局部环境中的时间和空间表达，可能导致新的治疗策略以增强SCI后的再生和功能恢复。