Elucidating the paradox of TrkC receptor isoforms causing either neuronal survival or degeneration: target validation and therapeutic rationale using isoform-selective pharmacological and biological tools.

阐明导致神经元存活或变性的 TrkC 受体异构体的悖论：使用异构体选择性药理学和生物学工具进行目标验证和治疗原理。

• 批准号: 390397
• 负责人: Saragovi Horacio U
• 金额: $ 99.2万
• 依托单位: Lady Davis Institute for Medical Research (Mtl)
• 依托单位国家: 加拿大
• 项目类别: Operating Grants
• 财政年份: 2018
• 资助国家: 加拿大
• 起止时间: 2018-09-01 至 2022-09-01
• 项目状态: 已结题
• 来源: https://webapps.cihr-irsc.gc.ca/decisions/p/project_details.html?applId=390397&lang=en
• 关键词: Agonist; Als; Antagonist; Cochlea; Hair Cells; Hearing Loss; Motor Neurons; Spinal Cord; Target Validation; Therapy

TrkC-FL is a receptor that when activated prevents the death of neurons. A truncated form of it is called TrkC.T1. When activated, TrkC.T1 causes neuronal death, in diseases causing blindness (Retinitis Pigmentosa, Glaucoma), in motor neuron disease (Amy

TrkC-FL是一种受体，当被激活时，可以防止神经元死亡。它的截断形式称为TrkC.T1。当TrkC.T1被激活时，会导致神经元死亡，在导致失明的疾病中(视网膜色素变性、青光眼)，在运动神经元疾病(AMY)中