Yang Q F, Fan M, Wan X C
Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing.
Sheng Li Ke Xue Jin Zhan. 1997 Jul;28(3):209-13.
Binding of neurotrophins and their receptors lead to dimerization and autophosphorylation of trks. Activated trkA initiates the Ras pathway and finally opens the transcriptions of immediate early genes and delayed response genes or participates directly in physiological responses. Target-derived neurotrophins bind to and induce phosphorylation of trk receptors at the axonal terminal. Active trk or NT-trk or other signal molecules can be retrogradely transported along the axon to transduct messages to neuronal nucleus. There are local autocrine and paracrine mechanisms besides target-derived NTs. Following nervous system injury, increased gene expressions of NTs and their receptors and increased retrograde axonal transport are helpful to survive and regenerate for injured neurons. Lacking NTs and their receptors will result in serious abnormal development of nervous system of mice.
神经营养因子与其受体的结合导致酪氨酸激酶受体（trks）二聚化和自身磷酸化。激活的trkA启动Ras信号通路，最终开启即刻早期基因和延迟反应基因的转录，或直接参与生理反应。靶源性神经营养因子在轴突末端与trk受体结合并诱导其磷酸化。活性trk或NT-trk或其他信号分子可沿轴突逆行运输，将信息传递至神经元细胞核。除了靶源性神经营养因子外，还存在局部自分泌和旁分泌机制。神经系统损伤后，神经营养因子及其受体的基因表达增加以及轴突逆行运输增加，有助于受损神经元存活和再生。缺乏神经营养因子及其受体将导致小鼠神经系统严重发育异常。
