神经生长因子通过激活大鼠嗜铬细胞瘤细胞（PC12细胞）中的丝裂原活化蛋白激酶（MAP激酶）途径上调垂体腺苷酸环化酶激活肽1型受体（PAC1）启动子。

Nerve growth factor upregulates the PAC1 promoter by activating the MAP kinase pathway in rat PC12 cells.

作者信息

Jamen F, Laden J C, Bouschet T, Rodriguez-Henche N, Bockaert J, Brabet P

机构信息

CNRS UPR 9023, 141, Rue de la Cardonille, 34094 Montpellier, France.

出版信息

Ann N Y Acad Sci. 2000;921:390-4. doi: 10.1111/j.1749-6632.2000.tb07002.x.

DOI:10.1111/j.1749-6632.2000.tb07002.x

PMID:11193862

Abstract

We report that: (1) An increase in the transcription activity is a mechanism by which trophic peptides may regulate the expression of PAC1. (2) An activation of the PAC1 promoter does not necessarily correlate with the neurotrophin-promoted neuritogenesis. (3) Activation of the PAC1 promoter is probably an early event since the EGF response is rather weak and transient in PC12 cells. (4) MAP kinase pathway activation is necessary for the NGF effect. The mechanism of the antagonism between PACAP and NGF observed on the PAC1 promoter activity and already described in regulating chromaffin cell proliferation, remains to be explained.

摘要

我们报告如下

（1）转录活性增加是营养肽调节PAC1表达的一种机制。（2）PAC1启动子的激活不一定与神经营养因子促进的神经突生长相关。（3）PAC1启动子的激活可能是一个早期事件，因为在PC12细胞中表皮生长因子反应相当微弱且短暂。（4）丝裂原活化蛋白激酶途径的激活对于神经生长因子的作用是必需的。垂体腺苷酸环化酶激活肽与神经生长因子在PAC1启动子活性上的拮抗作用机制，以及之前描述的在调节嗜铬细胞增殖方面的机制，仍有待解释。