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Ras/MEK pathway is required for NGF-induced expression of tyrosine hydroxylase gene.

Abstract：

:Neurotrophins are essential for the development and survival of catecholaminergic neurons. However, the critical pathway for expression of the tyrosine hydroxylase (TH) gene induced by neurotrophin is still unclear. Here we found that Ras/MEK pathway is required for NGF-induced expression of the TH gene in PC12D cells. Induction of TH mRNA by NGF was abolished by pretreatment of the cells with U0126, an inhibitor for MEK1/2, but not with inhibitors for p38 MAPK, PI3K, and PKA. U0126 inhibited TH promoter activity at the same concentration as it acted on ERK1/2 phosphorylation. A dominant-negative form of Ras suppressed the NGF-induced activation of the TH reporter gene, and transient transfection of cells with wild-type Ras and an active form of MEK1 increased the TH promoter activity. The reporter assay also demonstrated that the Ras/MEK pathway acted on both the AP-1-binding motif and the cAMP-responsive element in the TH promoter.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Suzuki T,Kurahashi H,Ichinose H

doi

10.1016/j.bbrc.2004.01.068

subject

Has Abstract

pub_date

2004-03-05 00:00:00

pages

389-96

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006291X04001123

journal_volume

315

pub_type

杂志文章

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