Please use this identifier to cite or link to this item:
|Title:||Stress-induced immediate-early gene, egr-1, involves activation of p38/JNK1|
|Authors:||Lim, C.P. |
|Citation:||Lim, C.P., Jain, N., Cao, X. (1998-06-04). Stress-induced immediate-early gene, egr-1, involves activation of p38/JNK1. Oncogene 16 (22) : 2915-2926. ScholarBank@NUS Repository.|
|Abstract:||The Ras/Raf/MAP kinase (ERK) pathway is a major signaling pathway induced by growth factors in mammalian cells. Two other types of mammalian MAP kinases, JNK (SAPK) and p38 (RK, CSBP), are induced by environmental stress. Although the immediate-early gene, egr-1, is induced by growth factors, cytokines, differentiation signals and DNA damaging agents, less is known about its induction by environmental stress and the mechanism involved. Here we report that in NIH3T3 cells, egr-1 is induced by various stress treatments such as heat shock, sodium arsenite, ultraviolet (U,V,) radiation, and anisomycin. p38 and JNK1, but not ERK2, were activated by these stress treatments. Induction of egr-1 by anisomycin is inhibited by a specific inhibitor of p38, SB 203580. We also show that p38 and JNK1 activated by their upstream kinases induce egr-1 promoter activity through activation of the ternary complex factor, Elk-1. The stress treatments also lead to an increase in Egr-1 protein phosphorylation and its DNA binding activity. Together, our data suggest that induction of egr-1 gene by growth factors and stress are mediated through different subgroups of MAP kinases which may also differentially affect egr-1 function on its target genes.|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Oct 19, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.