The C. elegans p38 MAPK rathway regulates nuclear ocalization of the transcription factor SKN-1 in oxidative stress response

被引:335
作者
Inoue, H
Hisamoto, N
An, JH
Oliveira, RP
Nishida, E
Blackwell, TK
Matsumoto, K [1 ]
机构
[1] Nagoya Univ, Dept Mol Biol, Grad Sch Sci, Inst Adv Res,Chikusa Ku, Nagoya, Aichi 4648602, Japan
[2] CREST, Japan Sci & Technol Corp, Chikusa Ku, Nagoya, Aichi 4648602, Japan
[3] Harvard Univ, Sch Med, Sect Dev & Stem Cell Biol, Joslin Diabet Ctr, Boston, MA 02215 USA
[4] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02215 USA
[5] Kyoto Univ, Dept Cell & Dev Biol, Grad Sch Biostudies, Sakyo Ku, Kyoto 6068502, Japan
关键词
C; elegans; oxidative stress; p38 MAP kinase; SKN-1;
D O I
10.1101/gad.1324805
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The evolutionarily conserved p38 mitogen-activated protein kinase (MAPK) cascade is an integral part of the response to a variety of environmental stresses. Here we show that the Caenorhabditis elegans PMK-1 p38 MAPK pathway regulates the oxidative stress response via the CNC transcription factor SKN-1. In response to oxidative stress, PMK-1 phosphorylates SKN-1, leading to its accumulation in intestine nuclei, where SKN-1 activates transcription of gcs-1, a phase II detoxification enzyme gene. These results delineate the C. elegans p38 MAPK signaling pathway leading to the nucleus that responds to oxidative stress.
引用
收藏
页码:2278 / 2283
页数:6
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