Role of Herp in the endoplasmic reticulum stress response

被引:102
作者
Hori, O [1 ]
Ichinoda, F
Yamaguchi, A
Tamatani, T
Taniguchi, M
Koyama, Y
Katayama, T
Tohyama, M
Stern, DM
Ozawa, K
Kitao, Y
Ogawa, S
机构
[1] Kanazawa Univ, Grad Sch Med, Dept Neuroanat Anat 3, Kanazawa, Ishikawa 9208640, Japan
[2] Osaka Univ, Grad Sch Med, Dept Anat & Neurosci, Suita, Osaka 5650871, Japan
[3] Med Coll Georgia, Augusta, GA 30912 USA
[4] JST, CREST, Kawaguchi, Saitama 3320012, Japan
关键词
D O I
10.1111/j.1356-9597.2004.00735.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Application of differential display to cultured rat astrocytes allowed cloning of Herp cDNA. Although Herp was strongly induced by endoplasmic reticulum (ER) stress, it decayed rapidly consequent to proteasome-mediated degradation. To investigate the role of this molecule in terms of the stress response, Herp knockout cells were developed using F9 embryonic carcinoma cells. F9 Herp null cells were more vulnerable to ER stress compared with F9 wild-type cells. In the early period of ER stress (0-8 h after tunicamycin treatment), Herp null cells displayed enhanced ER stress signalling and stabilization of an endogenous ERAD substrate, compared with wild-type cells. In the intermediate period (8-20 h after tunicamycin treatment), Herp null cells displayed reduced ER stress signalling, whereas in the late period (20-40 h after tunicamycin treatment), Herp null cells manifested irreversible cellular changes that lead to apoptotic cell death. Transfection analysis revealed that the N-terminal region, including the ubiquitin-like domain of Herp, was required for the survival of F9 cells under ER stress. These results indicate that Herp is a short-lived Ub-like protein improving the balance of folding capacity and protein loads in the ER and plays crucial roles for the ER stress resistance in F9 cells.
引用
收藏
页码:457 / 469
页数:13
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