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Role of Herp in the endoplasmic reticulum stress response
Author(s) -
Hori Osamu,
Ichinoda Fusae,
Yamaguchi Atsushi,
Tamatani Takashi,
Taniguchi Manabu,
Koyama Yoshihisa,
Katayama Taiichi,
Tohyama Masaya,
Stern David M.,
Ozawa Kentaro,
Kitao Yasuko,
Ogawa Satoshi
Publication year - 2004
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1356-9597.2004.00735.x
Subject(s) - tunicamycin , endoplasmic reticulum , unfolded protein response , biology , endoplasmic reticulum associated protein degradation , microbiology and biotechnology , null cell , transfection , chop , ubiquitin , cell culture , biochemistry , genetics , gene
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.