Facilitation of DNA damage-induced apoptosis by endoplasmic reticulum protein mitsugumin23

被引：10

作者：

Yamazaki, Tetsuo ^{[1
,2
]}

Sasaki, Nozomi ^{[2
]}

Nishi, Miyuki ^{[2
]}

Takeshima, Hiroshi ^{[2
]}

机构：

[1] Univ Tokushima, Dept Mol Cell Biol & Med, Inst Hlth Biosci, Grad Sch, Tokushima 7708505, Japan

[2] Kyoto Univ, Dept Biol Chem, Grad Sch Pharmaceut Sci, Kyoto 6068501, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2010年 / 392卷 / 02期

关键词：

Apoptosis; DNA damage; Endoplasmic reticulum; Etoposide; MG23; Radiation; P53; PROTEIN; DEATH; GENE; INDUCTION; CYTOMETRY; STRESS; CELLS; BCAP;

D O I：

10.1016/j.bbrc.2010.01.013

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The endoplasmic reticulum (ER) emanates context-dependent signals, thereby mediating cellular response to a variety of stresses. However, the underlying molecular mechanisms have been enigmatic. To better understand the signaling capacity of the ER, we focused on roles played by mitsugumin23 (MG23), a protein residing predominantly in this organelle. Overexpression of MG23 in human embryonic kidney 293T cells specifically enhanced apoptosis triggered by etoposide, a DNA-damaging anti-cancer drug. Conversely, genetic deletion of MG23 reduced susceptibility of thymocytes to DNA damage-induced apoptosis, which was demonstrated by whole-body irradiation experiments. In this setting, induction of the tumor-suppressor gene p53 was attenuated in MG23-knockout thymocytes as compared with their wild-type counterparts, consistent with the elevated radioresistance. It is therefore suggested that MG23 is an essential component of ER-generated lethal signals provoked upon DNA damage, specifying cell fate under pathophysiological conditions. (C) 2010 Elsevier Inc. All rights reserved,

引用

页码：196 / 200

页数：5

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