|
|||||
|
|
ATM blocks tunicamycin-induced endoplasmic reticulum stress |
|
| Authors: | Long He Osong Kwon Min Soo Kim Hiroyuki Osada Jong Seog Ahn Bo Yeon Kim |
| Affiliation: | a Korea Research Institute of Bioscience and Biotechnology (KRIBB), Yuseong, P.O. Box 115, Daejeon 305-806, Republic of Korea b Antibiotics Laboratory, Chemical Biology Department, Advanced Science Institute, RIKEN 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan c Department of Radiation Medicine, Georgetown University School of Medicine, Washington, DC 20057-1482, USA |
| Abstract: | Endoplasmic reticulum stress (ER-stress) is associated with ataxia telangiectasia mutated (ATM) gene. We present here conclusive data showing that ATM blocks ER-stress induced by tunicamycin or ionizing radiation (IR). X-box protein-1 (XBP-1) splicing, GRP78 expression and caspase-12 activation were increased by tunicamycin or IR in Atm-deficient AT5BIVA fibroblasts. Activation of caspase-12 and caspase-3 by tunicamycin was significantly reduced in cells transfected with wild-type Atm (AT5BIVA/wtATM). Atm knockdown by siRNA, however, noticeably elevated ER-stress and chemosensitivity to tunicamycin. In summary, we present substantial data demonstrating that ATM blocks the ER stress signaling associated with cancer cell proliferation. |
| Keywords: | Ataxia telangiectasia mutated ER stress Tunicamycin X-box protein-1 |
| 本文献已被 ScienceDirect 等数据库收录！ | |