Journal
FEBS LETTERS
Volume 583, Issue 5, Pages 903-908Publisher
WILEY
DOI: 10.1016/j.febslet.2009.02.002
Keywords
Ataxia telangiectasia mutated; ER stress; Tunicamycin; X-box protein-1
Funding
- Research Program for New Drug Target Discovery [M10748000346-07N4800-34610]
- Global Partnership Program of Korea Foundation for International Cooperation of Science and Technology (KICOS) [M6060200000106E0200- 00100]
- KRIBB Research Initiative Program
- Ministry of Education, Science Technology
- National R&D Program for Cancer Control [0820260]
- Ministry of Health Welfare, Korea
- Technology Development Program for Agriculture and Forestry
- Ministry for Agriculture, Forestry and Fisheries, Republic of Korea
- Korea Health Promotion Institute [0820260] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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