ATM blocks tunicamycin-induced endoplasmic reticulum stress

Cited 23 time in scopus
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Title
ATM blocks tunicamycin-induced endoplasmic reticulum stress
Author(s)
L He; Sun Ok Kim; O Song Kwon; Sook-Jung Jeong; Min-Soo KimHee Gu Lee; H Osada; M Jung; Jong Seog AhnBo Yeon Kim
Bibliographic Citation
FEBS Letters, vol. 583, no. 5, pp. 903-908
Publication Year
2009
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.
Keyword
Ataxia telangiectasia mutatedER stressTunicamycinX-box protein-1
ISSN
0014-5793
Publisher
Wiley
DOI
http://dx.doi.org/10.1016/j.febslet.2009.02.002
Type
Article
Appears in Collections:
Jeonbuk Branch Institute > Microbial Biotechnology Research Center > 1. Journal Articles
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Ochang Branch Institute > Anticancer Agent Research Center > 1. Journal Articles
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