ATM blocks tunicamycin-induced endoplasmic reticulum stress

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dc.contributor.authorL He-
dc.contributor.authorSun Ok Kim-
dc.contributor.authorO Song Kwon-
dc.contributor.authorSook-Jung Jeong-
dc.contributor.authorMin-Soo Kim-
dc.contributor.authorHee Gu Lee-
dc.contributor.authorH Osada-
dc.contributor.authorM Jung-
dc.contributor.authorJong Seog Ahn-
dc.contributor.authorBo Yeon Kim-
dc.date.accessioned2017-04-19T09:13:25Z-
dc.date.available2017-04-19T09:13:25Z-
dc.date.issued2009-
dc.identifier.issn00145793-
dc.identifier.uri10.1016/j.febslet.2009.02.002ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/8875-
dc.description.abstractEndoplasmic 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.-
dc.publisherWiley-
dc.titleATM blocks tunicamycin-induced endoplasmic reticulum stress-
dc.title.alternativeATM blocks tunicamycin-induced endoplasmic reticulum stress-
dc.typeArticle-
dc.citation.titleFEBS Letters-
dc.citation.number5-
dc.citation.endPage908-
dc.citation.startPage903-
dc.citation.volume583-
dc.contributor.affiliatedAuthorMin-Soo Kim-
dc.contributor.affiliatedAuthorHee Gu Lee-
dc.contributor.affiliatedAuthorJong Seog Ahn-
dc.contributor.affiliatedAuthorBo Yeon Kim-
dc.contributor.alternativeNameHe-
dc.contributor.alternativeName김선옥-
dc.contributor.alternativeName권오송-
dc.contributor.alternativeName정숙정-
dc.contributor.alternativeName김민수-
dc.contributor.alternativeName이희구-
dc.contributor.alternativeNameOsada-
dc.contributor.alternativeName정미라-
dc.contributor.alternativeName안종석-
dc.contributor.alternativeName김보연-
dc.identifier.bibliographicCitationFEBS Letters, vol. 583, no. 5, pp. 903-908-
dc.identifier.doi10.1016/j.febslet.2009.02.002-
dc.subject.keywordAtaxia telangiectasia mutated-
dc.subject.keywordER stress-
dc.subject.keywordTunicamycin-
dc.subject.keywordX-box protein-1-
dc.subject.localAtaxia telangiectasia mutated-
dc.subject.localER stress-
dc.subject.localTunicamycin-
dc.subject.localX-box protein-1-
dc.description.journalClassY-
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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