IEX-1-induced cell death requires BIM and is modulated by MCL-1
- Authors
- Yoon, Seongmin; Ha, Hye-Jung; Kim, Yong-Hak; Won, Miae; Park, Mira; Ko, Jeong-Jae; Lee, Kangseok; Bae, Jeehyeon
- Issue Date
- May-2009
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Apoptosis; BCL-2 family; MCL-1; IEX-1; BIM
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.382, no.2, pp 400 - 404
- Pages
- 5
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 382
- Number
- 2
- Start Page
- 400
- End Page
- 404
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/23191
- DOI
- 10.1016/j.bbrc.2009.03.037
- ISSN
- 0006-291X
1090-2104
- Abstract
- MCL-1 (myeloid cell leukemia-1) is a distinguished and pivotal member of the pro-survival BCL-2 family of proteins, and we isolated IEX-1 (immediate early response gene X-1) as a MCL-1-interacting protein using the yeast two-hybrid system and confirmed their endogenous association in human cells. The underlying mechanisms by which IEX-1 affects cell survival and death are largely unknown. Ectopic expression of IEX-1-induced caspase-dependent apoptosis in 293T cells. and the response was significantly modulated by changes in the MCL-1 expression level in cells. Forced expression of IEX-1 was unable to induce cell death or to perturb mitochondrial membrane potential in BIM-depleted cells. Additionally, knockouts of NOXA or PUMA did not affect the activities of IEX-1, indicating that the pro-death action of IEX-1 specifically requires BIM. Our findings provide insight into a new regulatory circuit that controls cell death and survival by the coordinated action of MCL-1, IEX-1, and BIM. (C) 2009 Elsevier Inc. All rights reserved.
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