The mitochondrial pathway and reactive oxygen species are critical contributors to interferon-alpha/beta-mediated apoptosis in Ubp43-deficient hematopoietic cells
- Authors
- Yim, Hwa Young; Yang, Young; Lim, Jong-Seok; Lee, Myeong Seok; Zhang, Dong-Er; Kim, Keun Il
- Issue Date
- Jun-2012
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- UBP43; USP18; Ubiquitin-like protein; ISG15; Interferon-alpha/beta; Apoptosis; Mitochondrial pathway; Reactive oxygen species (ROS)
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.423, no.2, pp 436 - 440
- Pages
- 5
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 423
- Number
- 2
- Start Page
- 436
- End Page
- 440
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/11880
- DOI
- 10.1016/j.bbrc.2012.05.154
- ISSN
- 0006-291X
1090-2104
- Abstract
- UBP43 (also known as USP18) plays a role in the negative regulation of interferon-alpha/beta signaling, and bone marrow cells in Ubp43-deficient mice exhibited hypersensitivity to interferon-alpha/beta-mediated apoptosis. Here, we show that the mitochondrial apoptotic pathway and reactive oxygen species are major contributors to the elevated interferon-alpha/beta-mediated apoptosis in Ubp43-deficient mouse bone marrow cells and in UBP43-knockdown THP-1 cells. Furthermore, TRAIL and FASL, which were proposed as apoptosis inducers upon interferon-alpha/beta treatment in UBP43-knockdown adherent cancer cells, did not cause apoptosis in these hematopoietic cells. Therefore, although UBP43 depletion can cause hypersensitivity to interferon-alpha/beta-mediated apoptosis in a broad range of cell types, the downstream pathway may vary depending on the cell type. (C) 2012 Elsevier Inc. All rights reserved.
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