期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 423, 期 2, 页码 436-440出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2012.05.154
关键词
UBP43; USP18; Ubiquitin-like protein; ISG15; Interferon-alpha/beta; Apoptosis; Mitochondrial pathway; Reactive oxygen species (ROS)
资金
- National Research Foundation (NRF) [2011-0002136, 2011-0006469]
- Korean government (MEST)
- NIH [HL091549]
- National Research Foundation of Korea [2011-0006469] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据