BAT3 negatively regulates lipopolysaccharide-induced NF-kappa B signaling through TRAF6
- Authors
- Lee, Yeojin; Lee, In Young; Yun, Hee Jae; Lee, Woo Sang; Kang, Seongman; Cho, Ssang-Goo; Lee, Ji Eun; Choi, Eui-Ju
- Issue Date
- 16-9월-2016
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- BAT3; Lipopolysaccharides; NF-kappa B; TRAF6
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.478, no.2, pp.784 - 790
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 478
- Number
- 2
- Start Page
- 784
- End Page
- 790
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/87503
- DOI
- 10.1016/j.bbrc.2016.08.025
- ISSN
- 0006-291X
- Abstract
- TNF receptor-associated factor 6 (TRAF6) plays a critical role in NF-kappa B and mitogen-activated protein kinase (MAPK) signaling pathways, both of which mediate macrophage activation in response to pathogen-associated molecular patterns such as bacterial endotoxin, lipopolysaccharides (LPS). In this study, we investigated whether HLA-B associated transcript-3 (BAT3) regulates LPS-induced macrophage activation. BAT3 physically interacted with TRAF6 in macrophages, and this interaction was enhanced in the cells after LPS treatment. Furthermore, BAT3 inhibited the homo-oligomerization of TRAF6 as well as the interaction between TRAF6 and its downstream kinase transforming growth factor beta-activated kinase 1 (TAK1), thereby suppressing TRAF6-mediated signaling events. Intriguingly, TRAF6 mediated ubiquitination of BAT3 and this ubiquitination was crucial for its inhibitory effect on TRAF6-mediated signaling. Depletion of BAT3 by RNA interference resulted in enhancement of LPS-induced activation of the NF-kappa B signaling with increasing expression levels of pro-inflammatory cytokines. These findings suggest that BAT3 functions as the negative regulator of LPS-induced macrophage activation. (C) 2016 Elsevier Inc. All rights reserved.
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