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UbcD4, an ortholog of E2-25K/Ube2K, is essential for activation of the immune deficiency pathway in Drosophila

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Abstract
Ubiquitination is a key regulatory mechanism in the immune deficiency (IMD) pathway in Drosophila. In this study, we first developed a simple immunoblot method to identify components involved in this pathway. Considering the emerging roles of ubiquitin-conjugating enzymes (E2s) in determining ubiquitin chain types and ubiquitination speed, we screened for E2s required for IMD activation. We found that UbcD4, in addition to the previously reported E2s Effete and Bendless, was required for activation of the IMD pathway. RNAi-mediated knockdown of the UbcD4 ortholog, E2-25K/Ube2K, inhibited TNFα- and LPS-mediated activation of the NF-κB pathway, implying that UbcD4 and E2-25K/Ube2K play a conserved role as positive regulators in both pathways. © 2015 Elsevier Inc. All rights reserved.
Author(s)
Park, Eun SilElangovan, MuthukumarKim, Young-JoonYoo, Yung Joon
Issued Date
2016-01
Type
Article
DOI
10.1016/j.bbrc.2015.12.062
URI
https://scholar.gist.ac.kr/handle/local/14426
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
Biochemical and Biophysical Research Communications, v.469, no.4, pp.891 - 896
ISSN
0006-291X
Appears in Collections:
Department of Life Sciences > 1. Journal Articles
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