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. 2010 Jul 15;6(7):e1000986. doi: 10.1371/journal.ppat.1000986

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Wang, Ryu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A and B) DDX3 rescued IRF signaling, which was inhibited by HBV Pol. HepG2 cells were transfected with indicated amounts of HBV Pol and DDX3 expression constructs. To induce IRF3 signaling, TBK1 (A) or IKKε (B) expression constructs (100 ng) were transfected. IRF3 activation was monitored as shown in Fig. 4. Data are expressed as the mean fold induction ± s.d. relative to control levels. The results are representative of at least two independent experiments each performed in triplicate. (C) HBV Pol disrupted the interaction between DDX3 and IKKε. HEK 293 cells were transfected with Flag-IKKε, HA-DDX3, and HBV Pol expression constructs. Cell lysates were analyzed by IP with the indicated antibodies to assess the interaction between DDX3 and IKKε. For the detection of the Flag-tagged IKKε, mouse anti-FLAG M2 antibody (Sigma, 1∶5,000) was used; anti-HA antibody (Amersham) was used to detect DDX3. The results are representative of three independent experiments.