ASK1 is Involved in EBV LMP1-induced NF-κB Activation
- Authors
- 송윤재
- Issue Date
- Mar-2012
- Publisher
- 대한미생물학회
- Keywords
- Epstein-Barr virus; Latent membrane protein 1; ASK1; NF-κB
- Citation
- Journal of Bacteriology and Virology, v.42, no.1, pp.63 - 68
- Journal Title
- Journal of Bacteriology and Virology
- Volume
- 42
- Number
- 1
- Start Page
- 63
- End Page
- 68
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/80794
- DOI
- 10.4167/jbv.2012.42.1.63
- ISSN
- 1598-2467
- Abstract
- Epstein-Barr virus (EBV) latent infection transforms B lymphocytes into proliferating lymphoblastoid cell lines (LCLs).
EBV latent infection membrane protein 1 (LMP1) is required for EBV-mediated B lymphocyte transformation, and LMP1-induced NF-κB activation is essential for LCL survival. Previously, it was reported that the level of reactive oxygen species (ROS) and the expression of apoptosis signal-regulating kinase 1 (ASK1) are elevated in EBV-positive Burkitt's lymphoma (BL) cells, the potential role of ASK1 in LMP1-induced NF-κB activation was thus investigated in this study. In EBV-positive BL cells, ASK1 was highly expressed and activated. In addition, TRAF6-ASK1 interaction was significantly increased in EBV-positive BL cells. Interestingly, the expression of LMP1 alone facilitated ASK1activation. The expression of a dominant negative ASK1 mutant (ASK1KM) strongly blocked LMP1-induced NF-κB activation. Furthermore, LMP1-induced NF-κB activation was significantly reduced in ASK1 knock out (ASK1-/-)mouse embryonic fibroblasts (MEFs). Taken together, these results demonstrate that ASK1 is activated by LMP1 and is critical for LMP1-induced NF-κB activation.
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