ASK1 is Involved in EBV LMP1-induced NF-kappaB Activation
Journal of Bacteriology and Virology
;
: 63-68, 2012.
Article
in English
| WPRIM
| ID: wpr-165304
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-kappaB 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-kappaB 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 ASK1 activation. The expression of a dominant negative ASK1 mutant (ASK1KM) strongly blocked LMP1-induced NF-kappaB activation. Furthermore, LMP1-induced NF-kappaB 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-kappaB activation.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
B-Lymphocytes
/
Lymphocyte Activation
/
Cell Line
/
NF-kappa B
/
Burkitt Lymphoma
/
Reactive Oxygen Species
/
Herpesvirus 4, Human
/
MAP Kinase Kinase Kinase 5
/
Fibroblasts
/
Membrane Proteins
Limits:
Animals
Language:
English
Journal:
Journal of Bacteriology and Virology
Year:
2012
Type:
Article
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