期刊
JOURNAL OF VIROLOGY
卷 78, 期 22, 页码 12694-12697出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.78.22.12694-12697.2004
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资金
- NCI NIH HHS [P50 CA096888, R37 CA 42245, P50 CA 96888, R37 CA042245] Funding Source: Medline
In addition to functioning as a transcriptional transactivator, Epstein-Barr virus EBNA2 interacts with Nur77 to protect against Nur77-mediated apoptosis. Estrogen-regulated EBNA2 in EREB2-5 cells was replaced by either EBNA2 or EBNA2 with a deletion of conserved region 4 (EBNA2DeltaCR4). Both EBNA2-converted and EBNA2DeltaCR4-converted EREB2-5 cells grew in the absence of estrogen and expressed LMP1. Treatment with tumor necrosis factor alpha did not induce apoptosis of EBNA2- or EBNA2DeltaCR4-expressing cells, but EBNA2DeltaCR4 cells were susceptible to etoposide and 5-fluorouracil, Nur77-mediated inducers of apoptosis. Thus, EBNA2 protects B cells against specific apoptotic agents against which LMP1 is not effective.
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