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EBNA2 is required for protection of latently Epstein-Barr virus-infected B cells against specific apoptotic stimuli.
J. Virol. 78, 12694-12697 (2004)
Publ. Version/Full Text Volltext
DOI
PMC
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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Publication type
Article: Journal article
Document type
Scientific Article
ISSN (print) / ISBN
0022-538X
e-ISSN
1098-5514
Journal
Journal of Virology
Quellenangaben
Volume: 78,
Issue: 22,
Pages: 12694-12697
Publisher
American Society for Microbiology (ASM)
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Research Unit Gene Vector (AGV)