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EBNA2 is required for protection of latently Epstein-Barr virus-infected B cells against specific apoptotic stimuli

Authors
 Jae Myun Lee  ;  Kyoung-Ho Lee  ;  S. Diane Hayward  ;  Jeon Han Park  ;  Bettina Kempkes  ;  Paul D. Ling  ;  Christopher J. Farrell 
Citation
 JOURNAL OF VIROLOGY, Vol.78(22) : 12694-12697, 2004 
Journal Title
 JOURNAL OF VIROLOGY 
ISSN
 0022-538X 
Issue Date
2004
Abstract
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 (EBNA2ΔCR4). Both EBNA2-converted and EBNA2ΔCR4-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 EBNA2ΔCR4-expressing cells, but EBNA2ΔCR4 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.
Files in This Item:
T200403655.pdf Download
DOI
10.1128/JVI.78.22.12694-12697.2004
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Park, Jeon Han(박전한) ORCID logo https://orcid.org/0000-0001-9604-3205
Lee, Jae Myun(이재면) ORCID logo https://orcid.org/0000-0002-5273-3113
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/112846
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