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 (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.
Publication types
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Apoptosis*
-
B-Lymphocytes / cytology
-
B-Lymphocytes / virology*
-
DNA-Binding Proteins / physiology
-
Epstein-Barr Virus Nuclear Antigens / physiology*
-
Herpesvirus 4, Human / physiology*
-
Nuclear Receptor Subfamily 4, Group A, Member 1
-
Receptors, Cytoplasmic and Nuclear
-
Receptors, Steroid
-
Transcription Factors / physiology
-
Tumor Necrosis Factor-alpha / pharmacology
-
Viral Matrix Proteins / physiology
-
Viral Proteins
-
Virus Latency
Substances
-
DNA-Binding Proteins
-
EBNA-2 protein, Human herpesvirus 4
-
EBV-associated membrane antigen, Epstein-Barr virus
-
Epstein-Barr Virus Nuclear Antigens
-
NR4A1 protein, human
-
Nuclear Receptor Subfamily 4, Group A, Member 1
-
Receptors, Cytoplasmic and Nuclear
-
Receptors, Steroid
-
Transcription Factors
-
Tumor Necrosis Factor-alpha
-
Viral Matrix Proteins
-
Viral Proteins