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Epstein-Barr virus nuclear protein EBNA3C is required for cell cycle progression and growth maintenance of lymphoblastoid cells

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Title: Epstein-Barr virus nuclear protein EBNA3C is required for cell cycle progression and growth maintenance of lymphoblastoid cells
Authors: Maruo, Seiji Browse this author →KAKEN DB
Wu, Yi Browse this author
Ishikawa, Satoko Browse this author
Kanda, Teru Browse this author
Iwakiri, Dai Browse this author
Takada, Kenzo Browse this author
Issue Date: 19-Dec-2006
Publisher: The National Academy of Sciences of the United States of America
Journal Title: Proceedings of the National Academy of Sciences of the United States of America
Volume: 103
Issue: 51
Start Page: 19500
End Page: 19505
Publisher DOI: 10.1073/pnas.0604919104
PMID: 17159137
Abstract: Epstein–Barr virus (EBV) infection converts primary human B cells into continuously proliferating lymphoblastoid cell lines (LCLs). To examine the role of EBV nuclear antigen (EBNA) 3C in the proliferation of LCLs, we established LCLs infected with an EBV recombinant that expresses EBNA3C with a C-terminal fusion to a 4-hydroxytamoxifen (4HT)-dependent mutant estrogen receptor, E3C–HT. In the presence of 4HT, LCLs expressed the E3C–HT protein and grew like WT LCLs. When E3C–HT EBV-infected LCLs were transferred to medium without 4HT, E3C–HT protein slowly disappeared, and the LCLs gradually ceased growing. WT EBNA3C expression from an oriP plasmid transfected into E3C–HT LCLs protected the LCLs from growth arrest in medium without 4HT, whereas expression of EBNA3A or EBNA3B did not. The expression of other EBNA proteins and of LMP1, CD21, CD23, and c-myc was unaffected by EBNA3C inactivation. However, EBNA3C inactivation resulted in the accumulation of p16INK4A, a decrease in the hyperphosphorylated form of the retinoblastoma protein, and a decrease in the proportion of cells in S or G2/M phase. These results indicate that EBNA3C has an essential role in cell cycle progression and the growth maintenance of LCLs.
Type: article (author version)
URI: http://hdl.handle.net/2115/30281
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 丸尾 聖爾

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