Latent membrane protein 1 of Epstein Barr virus regulates death-associated protein kinase 1 in lymphoblastoid cell line

Chun Wei Lee, Shr Jeng Jim Leu, Ruei Ying Tzeng, Sheng Fan Wang, Shu Chun Tsai, Kuang Hui Sun, Ruey Hwa Chen, Jason C. Huang*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

The Epstein-Barr virus (EBV) infects and transforms primary B cells into lymphoblastoid cell lines (LCLs). We observed death-associated protein kinase 1 (DAPK1) upregulation in B cells following EBV infection and high DAPK1 levels in LCLs. DAPK1 participates in several apoptosis-inducing pathways, yet DAPK1 expression increased during B cell transformation. Data from LMP1 overexpression in LCLs and HeLa cells and from knocked down LMP1 in LCLs suggest LMP1 regulation of DAPK1 expression. We observed NF-ΚB signaling in DAPK1 upregulation by LMP1 with CTAR deletion mutants failing to induce DAPK1 expression and with Bay11 blocking DAPK1 expression. DAPK1 is inactive in LCLs due to insufficient stimuli, and is not regulated by Ser308 phosphorylation. However, DAPK1 in LCLs is functional, as evidenced by its quick mediation of cell death following UV or H2O2 exposure, and increased survival among LCLs knocked down with DAPK. DAPK roles in EBV-infected B cells remain to be identified.

Original languageEnglish
Pages (from-to)19-25
Number of pages7
JournalVirology
Volume413
Issue number1
DOIs
StatePublished - 25 Apr 2011

Keywords

  • Apoptosis
  • Death-associated protein kinase 1
  • Epstein-Barr virus
  • Latent membrane protein 1
  • Lymphoblastoid cell line
  • NF-ΚB

Fingerprint

Dive into the research topics of 'Latent membrane protein 1 of Epstein Barr virus regulates death-associated protein kinase 1 in lymphoblastoid cell line'. Together they form a unique fingerprint.

Cite this