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

doi:10.1016/j.virol.2011.01.032

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^*

^*此作品的通信作者

醫學生物技術暨檢驗學系

研究成果: Article › 同行評審

6 引文斯高帕斯（Scopus）

摘要

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.

原文	English
頁（從 - 到）	19-25
頁數	7
期刊	Virology
卷	413
發行號	1
DOIs	https://doi.org/10.1016/j.virol.2011.01.032
出版狀態	Published - 25 4月 2011

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10.1016/j.virol.2011.01.032

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@article{94291354c4b14f1f942d68908a63f2b0,

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

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.",

keywords = "Apoptosis, Death-associated protein kinase 1, Epstein-Barr virus, Latent membrane protein 1, Lymphoblastoid cell line, NF-ΚB",

author = "Lee, {Chun Wei} and Leu, {Shr Jeng Jim} and Tzeng, {Ruei Ying} and Wang, {Sheng Fan} and Tsai, {Shu Chun} and Sun, {Kuang Hui} and Chen, {Ruey Hwa} and Huang, {Jason C.}",

note = "Funding Information: This research was supported by the Republic of China National Science Council ( NSC95-2320-B-010-048-MY2 ) and Taipei City Hospital (to J.C.H.). The authors would like to thank Prof. Ching-HwaTsai for her suggestions regarding this report, Dr. Chi-Ju Chen for providing vectors and LMP1 siRNA, Dr. Shao-Yin Chen for her insights regarding our original manuscript, and Jon Lindemann for his editing assistance. RNAi reagents were obtained from the National RNAi core facility, Academia Sinica.",

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AU - Lee, Chun Wei

AU - Leu, Shr Jeng Jim

AU - Tzeng, Ruei Ying

AU - Wang, Sheng Fan

AU - Tsai, Shu Chun

AU - Sun, Kuang Hui

AU - Chen, Ruey Hwa

AU - Huang, Jason C.

N1 - Funding Information: This research was supported by the Republic of China National Science Council ( NSC95-2320-B-010-048-MY2 ) and Taipei City Hospital (to J.C.H.). The authors would like to thank Prof. Ching-HwaTsai for her suggestions regarding this report, Dr. Chi-Ju Chen for providing vectors and LMP1 siRNA, Dr. Shao-Yin Chen for her insights regarding our original manuscript, and Jon Lindemann for his editing assistance. RNAi reagents were obtained from the National RNAi core facility, Academia Sinica.

PY - 2011/4/25

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N2 - 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.

AB - 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.

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KW - Death-associated protein kinase 1

KW - Epstein-Barr virus

KW - Latent membrane protein 1

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VL - 413

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JF - Virology

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ER -

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

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