Amort, Melanie; Nachbauer, Birgit; Tuzlak, Selma; Kieser, Arnd; Schepers, Aloys; Villunger, Andreas; Polacek, Norbert (2015). Expression of the vault RNA protects cells from undergoing apoptosis. Nature communications, 6(7030), p. 7030. Nature Publishing Group 10.1038/ncomms8030
|
Text
Amort et al_Nat Comm_2015.pdf - Published Version Available under License Creative Commons: Attribution (CC-BY). Download (1MB) | Preview |
Non-protein-coding RNAs are a functionally versatile class of transcripts exerting their biological roles on the RNA level. Recently, we demonstrated that the vault complex-associated RNAs (vtRNAs) are significantly upregulated in Epstein-Barr virus (EBV)-infected human B cells. Very little is known about the function(s) of the vtRNAs or the vault complex. Here, we individually express latent EBV-encoded proteins in B cells and identify the latent membrane protein 1 (LMP1) as trigger for vtRNA upregulation. Ectopic expression of vtRNA1-1, but not of the other vtRNA paralogues, results in an improved viral establishment and reduced apoptosis, a function located in the central domain of vtRNA1-1. Knockdown of the major vault protein has no effect on these phenotypes revealing that vtRNA1-1 and not the vault complex contributes to general cell death resistance. This study describes a NF-κB-mediated role of the non-coding vtRNA1-1 in inhibiting both the extrinsic and intrinsic apoptotic pathways.
Item Type: |
Journal Article (Original Article) |
---|---|
Division/Institute: |
08 Faculty of Science > Department of Chemistry, Biochemistry and Pharmaceutical Sciences (DCBP) |
Graduate School: |
Graduate School for Cellular and Biomedical Sciences (GCB) |
UniBE Contributor: |
Nachbauer, Birgit, Polacek, Norbert |
Subjects: |
500 Science > 570 Life sciences; biology 500 Science > 540 Chemistry |
ISSN: |
2041-1723 |
Publisher: |
Nature Publishing Group |
Language: |
English |
Submitter: |
Christina Schüpbach |
Date Deposited: |
21 May 2015 13:43 |
Last Modified: |
05 Dec 2022 14:47 |
Publisher DOI: |
10.1038/ncomms8030 |
BORIS DOI: |
10.7892/boris.68902 |
URI: |
https://boris.unibe.ch/id/eprint/68902 |