Please use this identifier to cite or link to this item: http://dl.umsu.ac.ir/handle/10722/132358
Title: An Epstein-Barr virus-encoded microRNA targets PUMA to promote host cell survival
Authors: Kok, KH;Kwong, DLW;Tsao, SW;Jin, DY;Choy, EYW;Siu, KL;Lung, RWM;To, KF;Tsang, CM
subject: Molecular Sequence Numbers
Year: 2008
Publisher: Rockefeller University Press. The Journal's web site is located at http://www.jem.org
United States
Description: Epstein-Barr virus (EBV) is a herpesvirus associated with nasopharyngeal carcinoma (NPC), gastric carcinoma (GC), and other malignancies. EBV is the first human virus found to express microRNAs (miRNAs), the functions of which remain largely unknown. We report on the regulation of a cellular protein named p53 up-regulated modulator of apoptosis (PUMA) by an EBV miRNA known as miR-BART5, which is abundantly expressed in NPC and EBV-GC cells. Modulation of PUMA expression by miR-BART5 and anti-miR-BART5 oligonucleotide was demonstrated in EBV-positive cells. In addition, PUMA was found to be significantly underexpressed in ∼60% of human NPC tissues. Although expression of miR- BART5 rendered NPC and EBV-GC cells less sensitive to proapoptotic agents, apoptosis can be triggered by depleting miR-BART5 or inducing the expression of PUMA. Collectively, our findings suggest that EBV encodes an miRNA to facilitate the establishment of latent infection by promoting host cell survival.
URI: http://www.scopus.com/mlt/select.url?eid=2-s2.0-58149145659&selection=ref&src=s&origin=recordpage
http://hub.hku.hk/handle/10722/132358
Standard no: Journal of Experimental Medicine, 2008, v. 205 n. 11, p. 2551-2560
5701484
10.1084/jem.20072581
1540-9538
2560
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
1123197
157390
WOS:000260603200012
0022-1007
11
PMC2571930
18838543
eid_2-s2.0-58149145659
2551
205
Appears in Collections:Department of Anatomy

Files in This Item:
Click on the URI links for accessing contents.


Items in HannanDL are protected by copyright, with all rights reserved, unless otherwise indicated.