File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: An Epstein-Barr virus-encoded microRNA targets PUMA to promote host cell survival

TitleAn Epstein-Barr virus-encoded microRNA targets PUMA to promote host cell survival
Authors
KeywordsMolecular Sequence Numbers
Issue Date2008
PublisherRockefeller University Press. The Journal's web site is located at http://www.jem.org
Citation
Journal of Experimental Medicine, 2008, v. 205 n. 11, p. 2551-2560 How to Cite?
AbstractEpstein-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.
Persistent Identifierhttp://hdl.handle.net/10722/132358
ISSN
2015 Impact Factor: 11.24
2015 SCImago Journal Rankings: 10.762
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Association for International Cancer Research07024
Fogarty International Center of National Institutes of HealthR01 TW06186-01
Funding Information:

This work was supported by Association for International Cancer Research (07024) and Fogarty International Center of National Institutes of Health (R01 TW06186-01).

References

 

DC FieldValueLanguage
dc.contributor.authorChoy, EYWen_HK
dc.contributor.authorSiu, KLen_HK
dc.contributor.authorKok, KHen_HK
dc.contributor.authorLung, RWMen_HK
dc.contributor.authorTsang, CMen_HK
dc.contributor.authorTo, KFen_HK
dc.contributor.authorKwong, DLWen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2011-03-28T09:23:33Z-
dc.date.available2011-03-28T09:23:33Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal of Experimental Medicine, 2008, v. 205 n. 11, p. 2551-2560en_HK
dc.identifier.issn0022-1007en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132358-
dc.description.abstractEpstein-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.en_HK
dc.languageengen_US
dc.publisherRockefeller University Press. The Journal's web site is located at http://www.jem.orgen_HK
dc.relation.ispartofJournal of Experimental Medicineen_HK
dc.subjectMolecular Sequence Numbersen_US
dc.titleAn Epstein-Barr virus-encoded microRNA targets PUMA to promote host cell survivalen_HK
dc.typeArticleen_HK
dc.identifier.emailKok, KH:khkok@hku.hken_HK
dc.identifier.emailKwong, DLW:dlwkwong@hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityKok, KH=rp01455en_HK
dc.identifier.authorityKwong, DLW=rp00414en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1084/jem.20072581en_HK
dc.identifier.pmid18838543en_HK
dc.identifier.pmcidPMC2571930-
dc.identifier.scopuseid_2-s2.0-58149145659en_HK
dc.identifier.hkuros157390-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58149145659&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume205en_HK
dc.identifier.issue11en_HK
dc.identifier.spage2551en_HK
dc.identifier.epage2560en_HK
dc.identifier.eissn1540-9538-
dc.identifier.isiWOS:000260603200012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.f10001123197-
dc.identifier.scopusauthoridChoy, EYW=23476516200en_HK
dc.identifier.scopusauthoridSiu, KL=7102312040en_HK
dc.identifier.scopusauthoridKok, KH=7006862631en_HK
dc.identifier.scopusauthoridLung, RWM=22980272500en_HK
dc.identifier.scopusauthoridTsang, CM=24831236400en_HK
dc.identifier.scopusauthoridTo, KF=7101911940en_HK
dc.identifier.scopusauthoridKwong, DLW=15744231600en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.citeulike5701484-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats