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Open Access Green as soon as Postprint is submitted to ZB.
Epstein-Barr virus maintains lymphomas via its miRNAs.
Oncogene 44, 1258-1264 (2014)
Epstein-Barr virus (EBV) has evolved exquisite controls over its host cells, human B lymphocytes, not only directing these cells during latency to proliferate and thereby expand the pool of infected cells, but also to survive and thereby persist for the lifetime of the infected individual. Although these activities ensure the virus is successful, they also make the virus oncogenic, particularly when infected people are immunosuppressed. Here we show, strikingly, that one set of EBV's microRNAs (miRNAs) both sustain Burkitt's lymphoma (BL) cells in the absence of other viral oncogenes and promote the transformation of primary B lymphocytes. BL cells were engineered to lose EBV and found to die by apoptosis and could be rescued by constitutively expressing viral miRNAs in them. Two of these EBV miRNAs were found to target caspase 3 to inhibit apoptosis at physiological concentrations.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
EBV; BART miRNAs; Apoptosis; RISC-IP; Burkitt's Lymphoma; Human Gamma-herpesviruses; Microrna Targets; Down-regulation; Lmp1 Oncogene; Protein; Ebv; Expression; Apoptosis; Cells; Bim
ISSN (print) / ISBN
0950-9232
e-ISSN
0950-9232
Journal
Oncogene
Quellenangaben
Volume: 44,
Issue: 10,
Pages: 1258-1264
Publisher
Nature Publishing Group
Publishing Place
London
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Research Unit Gene Vector (AGV)