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Open Access Green as soon as Postprint is submitted to ZB.
Notch1, Notch2, and Epstein-Barr virus-encoded nuclear antigen 2 signaling differentially affects proliferation and survival of Epstein-Barr virus-infected B cells.
Blood 113, 5506-5515 (2009)
The canonical mode of transcriptional activation by both the Epstein-Barr viral protein, Epstein-Barr virus-encoded nuclear antigen 2 (EBNA2), and an activated Notch receptor (Notch-IC) requires their recruitment to RBPJ, suggesting that EBNA2 uses the Notch pathway to achieve B-cell immortalization. To gain further insight into the biologic equivalence between Notch-IC and EBNA2, we performed a genome-wide expression analysis, revealing that Notch-IC and EBNA2 exhibit profound differences in the regulation of target genes. Whereas Notch-IC is more potent in regulating genes associated with differentiation and development, EBNA2 is more potent in inducing viral and cellular genes involved in proliferation, survival, and chemotaxis. Because both EBNA2 and Notch-IC induced the expression of cell cycle associated genes, we analyzed whether Notch1-IC or Notch2-IC can replace EBNA2 in B-cell immortalization. Although Notch-IC could drive quiescent B cells into the cell cycle, B-cell immortalization was not maintained, partially due to an increased apoptosis rate in Notch-IC expressing cells. Expression analysis revealed that both EBNA2 and Notch-IC induced the expression of proapoptotic genes, but only in EBNA2-expressing cells were antiapoptotic genes strongly up-regulated. These findings suggest that Notch signaling in B cells and B-cell lymphomas is only compatible with proliferation if pathways leading to antiapototic signals are active.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
rbp-j-kappa; c-myc; binding-protein; activated notch1; direct target; cyclin d1; expression; ebna2; recombination; membrane
Language
english
Publication Year
2009
HGF-reported in Year
2009
ISSN (print) / ISBN
0006-4971
e-ISSN
1528-0020
Journal
Blood
Quellenangaben
Volume: 113,
Issue: 22,
Pages: 5506-5515
Publisher
American Society of Hematology
Reviewing status
Peer reviewed
Institute(s)
Research Unit Gene Vector (AGV)
Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)
Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)
POF-Topic(s)
30203 - Molecular Targets and Therapies
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s)
Immune Response and Infection
PSP Element(s)
G-501500-003
G-501400-001
G-501400-001
PubMed ID
19339697
Scopus ID
67049097357
Erfassungsdatum
2009-12-31