EBNA2 and Notch signalling in Epstein–Barr virus mediated immortalization of B lymphocytes

Zimber-Strobl, Ursula; Strobl, Lothar J.

doi:10.1006/scbi.2001.0409

Cited by 117 publications

(96 citation statements)

References 141 publications

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“…Notch target genes and herpes viruses (Epstein-Barr and Kaposi s sarcoma-associated herpes viruses) The Epstein-Barr virus nuclear antigen 2 (EBNA2) and NICD have been shown to be partially interchangeable, reviewed in [166]. Therefore EBNA2 has been proposed to be the functional homolog of NICD.…”

Section: Notch and Leukemiamentioning

confidence: 99%

“…Recombinant viruses carrying an EBNA2 gene that lacks the RBP-J interaction domain are no longer able to immortalize B-cells [171]. EBNA2 and NICD are found to regulate the same cellular and viral promoters and both have been shown to be partially interchangeable in regard to activation of target genes in B-cell lines and modulation of differentiation processes, reviewed in [166]. In addition to EBV, the lytic switch protein RTA of Kaposi s sarcoma-associated herpes virus (KSHV) has been found to bind to RBP-J [172], reviewed in [173].…”

Section: Notch and Leukemiamentioning

confidence: 99%

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The Notch signaling pathway: Transcriptional regulation at Notch target genes

Borggrefe

Oswald

2009

Cell. Mol. Life Sci.

573

499

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. The Notch gene encodes a transmembrane receptor that gave the name to the evolutionary highly conserved Notch signaling cascade. It plays a pivotal role in the regulation of many fundamental cellular processes such as proliferation, stem cell maintenance and differentiation during embryonic and adult development. After specific ligand binding, the intracellular part of the Notch receptor is cleaved off and translocates to the nucleus, where it binds to the transcription factor RBP-J. In the absence of activated Notch, RBP-J represses Notch target genes by recruiting a corepressor complex. Here, we review Notch signaling with a focus on gene regulatory events at Notch target genes. This is of utmost importance to understand Notch signaling since certain RBP-J associated cofactors and particular epigenetic marks determine the specificity of Notch target gene expression in different cell types. We subsequently summarize the current knowledge about Notch target genes and the physiological significance of Notch signaling in development and cancer.

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Section: Notch and Leukemiamentioning

confidence: 99%

Section: Notch and Leukemiamentioning

confidence: 99%

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Borggrefe

Oswald

2009

Cell. Mol. Life Sci.

573

499

View full text Add to dashboard Cite

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“…All three proteins bind to a cellular DNAbinding protein known as CBF1 or RBP-JK. This factor also binds to, and targets to DNA, the EBV transactivator protein EBNA2 and also the IC-Notch effector of the Notch signaling pathway (30). EBNA3A, -3B, and -3C can all repress EBNA2-mediated transactivation of the EBV LMP-2 promoter (31) and EBNA3A and -3C can repress reporter plasmids containing the RBP-JK/CBF1 sites from the EBV Cp promoter independently of EBNA2-mediated activation (32).…”

Section: Waf1mentioning

confidence: 99%

Two Nonconsensus Sites in the Epstein-Barr Virus Oncoprotein EBNA3A Cooperate to Bind the Co-repressor Carboxyl-terminal-binding Protein (CtBP)

Hickabottom

Parker

Freemont

et al. 2002

Journal of Biological Chemistry

120

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“…Pegman et al (2006) demonstrated that in EBV-negative BL-derived cell lines EBNA2 up-regulates bfl-1 expression by interacting with EBNA2-CBF-1 (Cp-binding factor 1, also known as RPR-JK) (Zimber-Strobl and Strobl, 2001;Hayward, 2004). These interactions involve receptors of the classical Notch pathway.…”

Section: Barf1 Activates Bcl-2mentioning

confidence: 99%

Epstein-Barr virus interactions with the Bcl-2 protein family and apoptosis in human tumor cells

Mao

2013

J. Zhejiang Univ. Sci. B

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Epstein-Barr virus (EBV), a human gammaherpesvirus carried by more than 90% of the world's population, is associated with malignant tumors such as Burkitt's lymphoma (BL), Hodgkin lymphoma, post-transplant lymphoma, extra-nodal natural killer/T cell lymphoma, and nasopharyngeal and gastric carcinomas in immune-compromised patients. In the process of infection, EBV faces challenges: the host cell environment is harsh, and the survival and apoptosis of host cells are precisely regulated. Only when host cells receive sufficient survival signals may they immortalize. To establish efficiently a lytic or long-term latent infection, EBV must escape the host cell immunologic mechanism and resist host cell apoptosis by interfering with multiple signaling pathways. This review details the apoptotic pathway disrupted by EBV in EBV-infected cells and describes the interactions of EBV gene products with host cellular factors as well as the function of these factors, which decide the fate of the host cell. The relationships between other EBV-encoded genes and proteins of the B-cell leukemia/lymphoma (Bcl) family are unknown. Still, EBV seems to contribute to establishing its own latency and the formation of tumors by modifying events that impact cell survival and proliferation as well as the immune response of the infected host. We discuss potential therapeutic drugs to provide a foundation for further studies of tumor pathogenesis aimed at exploiting novel therapeutic strategies for EBV-associated diseases.

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EBNA2 and Notch signalling in Epstein–Barr virus mediated immortalization of B lymphocytes

Cited by 117 publications

References 141 publications

The Notch signaling pathway: Transcriptional regulation at Notch target genes

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Two Nonconsensus Sites in the Epstein-Barr Virus Oncoprotein EBNA3A Cooperate to Bind the Co-repressor Carboxyl-terminal-binding Protein (CtBP)

Epstein-Barr virus interactions with the Bcl-2 protein family and apoptosis in human tumor cells

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