Viral interactions with the Notch pathway

Hayward, S. Diane

doi:10.1016/j.semcancer.2004.04.018

Cited by 89 publications

(64 citation statements)

References 142 publications

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“…To monitor the activation status of the Notch pathway, we utilized CBF1-luc reporters containing four (30) or eight binding sites (31) for CBF1, a CSL transcription factor activated by Notch (11). NIH3T3 cells were transiently co-transfected with mouse Notch1 and a Notch reporter and co-cultured with CHO cells stably transfected with Dll1 (CHO.Dll1) or with empty vector (CHO.Vec).…”

Section: Resultsmentioning

confidence: 99%

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Proteolytic Processing of Delta-like 1 by ADAM Proteases

Dyczynska

Sun

et al. 2007

Journal of Biological Chemistry

118

114

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Delta-like 1 (Dll1) is a mammalian ligand for Notch receptors.Interactions between Dll1 and Notch in trans activate the Notch pathway, whereas Dll1 binding to Notch in cis inhibits Notch signaling. Dll1 undergoes proteolytic processing in its extracellular domain by ADAM10. In this work we demonstrate that Dll1 represents a substrate for several other members of the ADAM family. In co-transfected cells, Dll1 is constitutively cleaved by ADAM12, and the N-terminal fragment of Dll1 is released to medium. ADAM12-mediated cleavage of Dll1 is cell density-dependent, takes place in cis orientation, and does not require the presence of the cytoplasmic domain of ADAM12. Full-length Dll1, but not its N-or C-terminal proteolytic fragment, co-immunoprecipitates with ADAM12. By using a Notch reporter construct, we show that Dll1 processing by ADAM12 increases Notch signaling in a cell-autonomous manner. Furthermore, ADAM9 and ADAM17 have the ability to process Dll1. In contrast, ADAM15 does not cleave Dll1, although the two proteins still co-immunoprecipitate with each other. Asn-353 present in the catalytic motif of ADAM12 and other Dll1-processing ADAMs, but absent in ADAM15, is necessary for Dll1 cleavage. Dll1 cleavage is reduced in ADAM9/12/15 ؊/؊ mouse embryonic fibroblasts (MEFs), suggesting that the endogenous ADAM9 and/or ADAM12 present in wild type MEFs contribute to Dll1 processing. Finally, the endogenous Dll1 present in primary mouse myoblasts undergoes cleavage in confluent, differentiating myoblast cultures, and this cleavage is decreased by ADAM12 small interfering RNAs. Our findings expand the role of ADAM proteins in the regulation of Notch signaling.

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Section: Resultsmentioning

confidence: 99%

“…This is followed by the cleavage at the S3 site in the transmembrane domain of Notch by a ␥-secretase complex (9,10). The intracellular domain of Notch translocates to the nucleus, where it interacts with CSL (CBF1, Su(H), Lag-1) transcription factors and activates expression of target genes (11).…”

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confidence: 99%

Proteolytic Processing of Delta-like 1 by ADAM Proteases

Dyczynska

Sun

et al. 2007

Journal of Biological Chemistry

118

114

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“…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]. KSHV establishes latency in B-cells, like EBV, but can also infect endothelial cells.…”

Section: Notch and Leukemiamentioning

confidence: 99%

“…KSHV establishes latency in B-cells, like EBV, but can also infect endothelial cells. Other viruses that have interactions with the Notch pathway are adenovirus, HPV and simian virus 40 (SV40), reviewed [173]. The first association of adenovirus came from the recognition of a RBP-J binding site in the pIX promoter [5].…”

Section: Notch and Leukemiamentioning

confidence: 99%

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Borggrefe

Oswald

2009

Cell. Mol. Life Sci.

577

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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“…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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Viral interactions with the Notch pathway

Cited by 89 publications

References 142 publications

Proteolytic Processing of Delta-like 1 by ADAM Proteases

Proteolytic Processing of Delta-like 1 by ADAM Proteases

The Notch signaling pathway: Transcriptional regulation at Notch target genes

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

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