The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Epstein-Barr Virus-Induced miR-155 Attenuates NF-κB Signaling and Stabilizes Latent Virus Persistence
Abstract
MicroRNAs have been implicated in the modulation of gene expression programs important for normal and cancer cell development. miR-155 is known to play a role in B-cell development and is upregulated in various B-cell lymphomas, including several that are latently infected with Epstein-Barr virus (EBV). We show here that EBV infection of primary human B lymphocytes leads to the sustained elevation of miR-155 and its precursor RNA, BIC. The EBV-encoded latency membrane protein 1 (LMP1) can partially reconstitute BIC activation in B lymphocytes but not in epithelial cell cultures. LMP1 is a potent activator of NF-κB signaling pathways and is essential for EBV immortalization of B lymphocytes. An inhibitor to miR-155 further stimulated NF-κB responsive gene transcription, and IKKε was identified as a potential target of miR-155 translational repression. Remarkably, miR-155 inhibitor reduced EBNA1 mRNA and the EBV copy number in latently infected cells. This suggests that miR-155 contributes to EBV immortalization by modulation of NF-κB signaling and the suppression of host innate immunity to latent viral infection.
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“The miR-155 is a multifunctional microRNA and it can modulate inflammatory responses in both a positive and negative way [40-48].”
From miR-155 induction in microglial cells suppresses Japanese encephalitis virus replication and negatively modulates innate immune responses (2014) · cites this paper as [46]
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“Besides its positive role in NF-κB activation and subsequent pro-inflammatory response, accumulating evidence has demonstrated that it can constitute a negative feedback loop in the NF-κB signaling pathway by targeting multiple key proteins, which ultimately leads to repression of, or at least the limitation of NF-κB activation in response to viral or microbial stimuli [41,42,45-48].”
From miR-155 induction in microglial cells suppresses Japanese encephalitis virus replication and negatively modulates innate immune responses (2014) · cites this paper as [46]
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Citations
Cites
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Cited by
Sorted by citations
miR-155 in cancer drug resistance and as target for miRNA-based therapeutics
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Metadata
- Authors
- Lu, F., Weidmer, A., Liu, C.-G., Volinia, S., Croce, C. M., & Lieberman, P. M.
- Affiliations
- The Wistar Institute, Philadelphia, Pennsylvania 19104
- Comprehensive Cancer Center, Ohio State University, Columbus, Ohio 43210
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2008-11
- Volume
- 82
- Issue
- 21
- Pages
- 10436-10443
- ISSN
- 0022-538X
- 1098-5514
- Cited by
- 190
- References
- 3
- Language
- en
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