The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Reciprocal Inhibition between Intracellular Antiviral Signaling and the RNAi Machinery in Mammalian Cells
Open accessAbstract
SUMMARY RNA interference (RNAi) is an established antiviral defense mechanism in plants and invertebrates. Whether RNAi serves a similar function in mammalian cells remains unresolved. We find that in some cell types, mammalian RNAi activity is reduced shortly after viral infection via poly ADP-ribosylation of the RNA induced silencing complex (RISC), a core component of RNAi. Well-established antiviral signaling pathways, including RIG-I/MAVS and RNAseL, contribute to inhibition of RISC. In the absence of virus infection, microRNAs repress interferon-stimulated genes (ISGs) associated with cell death and proliferation, thus maintaining homeostasis. Upon detection of intracellular pathogen-associated molecular patterns, RISC activity decreases, contributing to increased expression of ISGs. Our results suggest that unlike in lower eukaryotes, mammalian RISC is not antiviral in some contexts, but rather, RISC has been co-opted to negatively regulate toxic host antiviral effectors via microRNAs.
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Taganov, K. D., Boldin, M. P., Chang, K.-J., & Baltimore, D. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0605298103 · Cited by 4,317
Seth, R. B., Sun, L., Ea, C.-K., & Chen, Z. J. (2005) · Cell · doi:10.1016/j.cell.2005.08.012 · Cited by 3,329
Interferon-inducible antiviral effectors
Sadler, A. J., & Williams, B. R. G. (2008) · Nature Reviews Immunology · doi:10.1038/nri2314 · Cited by 2,160
MicroRNA-155 is induced during the macrophage inflammatory response
O'Connell, R. M., Taganov, K. D., Boldin, M. P., Cheng, G., & Baltimore, D. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0610731104 · Cited by 1,866
The miR-17-5p microRNA is a key regulator of the G1/S phase cell cycle transition
Cloonan, N., Brown, M. K., Steptoe, A. L., Wani, S., Chan, W. L., Forrest, A. R., Kolle, G., Gabrielli, B., & Grimmond, S. M. (2008) · Genome Biology · doi:10.1186/gb-2008-9-8-r127 · Cited by 304
Cited by
Regulation of microRNA biogenesis
Ha, M., & Kim, V. N. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3838 · Cited by 5,462
Regulation of microRNA function in animals
Gebert, L. F. R., & MacRae, I. J. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0045-7 · Cited by 2,284
PARPs and ADP-ribosylation: recent advances linking molecular functions to biological outcomes
Gupte, R., Liu, Z., & Kraus, W. L. (2017) · Genes & Development · doi:10.1101/gad.291518.116 · Cited by 681
“PARP-13 also induces the expression of genes that attenuate the RISCmediated transcript silencing, which promotes the accumulation of cytotoxic transcripts that promote the innate antiviral defense (Seo et al. 2013).”
BackgroundDiscriminating self from non-self in nucleic acid sensing
Schlee, M., & Hartmann, G. (2016) · Nature Reviews Immunology · doi:10.1038/nri.2016.78 · Cited by 593
Double-Stranded RNA Sensors and Modulators in Innate Immunity
Hur, S. (2019) · Annual Review of Immunology · doi:10.1146/annurev-immunol-042718-041356 · Cited by 420
Metadata
- Authors
- Seo, G. J., Kincaid, R. P., Phanaksri, T., Burke, J. M., Pare, J. M., Cox, J. E., Hsiang, T.-Y., Krug, R. M., & Sullivan, C. S.
- Venue
- Cell Host & Microbe
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 14
- Issue
- 4
- Pages
- 435-445
- ISSN
- 1931-3128 (ISSN-L)
- OpenAlex
- W2086896986
- Cited by
- 189
- References
- 5
- FWCI
- 9.60
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Seo, G. J., Kincaid, R. P., Phanaksri, T., Burke, J. M., Pare, J. M., Cox, J. E., Hsiang, T.-Y., Krug, R. M., & Sullivan, C. S. (2013). Reciprocal Inhibition between Intracellular Antiviral Signaling and the RNAi Machinery in Mammalian Cells. Cell Host & Microbe. https://doi.org/10.1016/j.chom.2013.09.002
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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