The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.
Isoforms of RNA-Editing Enzyme ADAR1 Independently Control Nucleic Acid Sensor MDA5-Driven Autoimmunity and Multi-organ Development
Open accessAbstract
Summary Mutations in the ADAR gene that encodes the ADAR1 RNA editing enzyme cause Aicardi-Goutières Syndrome (AGS), a severe autoimmune disease associated with an aberrant type I interferon response. How ADAR1 prevents autoimmunity remains incompletely defined. Here, we demonstrate that ADAR1 is a specific and essential negative regulator of the MDA5-MAVS RNA sensing pathway. Moreover, we uncovered a MDA5-MAVS-independent function for ADAR1 in the development of multiple organs. We showed that the p150 isoform of ADAR1 uniquely regulated the MDA5 pathway, whereas both the p150 and p110 isoforms contributed to development. Abrupt deletion of ADAR1 in adult mice revealed that both of these functions were required throughout life. Our findings delineate genetically separable roles for both ADAR1 isoforms in vivo, with implications for the human diseases caused by ADAR mutations.
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Cites
STAR: ultrafast universal RNA-seq aligner
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Differential roles of MDA5 and RIG-I helicases in the recognition of RNA viruses
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“129S4Meox2 cross were subsequently bred to Tmem173 / (Sting / ) mice (Ishikawa et al., 2009), Mavs / mice (Gall et al.”
BackgroundSAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx
Laguette, N., Sobhian, B., Casartelli, N., Ringeard, M., Chable-Bessia, C., Ségéral, E., Yatim, A., Emiliani, S., Schwartz, O., & Benkirane, M. (2011) · Nature · doi:10.1038/nature10117 · Cited by 1,511
Cell Type-Specific Involvement of RIG-I in Antiviral Response
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Trex1 prevents cell-intrinsic initiation of autoimmunity
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Self-citationEating disorder and epilepsy in mice lacking 5-HT2C serotonin receptors
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RNA Editing by Adenosine Deaminases That Act on RNA
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Vpx relieves inhibition of HIV-1 infection of macrophages mediated by the SAMHD1 protein
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“Similarly, SAMHD1 is a dNTP phosphohydrolase that prevents cDNA synthesis by retroviral reverse transcriptase enzymes, strongly suggesting that the cGAS-STING pathway also drives autoimmunity in AGS caused by SAMHD1 mutations (Goldstone et al., 2011; Hrecka et al., 2011; Laguette et al., 2011; Rehwinkel et al., 2013).”
Background
Cited by
A-to-I RNA editing — immune protector and transcriptome diversifier
Eisenberg, E., & Levanon, E. Y. (2018) · Nature Reviews Genetics · doi:10.1038/s41576-018-0006-1 · Cited by 624
Recognition of Endogenous Nucleic Acids by the Innate Immune System
Roers, A., Hiller, B., & Hornung, V. (2016) · Immunity · doi:10.1016/j.immuni.2016.04.002 · Cited by 541
Human ADAR1 Prevents Endogenous RNA from Triggering Translational Shutdown
Chung, H., Calis, J. J. A., Wu, X., Sun, T., Yu, Y., Sarbanes, S. L., Dao Thi, V. L., Shilvock, A. R., Hoffmann, H.-H., Rosenberg, B. R., et al. (2018) · Cell · doi:10.1016/j.cell.2017.12.038 · Cited by 538
The type I interferonopathies: 10 years on
Crow, Y. J., & Stetson, D. B. (2022) · Nature Reviews Immunology · doi:10.1038/s41577-021-00633-9 · Cited by 489
Self-citationBreaching Self-Tolerance to Alu Duplex RNA Underlies MDA5-Mediated Inflammation
Ahmad, S., Mu, X., Yang, F., Greenwald, E., Park, J. W., Jacob, E., Zhang, C.-Z., & Hur, S. (2018) · Cell · doi:10.1016/j.cell.2017.12.016 · Cited by 449
Metadata
- Authors
- Pestal, K., Funk, C. C., Snyder, J. M., Price, N. D., Treuting, P. M., & Stetson, D. B.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2015-11
- Volume
- 43
- Issue
- 5
- Pages
- 933-944
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2173666904
- Cited by
- 513
- References
- 50
- FWCI
- 11.96
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Pestal, K., Funk, C. C., Snyder, J. M., Price, N. D., Treuting, P. M., & Stetson, D. B. (2015). Isoforms of RNA-Editing Enzyme ADAR1 Independently Control Nucleic Acid Sensor MDA5-Driven Autoimmunity and Multi-organ Development. Immunity. https://doi.org/10.1016/j.immuni.2015.11.001
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