The DOI matches its Crossref record; 73 of the 73 references it cites were found in a registry or an index.
The SARS Coronavirus 3a Protein Causes Endoplasmic Reticulum Stress and Induces Ligand-Independent Downregulation of the Type 1 Interferon Receptor
Open accessAbstract
The Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) is reported to cause apoptosis of infected cells and several of its proteins including the 3a accessory protein, are pro-apoptotic. Since the 3a protein localizes to the endoplasmic reticulum (ER)-Golgi compartment, its role in causing ER stress was investigated in transiently transfected cells. Cells expressing the 3a proteins showed ER stress based on activation of genes for the ER chaperones GRP78 and GRP94. Since ER stress can cause differential modulation of the unfolded protein response (UPR), which includes the inositol-requiring enzyme 1 (IRE-1), activating transcription factor 6 (ATF6) and PKR-like ER kinase (PERK) pathways, these were individually tested in 3a-expressing cells. Only the PERK pathway was found to be activated in 3a-expressing cells based on (1) increased phosphorylation of eukaryotic initiation factor 2 alpha (eIF2alpha) and inhibitory effects of a dominant-negative form of eIF2alpha on GRP78 promoter activity, (2) increased translation of activating transcription factor 4 (ATF4) mRNA, and (3) ATF4-dependent activation of the C/EBP homologous protein (CHOP) gene promoter. Activation of PERK affects innate immunity by suppression of type 1 interferon (IFN) signaling. The 3a protein was found to induce serine phosphorylation within the IFN alpha-receptor subunit 1 (IFNAR1) degradation motif and to increase IFNAR1 ubiquitination. Confocal microscopic analysis showed increased translocation of IFNAR1 into the lysosomal compartment and flow cytometry showed reduced levels of IFNAR1 in 3a-expressing cells. These results provide further mechanistic details of the pro-apoptotic effects of the SARS-CoV 3a protein, and suggest a potential role for it in attenuating interferon responses and innate immunity.
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IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA
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Interplay between SARS-CoV-2 and the type I interferon response
Sa Ribero, M., Jouvenet, N., Dreux, M., & Nisole, S. (2020) · PLOS Pathogens · doi:10.1371/journal.ppat.1008737 · Cited by 443
Miao, G., Zhao, H., Li, Y., Ji, M., Chen, Y., Shi, Y., Bi, Y., Wang, P., & Zhang, H. (2021) · Developmental Cell · doi:10.1016/j.devcel.2020.12.010 · Cited by 354
“, 2018), elicits ER stress (Minakshi et al., 2009), activates NF-kB and the NLRP3 inflammasome (Siu et al.”
BackgroundSARS-CoV-2-Specific Immune Response and the Pathogenesis of COVID-19
Gusev, E., Sarapultsev, A., Solomatina, L., & Chereshnev, V. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23031716 · Cited by 281
HIV-1 modulates the tRNA pool to improve translation efficiency
van Weringh, A., Ragonnet-Cronin, M., Pranckeviciene, E., Pavon-Eternod, M., Kleiman, L., & Xia, X. (2011) · Molecular Biology and Evolution · doi:10.1093/molbev/msr005 · Cited by 130
Metadata
- Authors
- Minakshi, R., Padhan, K., Rani, M., Khan, N., Ahmad, F., & Jameel, S.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2009-12-17
- Volume
- 4
- Issue
- 12
- Pages
- e8342
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W2156333187
- Cited by
- 257
- References
- 73
- FWCI
- 2.08
- Type
- journal article
- Language
- en
- Open access
- gold
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- Minakshi, R., Padhan, K., Rani, M., Khan, N., Ahmad, F., & Jameel, S. (2009). The SARS Coronavirus 3a Protein Causes Endoplasmic Reticulum Stress and Induces Ligand-Independent Downregulation of the Type 1 Interferon Receptor. PLoS ONE. https://doi.org/10.1371/journal.pone.0008342
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