ArticleJournal of virology2000
RNase L-independent specific 28S rRNA cleavage in murine coronavirus-infected cells.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- SARS-CoV-2 3CLpro whole human proteome cleavage prediction and enrichment/depletion analysis.Computational biology and chemistry · 2022Article
- The interface between coronaviruses and host cell RNA biology: Novel potential insights for future therapeutic intervention.Wiley interdisciplinary reviews. RNA · 2020Review
- Public Database-Driven Insights Into Aging Stress-Associated Defective Gut Barrier With Low SARS-CoV-2 Receptors.Frontiers in medicine · 2020Article
- Tick-borne encephalitis virus inhibits rRNA synthesis and host protein production in human cells of neural origin.PLoS neglected tropical diseases · 2019Article
- Interplay between coronavirus, a cytoplasmic RNA virus, and nonsense-mediated mRNA decay pathway.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Review
- RNA disruption is associated with response to multiple classes of chemotherapy drugs in tumor cell lines.BMC cancer · 2016Article
- Viral and Cellular mRNA Translation in Coronavirus-Infected Cells.Advances in virus research · 2016Review
- Ribonuclease L and metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs.Nucleic acids research · 2014Article
- Tinkering with translation: protein synthesis in virus-infected cells.Cold Spring Harbor perspectives in biology · 2013Review
- Targets and intracellular signaling mechanisms for deoxynivalenol-induced ribosomal RNA cleavage.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- Aberrant expression of miR-638 contributes to benzo(a)pyrene-induced human cell transformation.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- Article
- Inhibition of protein kinase R activation and upregulation of GADD34 expression play a synergistic role in facilitating coronavirus replication by maintaining de novo protein synthesis in virus-infected cells.Journal of virology · 2009Article
- A two-pronged strategy to suppress host protein synthesis by SARS coronavirus Nsp1 protein.Nature structural & molecular biology · 2009Article
- Apoptotic signals induce specific degradation of ribosomal RNA in yeast.Nucleic acids research · 2008Article
- Coronavirus infection modulates the unfolded protein response and mediates sustained translational repression.Journal of virology · 2008Article
- Viral encounters with 2',5'-oligoadenylate synthetase and RNase L during the interferon antiviral response.Journal of virology · 2007Review
- Novel small-molecule inhibitors of transmissible gastroenteritis virus.Antimicrobial agents and chemotherapy · 2007Article
- Mouse hepatitis coronavirus replication induces host translational shutoff and mRNA decay, with concomitant formation of stress granules and processing bodies.Cellular microbiology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
We characterized a novel 28S rRNA cleavage in cells infected with the murine coronavirus mouse hepatitis virus (MHV). The 28S rRNA cleavage occurred as early as 4 h postinfection (p.i.) in MHV-infected DBT cells, with the appearance of subsequent cleavage products and a decrease in the amount of intact 28S rRNA with increasing times of infection; almost all of the intact 28S rRNA disappeared by 24 h p.i. In contrast, no specific 18S rRNA cleavage was detected in infected cells. MHV-induced 28S rRNA cleavage was detected in all MHV-susceptible cell lines and all MHV strains tested. MHV replication was required for the 28S rRNA cleavage, and mature cytoplasmic 28S rRNA underwent cleavage. In certain combination of cells and viruses, pretreatment of virus-infected cells with interferon activates a cellular endoribonuclease, RNase L, that causes rRNA degradation. No interferon was detected in the inoculum used for MHV infection. Addition of anti-interferon antibody to MHV-infected cells did not inhibit 28S rRNA cleavage. Furthermore, 28S rRNA cleavage occurred in an MHV-infected mouse embryonic fibroblast cell line derived from RNase L knockout mice. Thus, MHV-induced 28S rRNA cleavage was independent of the activation of RNase L. MHV-induced 28S rRNA cleavage was also different from apoptosis-related rRNA degradation, which usually occurs concomitantly with DNA fragmentation. In MHV-infected 17Cl-1 cells, 28S rRNA cleavage preceded DNA fragmentation by at least 18 h. Blockage of apoptosis in MHV-infected 17Cl-1 cells by treatment with a caspase inhibitor did not block 28S rRNA cleavage. Furthermore, MHV-induced 28S rRNA cleavage occurred in MHV-infected DBT cells that do not show apoptotic signs, including activation of caspase-3 and DNA fragmentation. Thus, MHV-induced 28S rRNA cleavage appeared to differ from any rRNA degradation mechanism described previously.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.