ArticleJournal of virology2006
7a protein of severe acute respiratory syndrome coronavirus inhibits cellular protein synthesis and activates p38 mitogen-activated protein kinase.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
101 citing papers in PubMed, 177 citations in OpenAlex.
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- The role of cell death in SARS-CoV-2 infection.Signal transduction and targeted therapy · 2023Review
- SARS-CoV-2 viral protein Nsp2 stimulates translation under normal and hypoxic conditions.Virology journal · 2023Article
- Severe acute respiratory syndrome coronaviruses contributing to mitochondrial dysfunction: Implications for post-COVID complications.Mitochondrion · 2023Review
- Host microRNAs exhibit differential propensity to interact with SARS-CoV-2 and variants of concern.Biochimica et biophysica acta. Molecular basis of disease · 2023Article
- Contribution to pathogenesis of accessory proteins of deadly human coronaviruses.Frontiers in cellular and infection microbiology · 2023Review
- Recent advances in ZBP1-derived PANoptosis against viral infections.Frontiers in immunology · 2023Review
- Ubiquitination of SARS-CoV-2 ORF7a Prevents Cell Death Induced by Recruiting BclXL To Activate ER Stress.Microbiology spectrum · 2022Article
- Recent clinical findings on the role of kinase inhibitors in COVID-19 management.Life sciences · 2022Review
- Papaverine, a promising therapeutic agent for the treatment of COVID-19 patients with underlying cardiovascular diseases (CVDs).Drug development research · 2022Article
- Development of antibody resistance in emerging mutant strains of SARS CoV-2: Impediment for COVID-19 vaccines.Reviews in medical virology · 2022Review
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- Cell deaths: Involvement in the pathogenesis and intervention therapy of COVID-19.Signal transduction and targeted therapy · 2022Review
- Cell death mechanisms involved in cell injury caused by SARS-CoV-2.Reviews in medical virology · 2022Review
- Neutralizing the free radicals could alleviate the disease severity following an infection by positive strand RNA viruses.Cell stress & chaperones · 2022Review
- Programmed cell death: the pathways to severe COVID-19?The Biochemical journal · 2022Review
- Overview of SARS-CoV-2 genome-encoded proteins.Science China. Life sciences · 2022Review
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
It was recently shown that the 7a protein of severe acute respiratory syndrome coronavirus induces biochemical changes associated with apoptosis. In this study, the mechanism by which the 7a protein induces apoptosis was examined. The 7a protein was tested for the ability to inhibit cellular gene expression because several proapoptotic viral proteins with this function have previously been identified. 7a protein inhibited expression of luciferase from an mRNA construct that specifically measures translation, whereas inhibitors of transcription and nucleocytoplasmic transport did not. The inhibition of translation and other cellular processes of gene expression have been associated with the induction of a stress response in cells. Western blot analysis using phosphospecific antibodies indicated that 7a protein activated p38 mitogen-activated protein kinase (MAPK), but not c-Jun N-terminal protein kinase/stress-activated protein kinase. Taken together, these data indicate that the induction of apoptosis by the 7a protein may be related to its ability to inhibit cellular translation and activate p38 MAPK.
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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.