ArticleVirus research2010
SARS-coronavirus protein 6 conformations required to impede protein import into the nucleus.
Article in Virus research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed.
- M-Motif, a potential non-conventional NLS in YAP/TAZ and other cellular and viral proteins that inhibits classic protein import.iScience · 2025Article
- Transmission cluster of COVID-19 cases from Uruguay: emergence and spreading of a novel SARS-CoV-2 ORF6 deletion.Memorias do Instituto Oswaldo Cruz · 2022Article
- Potential Drug Strategies to Target Coronaviruses.Advances in experimental medicine and biology · 2021Article
- SARS-CoV-2 nsp13, nsp14, nsp15 and orf6 function as potent interferon antagonists.Emerging microbes & infections · 2020Article
- The molecular virology of coronaviruses.The Journal of biological chemistry · 2020Review
- Phage display technique identifies the interaction of severe acute respiratory syndrome coronavirus open reading frame 6 protein with nuclear pore complex interacting protein NPIPB3 in modulating Type I interferon antagonism.Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi · 2017Article
- Continuous and Discontinuous RNA Synthesis in Coronaviruses.Annual review of virology · 2015Review
- Accessory proteins of SARS-CoV and other coronaviruses.Antiviral research · 2014Review
- The role of severe acute respiratory syndrome (SARS)-coronavirus accessory proteins in virus pathogenesis.Viruses · 2012Review
- SARS coronavirus pathogenesis: host innate immune responses and viral antagonism of interferon.Current opinion in virology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The severe acute respiratory syndrome coronavirus (SARS-CoV) genome encodes eight accessory proteins. Accessory protein 6 is a 63-residue amphipathic peptide that accelerates coronavirus infection kinetics in cell culture and in mice. Protein 6 is minimally bifunctional, with an N-terminal lipophilic part implicated in accelerating viral growth and a C-terminal hydrophilic part interfering with general protein import into the nucleus. This interference with nuclear import requires interaction between protein 6 and cellular karyopherins, a process that typically involves nuclear localization signal (NLS) motifs. Here we dissected protein 6 using site-directed mutagenesis and found no evidence for a classical NLS. Furthermore, we found that the C-terminal tail of protein 6 impeded nuclear import only in the context of a lipophilic N-terminus, which could be derived from membrane proteins unrelated to protein 6. These findings are discussed in the context of the proposed protein 6 structure.
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What OpenQuestion holds
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.