Evidence map›Paper›PMID 21637748›Full record

ArticlePloS one2011

SARS-CoV 9b protein diffuses into nucleus, undergoes active Crm1 mediated nucleocytoplasmic export and triggers apoptosis when retained in the nucleus.

Kulbhushan Sharma, Sara Åkerström, Anuj Kumar Sharma, Vincent T K Chow, Shumein Teow, Bernard Abrenica, Stephanie A Booth, Timothy F Booth, Ali Mirazimi, Sunil K Lal

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Contribution to pathogenesis of accessory proteins of deadly human coronaviruses.Frontiers in cellular and infection microbiology · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. The adaptation of SARS-CoV-2 to humans.Memorias do Instituto Oswaldo Cruz · 2022
    Article
  11. Clinical drug therapies and biologicals currently used or in clinical trial to treat COVID-19.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. The molecular virology of coronaviruses.The Journal of biological chemistry · 2020
    Review
  20. Coding potential and sequence conservation of SARS-CoV-2 and related animal viruses.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2020
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 6 institutions in 4 countries.

Kulbhushan SharmaVirology Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India.
Sara Åkerström
Anuj Kumar Sharma
Vincent T K Chow
Shumein Teow
Bernard Abrenica
Stephanie A Booth
Timothy F Booth
Ali Mirazimi
Sunil K Lal
Public Health Agency of Canada · CAInternational Centre for Genetic Engineering and Biotechnology · INSwedish Institute · SEJawaharlal Nehru University · INNational University of Singapore · SGUniversity of Manitoba · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background9b is an accessory protein of the SARS-CoV. It is a small protein of 98 amino acids and its structure has been solved recently. 9b is known to localize in the extra-nuclear region and has been postulated to possess a nuclear export signal (NES), however the role of NES in 9b functioning is not well understood. PRINCIPAL FINDINGS/METHODOLOGY: In this report, we demonstrate that 9b in the absence of any nuclear localization signal (NLS) enters the nucleus by passive transport. Using various cell cycle inhibitors, we have shown that the nuclear entry of 9b is independent of the cell cycle. Further, we found that 9b interacts with the cellular protein Crm1 and gets exported out of the nucleus using an active NES. We have also revealed that this NES activity influences the half-life of 9b and affects host cell death. We found that an export signal deficient SARS-CoV 9b protein induces apoptosis in transiently transfected cells and showed elevated caspase-3 activity. CONCLUSION/SIGNIFICANCE: Here, we showed that nuclear shuttling of 9b and its interaction with Crm1 are essential for the proper degradation of 9b and blocking the nuclear export of this protein induces apoptosis. This phenomenon may be critical in providing a novel role to the 9b accessory protein of SARS-CoV.

Indexed as

ApoptosisActive Transport, Cell NucleusAnimalsCell CycleCell NucleusChlorocebus aethiopsDiffusionExportin 1 ProteinIntracellular SpaceKaryopherinsModels, BiologicalNuclear Export SignalsNuclear Localization SignalsProtein Processing, Post-TranslationalProtein TransportReceptors, Cytoplasmic and NuclearExportin 1 ProteinKaryopherinsNuclear Export SignalsNuclear Localization SignalsReceptors, Cytoplasmic and NuclearViral Proteins

Identifiers

PMID21637748
PMCPMC3103500
OpenAlexW2058772313

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.