Evidence map›Paper›PMID 24109239›Full record

ArticleJournal of virology2013

Merkel cell polyomavirus small T antigen targets the NEMO adaptor protein to disrupt inflammatory signaling.

David A Griffiths, Hussein Abdul-Sada, Laura M Knight, Brian R Jackson, Kathryn Richards, Emma L Prescott, A Howard S Peach, G Eric Blair, Andrew Macdonald, Adrian Whitehouse

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Merkel cell polyomavirus and Langerhans cell neoplasm.Cell communication and signaling : CCS · 2018
    Pooled it
  2. Review
  3. Article
  4. Polyomavirus ALTOs, but not MTs, downregulate viral early gene expression by activating the NF-κB pathway.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Merkel Cell Carcinoma from Molecular Pathology to Novel Therapies.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Protein phosphatases in TLR signaling.Cell communication and signaling : CCS · 2021
    Review
  20. Article

7 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

David A GriffithsSchool of Molecular and Cellular Biology, Faculty of Biological Sciences.
Hussein Abdul-Sada
Laura M Knight
Brian R Jackson
Kathryn Richards
Emma L Prescott
A Howard S Peach
G Eric Blair
Andrew Macdonald
Adrian Whitehouse
University of Leeds · GBLeeds Teaching Hospitals NHS Trust · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council MR/K012665/1
6 · The paper itself

Abstract

Merkel cell carcinoma (MCC) is a highly aggressive nonmelanoma skin cancer arising from epidermal mechanoreceptor Merkel cells. In 2008, a novel human polyomavirus, Merkel cell polyomavirus (MCPyV), was identified and is strongly implicated in MCC pathogenesis. Currently, little is known regarding the virus-host cell interactions which support virus replication and virus-induced mechanisms in cellular transformation and metastasis. Here we identify a new function of MCPyV small T antigen (ST) as an inhibitor of NF-κB-mediated transcription. This effect is due to an interaction between MCPyV ST and the NF-κB essential modulator (NEMO) adaptor protein. MCPyV ST expression inhibits IκB kinase α (IKKα)/IKKβ-mediated IκB phosphorylation, which limits translocation of the NF-κB heterodimer to the nucleus. Regulation of this process involves a previously undescribed interaction between MCPyV ST and the cellular phosphatase subunits, protein phosphatase 4C (PP4C) and/or protein phosphatase 2A (PP2A) Aβ, but not PP2A Aα. Together, these results highlight a novel function of MCPyV ST to subvert the innate immune response, allowing establishment of early or persistent infection within the host cell.

Indexed as

Antigens, Viral, TumorCarcinoma, Merkel CellCell LineHumansI-kappa B KinaseImmunity, InnateMerkel cell polyomavirusNF-kappa BPhosphorylationPolyomavirus InfectionsProtein BindingTumor Virus InfectionsAntigens, Viral, TumorI-kappa B KinaseIKBKG protein, humanNF-kappa B

Identifiers

PMID24109239
PMCPMC3838273
OpenAlexW1982818976

What OpenQuestion holds

Textmetadata
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.