Evidence map›Paper›PMID 34901388›Full record

ArticleMolecular therapy oncolytics2021

AXL receptor is required for Zika virus strain MR-766 infection in human glioblastoma cell lines.

Samuel D Zwernik, Beau H Adams, Daniel A Raymond, Catherine M Warner, Amin B Kassam, Richard A Rovin, Parvez Akhtar

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. AXL signaling in cancer: from molecular insights to targeted therapies.Signal transduction and targeted therapy · 2025
    Review
  8. Article
  9. Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.Journal of the Egyptian National Cancer Institute · 2024
    Review
  10. Zika Virus Neuropathogenesis-Research and Understanding.Pathogens (Basel, Switzerland) · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Samuel D ZwernikAdvocate Aurora Research Institute, Advocate Aurora Health, Milwaukee, WI 53233, USA.
Beau H AdamsAdvocate Aurora Research Institute, Advocate Aurora Health, Milwaukee, WI 53233, USA.
Daniel A RaymondAdvocate Aurora Research Institute, Advocate Aurora Health, Milwaukee, WI 53233, USA.
Catherine M WarnerAdvocate Aurora Research Institute, Advocate Aurora Health, Milwaukee, WI 53233, USA.
Amin B KassamAurora Neuroscience Innovation Institute, Advocate Aurora Health, Milwaukee, WI 53215, USA.
Richard A RovinAurora Neuroscience Innovation Institute, Advocate Aurora Health, Milwaukee, WI 53215, USA.
Parvez AkhtarAdvocate Aurora Research Institute, Advocate Aurora Health, Milwaukee, WI 53233, USA.
Aurora Health Care · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent reports have shown that Zika virus (ZIKV) has oncolytic potential against human glioblastoma (GBM); however, the mechanisms underlying its tropism and cell entry are not completely understood. The receptor tyrosine kinase AXL has been identified as an entry receptor for ZIKV in a cell-type-specific manner. Interestingly, AXL is frequently overexpressed in GBM patients. Using commercially available GBM cell lines, we first show that cells expressing AXL are permissive for ZIKV infection, while cells that do not express AXL are not. Furthermore, inhibition of AXL kinase using R428 and antibody blockade of AXL receptor strongly attenuated virus entry in GBM cell lines. Additionally, CRISPR knockout of the AXL gene in GBM cell lines completely abolished ZIKV infection, significantly inhibited viral replication, and significantly reduced apoptosis compared with parental lines. Lastly, introduction of AXL receptor into non-expressing cell lines renders the cells susceptible to ZIKV infection. Together, these findings demonstrate that ZIKV entry into GBM cells

Indexed as

AXL receptorBrain tumorGBMOncolytic virusZika virus

Identifiers

PMID34901388
PMCPMC8626839
OpenAlexW3213422233

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.