Evidence map›Paper›PMID 32182205›Full record

ArticleThe Journal of general virology2020

Human papillomavirus type 16 infection activates the host serine arginine protein kinase 1 (SRPK1) - splicing factor axis.

Sarah Mole, Arwa Ali A Faizo, Hegel Hernandez-Lopez, Megan Griffiths, Andrew Stevenson, Sally Roberts, Sheila V Graham

Open access · hybridAbstract read
In one paragraph

Article in The Journal of general virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  5. Article
  6. Viral Modulation of Host Splicing.Annual review of virology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
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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 5 institutions in 3 countries.

Sarah MoleMRC - University of Glasgow Centre for Virus Research, Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Garscube Estate, Glasgow G61 1QH, UK.
Arwa Ali A FaizoMRC - University of Glasgow Centre for Virus Research, Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Garscube Estate, Glasgow G61 1QH, UK.
Hegel Hernandez-LopezMRC - University of Glasgow Centre for Virus Research, Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Garscube Estate, Glasgow G61 1QH, UK.
Megan GriffithsMRC - University of Glasgow Centre for Virus Research, Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Garscube Estate, Glasgow G61 1QH, UK.
Andrew StevensonMRC - University of Glasgow Centre for Virus Research, Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Garscube Estate, Glasgow G61 1QH, UK.
Sally RobertsInstitute of Cancer and Genomic Sciences, Institute of Biomedical Research West, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK.
Sheila V GrahamMRC - University of Glasgow Centre for Virus Research, Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Garscube Estate, Glasgow G61 1QH, UK.
MRC University of Glasgow Centre for Virus Research · GBBristol-Myers Squibb (United States) · USGlaxoSmithKline (United Kingdom) · GBKing Abdulaziz University · SAUniversity of Birmingham · GB

Funding

Medical Research Council MC_UU_12014Medical Research Council MC_UU_12014/9Wellcome Trust
6 · The paper itself

Abstract

The infectious life cycle of human papillomaviruses (HPVs) is tightly linked to keratinocyte differentiation. Evidence suggests a sophisticated interplay between host gene regulation and virus replication. Alternative splicing is an essential process for host and viral gene expression, and is generally upregulated by serine arginine-rich splicing factors (SRSFs). SRSF activity can be positively or negatively controlled by cycles of phosphorylation/dephosphorylation. Here we show that HPV16 infection leads to accumulation of the paradigm SRSF protein, SRSF1, in the cytoplasm in a keratinocyte differentiation-specific manner. Moreover, HPV16 infection leads to increased levels of cytoplasmic and nuclear phosphorylated SRSF1. SR protein kinase 1 (SRPK1) phosphorylates SRSF1. Similar to HPV upregulation of SRSF1, we demonstrate HPV upregulation of SRPK1 via the viral E2 protein. SRPK1 depletion or drug inhibition of SRPK1 kinase activity resulted in reduced levels of SRSF1, suggesting that phosphorylation stabilizes the protein in differentiated HPV-infected keratinocytes. Together, these data indicate HPV infection stimulates the SRPK1-SRSF axis in keratinocytes.

Indexed as

3T3 CellsAlternative SplicingAnimalsHeLa CellsHuman papillomavirus 16HumansKeratinocytesMicePapillomavirus InfectionsPhosphorylationProtein Serine-Threonine KinasesSerine-Arginine Splicing FactorsUp-RegulationViral ProteinsVirus ReplicationProtein Serine-Threonine KinasesSerine-Arginine Splicing FactorsSRPK1 protein, humanViral Proteinscervical cancerepithelial differentiationhuman papillomavirusinfectiontumour progression

Identifiers

PMID32182205
PMCPMC7414453
OpenAlexW3005728216

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.