Evidence map›Paper›PMID 9029152›Full record

ArticleThe EMBO journal1997

Abrogation of a mitotic checkpoint by E2 proteins from oncogenic human papillomaviruses correlates with increased turnover of the p53 tumor suppressor protein.

M G Frattini, S D Hurst, H B Lim, S Swaminathan, L A Laimins

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 83 citations in OpenAlex.

  1. Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Human papillomavirus oncoproteins and apoptosis (Review).Experimental and therapeutic medicine · 2014
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Human papillomaviruses: a growing field.Genes & development · 2009
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Molecular biology of cervical cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2007
    Review
  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

5 authors at 1 institution in 1 country.

M G FrattiniDepartment of Microbiology-Immunology, Northwestern University, Chicago, IL 60611, USA.
S D Hurst
H B Lim
S Swaminathan
L A Laimins
Northwestern University · US

Funding

PATHOGENESIS OF HUMAN PAPILLOMAVIRUSES IN VITROU01AI034637 · NIAID · UNIVERSITY OF CHICAGO · PI LAIMINS, LAIMONIS A · 1993 to 1996
–
NIAID NIH HHS AI34637
6 · The paper itself

Abstract

Human papillomavirus (HPV) E2 and E1 proteins are required for the replication of viral genomes in vivo. We have examined the effects of increasing the level of E2 on viral and cellular replication using recombinant adenoviruses. Infection of cells which maintain HPV 31 DNA episomally with E2 recombinant adenoviruses resulted in a 5-fold increase in genome copy number as well as an S phase arrest allowing for the continued replication of cellular DNA. Similar effects on cell cycle progression were seen following infection of normal human foreskin keratinocytes, the natural host cell. The DNA content of these cells increased beyond 4N indicating that multiple rounds of replication had occurred without an intervening mitotic event. In addition, increased cyclin A and E associated kinase activity was observed, while no change was detected in cyclin B associated kinase activity or in the activation state of cdc2 kinase. Interestingly, the levels of the p53 tumor suppresser protein were dramatically reduced through a post-transcriptional mechanism following infection. These data suggest a role for E2 in regulating viral and cellular replication by abrogation of a mitotic checkpoint, which is, at least in part, controlled by p53.

Indexed as

MitosisAdenoviridaeCDC2 Protein KinaseCell CycleCell NucleusDNA-Binding ProteinsDNA, ViralEnzyme ActivationFlow CytometryGene Expression Regulation, ViralGenetic VectorsHalf-LifeHumansPapillomaviridaeProtein KinasesRecombinant ProteinsCDC2 Protein KinaseDNA-Binding ProteinsDNA, ViralE2 protein, Human papillomavirus type 31histone H1 kinaseProtein KinasesRecombinant ProteinsTumor Suppressor Protein p53Viral Proteins

Identifiers

PMID9029152
PMCPMC1169638
OpenAlexW2023228900

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.