Evidence map›Paper›PMID 10618715›Full record

ArticleOncogene1999

Interaction between the HPV-16 E2 transcriptional activator and p53.

P Massimi, D Pim, C Bertoli, V Bouvard, L Banks

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. 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
3.5field-weighted citation impact, top 7% 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, 89 citations in OpenAlex.

  1. Article
  2. Viral vector-based therapeutic HPV vaccines.Clinical and experimental medicine · 2024
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Human papillomavirus infections: warts or cancer?Cold Spring Harbor perspectives in biology · 2013
    Review
  16. HPV-18 E6 mutants reveal p53 modulation of viral DNA amplification in organotypic cultures.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  17. Review
  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

5 authors at 2 institutions in 2 countries.

P MassimiInternational Centre for Genetic Engineering and Biotechnology, Padriciano 99, I-34012 Trieste, Italy.
D Pim
C Bertoli
V Bouvard
L Banks
International Centre for Genetic Engineering and Biotechnology · ITCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The HPV-16 E2 protein is a major regulator of viral DNA replication and gene expression. Through interactions with the viral origin binding protein, E1, it localizes E1 to the origin of replication and stimulates the initiation of viral DNA replication. However, several recent reports have described a number of diverse activities of E2 relating to the induction of apoptosis through both p53 dependent and independent mechanisms, and to induction of growth arrest in both the G1 and G2M phases of the cell cycle. Recent studies have also shown that p53 can specifically inhibit HPV DNA replication, albeit through an unknown mechanism. Since p53 has been described in the replication centres of Herpes Viruses, Adenovirus and SV40 we decided to investigate whether any of the above activities of E2 may be related to an association with p53. We show, in a series of in vitro assays, specific interaction between p53 and HPV-16 E2 via residues in the carboxy terminal half of the E2 protein. Mutational analysis of p53 indicates that sequences in both the DNA binding and oligomerization domains are essential for the interaction, and a mutant of p53 which is unable to bind E2 is also unable to inhibit HPV DNA replication. Finally, using an inducible system of p53 expression we also show that E2 will complex with p53 in vivo. These results raise the intriguing possibility that p53 may also be involved in HPV DNA replication centres, and also provides explanations for some of the diverse activities reported for the HPV E2 proteins.

Indexed as

DNA-Binding ProteinsAmino Acid SequenceBinding SitesDNA ReplicationHumansModels, MolecularMolecular Sequence DataOncogene Proteins, ViralPapillomaviridaeProtein Structure, SecondaryRecombinant Fusion ProteinsTrans-ActivatorsTransfectionTumor Cells, CulturedTumor Suppressor Protein p53DNA-Binding ProteinsE2 protein, Human papillomavirus type 16Oncogene Proteins, ViralRecombinant Fusion ProteinsTrans-ActivatorsTumor Suppressor Protein p53

Identifiers

PMID10618715
OpenAlexW2334731906

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.