Evidence map›Paper›PMID 9765437›Full record

ArticleJournal of virology1998

Role of glutamine 17 of the bovine papillomavirus E5 protein in platelet-derived growth factor beta receptor activation and cell transformation.

O Klein, G W Polack, T Surti, D Kegler-Ebo, S O Smith, D DiMaio

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1998. 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
2.6field-weighted citation impact, top 11% 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, 56 citations in OpenAlex.

  1. Two transmembrane dimers of the bovine papillomavirus E5 oncoprotein clamp the PDGF β receptor in an active dimeric conformation.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  2. De novo selection of oncogenes.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  3. Viral miniproteins.Annual review of microbiology · 2014
    Review
  4. Article
  5. The E5 proteins.Virology · 2013
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. 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

6 authors at 1 institution in 1 country.

O KleinDepartment of Genetics, Yale University School of Medicine, New Haven, Connecticut 06510, USA.
G W Polack
T Surti
D Kegler-Ebo
S O Smith
D DiMaio
Yale University · US

Funding

CELL TRANSFORMATION BY BOVINE PAPILLOMAVIRUSR01CA037157 · NCI · YALE UNIVERSITY · PI DIMAIO, DANIEL C. · 1985 to 2019
$9.9M
CELL TRANSFORMATION BY BOVINE PAPILLOMAVIRUSR37CA037157 · NCI · YALE UNIVERSITY · PI DIMAIO, DANIEL · 1992 to 1999
–
NCI NIH HHS CA37157NCI NIH HHS R01 CA037157NCI NIH HHS R37 CA037157
6 · The paper itself

Abstract

The bovine papillomavirus E5 protein is a small, homodimeric transmembrane protein that forms a stable complex with the cellular platelet-derived growth factor (PDGF) beta receptor through transmembrane and juxtamembrane interactions, resulting in receptor activation and cell transformation. Glutamine 17 in the transmembrane domain of the 44-amino-acid E5 protein is critical for complex formation and receptor activation, and we previously proposed that glutamine 17 forms a hydrogen bond with threonine 513 of the PDGF beta receptor. We have constructed and analyzed mutant E5 proteins containing all possible amino acids at position 17 and examined the ability of these proteins to transform C127 fibroblasts, which express endogenous PDGF beta receptor. Although several position 17 mutants were able to transform cells, mutants containing amino acids with side groups that were unable to participate in hydrogen bonding interactions did not form a stable complex with the PDGF beta receptor or transform cells, in agreement with the proposed interaction between position 17 of the E5 protein and threonine 513 of the receptor. The nature of the residue at position 17 also affected the ability of the E5 proteins to dimerize. Overall, there was an excellent correlation between the ability of the various E5 mutant proteins to bind the PDGF beta receptor, lead to receptor tyrosine phosphorylation, and transform cells. Similar results were obtained in Ba/F3 hematopoietic cells expressing exogenous PDGF beta receptor. In addition, treatment of E5-transformed cells with a specific inhibitor of the PDGF receptor tyrosine kinase reversed the transformed phenotype. These results confirm the central importance of the PDGF beta receptor in mediating E5 transformation and highlight the critical role of the residue at position 17 of the E5 protein in the productive interaction with the PDGF beta receptor. On the basis of molecular modeling analysis and the known chemical properties of the amino acids, we suggest a structural basis for the role of the residue at position 17 in E5 dimerization and in complex formation between the E5 protein and the PDGF beta receptor.

Indexed as

Cell Transformation, ViralAnimalsBovine papillomavirus 1CattleCell LineCOS CellsDimerizationGenes, ViralGlutamineModels, MolecularMutationOncogene Proteins, ViralProtein ConformationReceptor, Platelet-Derived Growth Factor betaReceptors, Platelet-Derived Growth FactorGlutamineoncogene protein E5, Bovine papillomavirus type 1Oncogene Proteins, ViralReceptor, Platelet-Derived Growth Factor betaReceptors, Platelet-Derived Growth Factor

Identifiers

PMID9765437
PMCPMC110309
OpenAlexW1863728155

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.