Evidence map›Paper›PMID 21330137›Full record

ReviewTrends in microbiology2011

Opposing oncogenic activities of small DNA tumor virus transforming proteins.

G Chinnadurai

Open access · greenAbstract readReview
In one paragraph

Review in Trends in microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. human adenoviruses role in ophthalmic pterygium formation.Jundishapur journal of microbiology · 2015
    Article
  6. Article
  7. Article
  8. Article
  9. Adenovirus and miRNAs.Biochimica et biophysica acta
    Review
  10. 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

1 author at 1 institution in 1 country.

G ChinnaduraiInstitute for Molecular Virology, Doisy Research Center, Saint Louis University Medical School, 1100 South Grand Blvd., 6th Floor, St. Louis, MO 63104, USA. chinnag@slu.edu
Saint Louis University · US

Funding

PROMOTION OF CELL SURVIVAL BY ADENOVIRUS E1B 19K PROTEINR01CA033616 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 1985 to 2015
$4.0M
Modulation of Oncogenesis by E1A--Role of CtBP and CtIPR01CA084941 · NCI · SAINT LOUIS UNIVERSITY · PI CHINNADURAI, GOVINDASWAMY · 2001 to 2011
$2.5M
NCI NIH HHS CA-033616NCI NIH HHS CA-084941NCI NIH HHS R01 CA033616NCI NIH HHS R01 CA084941
6 · The paper itself

Abstract

The E1A gene of species C human adenovirus is an intensely investigated model viral oncogene that immortalizes primary cells and mediates oncogenic cell transformation in cooperation with other viral or cellular oncogenes. Investigations using E1A proteins have illuminated important paradigms in cell proliferation and about the functions of cellular proteins such as the retinoblastoma protein. Studies with E1A have led to the unexpected discovery that E1A also suppresses cell transformation and oncogenesis. Here, I review our current understanding of the transforming and tumor-suppressive functions of E1A, and how E1A studies led to the discovery of a related tumor-suppressive function in benign human papillomaviruses. The potential role of these opposing functions in viral replication in epithelial cells is also discussed.

Indexed as

AdenoviridaeAdenovirus E1A ProteinsHumansOncogene Proteins, ViralTumor Suppressor ProteinsVirulence FactorsAdenovirus E1A ProteinsOncogene Proteins, ViralTumor Suppressor ProteinsVirulence Factors

Identifiers

PMID21330137
PMCPMC3095844
OpenAlexW2078229816

What OpenQuestion holds

Textmetadata
LicenceTDM
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.