Evidence map›Paper›PMID 16170362›Full record

ArticleOncogene2006

Transformation by the simian virus 40 T antigen is regulated by IGF-I receptor and IRS-1 signaling.

T DeAngelis, J Chen, A Wu, M Prisco, R Baserga

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
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  8. Inhibition of Cullin-RING E3 ubiquitin ligase 7 by simian virus 40 large T antigen.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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

5 authors at 2 institutions in 1 country.

T DeAngelisKimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.
J Chen
A Wu
M Prisco
R Baserga
Sidney Kimmel Cancer Center · USThomas Jefferson University · US

Funding

BIOLOGY OF THE P53 PROTEINR01CA089640 · NCI · THOMAS JEFFERSON UNIVERSITY · PI BASERGA, RENATO LUIGI · 2001 to 2009
$2.0M
A Role of the IGF-1 Receptor In AgingR01AG020956 · NIA · THOMAS JEFFERSON UNIVERSITY · PI BASERGA, RENATO LUIGI · 2001 to 2005
$1.5M
NCI NIH HHS CA89640NIA NIH HHS AG 20956
6 · The paper itself

Abstract

Previous work has shown that the Simian Virus 40 T antigen (T antigen) cannot transform mouse embryo fibroblasts (MEFs) that do not express the type 1 insulin-like growth factor receptor (IGF-IR). We have now investigated the mechanism(s) by which the transforming activity of T antigen is affected by IGF-IR signaling. We demonstrate that transformation by T antigen of MEFs and several other cell lines requires an insulin receptor substrate-1 (IRS-1) phosphorylated on tyrosines. If IRS-1 is not expressed, or is serine phosphorylated or otherwise inactive, T antigen fails to transform cells in culture. For instance, while T antigen cannot transform 32D myeloid cells (that do not express IRS-1), its transforming activity is restored by the expression of a wild-type IRS-1, but not of an IRS-1 mutated at the PI3K binding sites. The importance of IRS-1 activation of PI3K in T-antigen transformation is supported by the finding that a constitutively activated p110 subunit of PI3K, a target of IRS-1, overcomes the inability of T antigen to transform MEFs with a serine phosphorylated IRS-1. Taken together, these results indicate that the IRS-1/PI3K signaling is one of the mechanisms regulating transformation by the SV40 T antigen. We propose that the requirement for a tyrosyl-phosphorylated IRS-1 provides a mechanism to explain the failure of T antigen to transform MEFs with deleted IGF-IR genes.

Indexed as

Cell Line, TransformedAgarAnimalsAntigens, Polyomavirus TransformingAntigens, Viral, TumorBinding SitesBlotting, WesternBreast NeoplasmsCell LineCells, CulturedCell SurvivalCell Transformation, NeoplasticFibroblastsGene DeletionInsulin Receptor Substrate ProteinsMiceAgarAntigens, Polyomavirus TransformingAntigens, Viral, TumorInsulin Receptor Substrate ProteinsIrs1 protein, mousePhosphatidylinositol 3-KinasesPhosphoproteinsPol1 Transcription Initiation Complex ProteinsReceptor, IGF Type 1RNARNA, RibosomalSerinetranscription factor UBFTyrosine

Identifiers

PMID16170362
OpenAlexW1995758629

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.