Evidence map›Paper›PMID 22261717›Full record

ArticleEMBO reports2012

Nuclear IGF1R is a transcriptional co-activator of LEF1/TCF.

Dudi Warsito, Sylvia Sjöström, Sandra Andersson, Olle Larsson, Bita Sehat

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.2field-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

58 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  4. IGF-1R targeting in cancer - does sub-cellular localization matter?Journal of experimental & clinical cancer research : CR · 2023
    Review
  5. Review
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  8. Molecularly Defined Subsets of Ewing Sarcoma Tumors Differ in Their Responses to IGF1R and WEE1 Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. IGFBP-3 functions as a molecular switch that mediates mitochondrial and metabolic homeostasis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  15. Article
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  17. Review
  18. 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.

Dudi WarsitoDepartment of Oncology and Pathology, Karolinska Institutet, Cancer Center Karolinska, R8:04, Karolinska University Hospital, SE-171 76 Stockholm, Sweden.
Sylvia Sjöström
Sandra Andersson
Olle Larsson
Bita Sehat
Karolinska University Hospital · SEKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent findings suggest that nuclear IGF1R binds to enhancer regions and functions as a transcriptional cofactor. However, the downstream transcriptional regulators of this pathway remain to be defined. Here, we show that nuclear IGF1R associates with the transcription factor LEF1 and increases promoter activity of LEF1 downstream target genes cyclin D1 and axin2. Furthermore, nuclear IGF1R augments protein levels of cyclin D1 and axin2. Our findings suggest a novel function for IGF1R, thus further emphasizing the important role of this receptor in cancer biology.

Indexed as

Axin Proteinbeta CateninCell LineCell NucleusCyclin D1Gene Expression RegulationHumansInsulin Receptor Substrate ProteinsLymphoid Enhancer-Binding Factor 1Promoter Regions, GeneticProtein BindingProtein TransportReceptor, IGF Type 1Receptors, Cytoplasmic and NuclearTranscriptional ActivationAxin Proteinbeta CateninCyclin D1Insulin Receptor Substrate ProteinsLymphoid Enhancer-Binding Factor 1Receptor, IGF Type 1Receptors, Cytoplasmic and Nuclear

Identifiers

PMID22261717
PMCPMC3323138
OpenAlexW2003340108

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.