Evidence map›Paper›PMID 24416643›Full record

ReviewJAK-STAT2013

Genomic and computational approaches to dissect the mechanisms of STAT3's universal and cell type-specific functions.

Andrew Paul Hutchins, Diego Diez, Diego Miranda-Saavedra

Open access · bronzeAbstract readReview
In one paragraph

Review in JAK-STAT, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Emerging therapeutic targets for cardiac hypertrophy.Expert opinion on therapeutic targets · 2022
    Review
  6. Review
  7. Review
  8. Article
  9. Inhibition of STAT3 blocks protein synthesis and tumor metastasis in osteosarcoma cells.Journal of experimental & clinical cancer research : CR · 2018
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Differential effects of STAT proteins on growth hormone-mediated IGF-I gene expression.American journal of physiology. Endocrinology and metabolism · 2014
    Article
  19. Review
  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

3 authors at 2 institutions in 2 countries.

Andrew Paul HutchinsBioinformatics and Genomics Laboratory; World Premier International (WPI) Immunology Frontier Research Center (IFReC); Osaka University; Suita, Osaka Japan.
Diego DiezBioinformatics and Genomics Laboratory; World Premier International (WPI) Immunology Frontier Research Center (IFReC); Osaka University; Suita, Osaka Japan.
Diego Miranda-SaavedraBioinformatics and Genomics Laboratory; World Premier International (WPI) Immunology Frontier Research Center (IFReC); Osaka University; Suita, Osaka Japan.
Institut thématique Génétique, génomique et bioinformatique · FROsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STAT3 is the quintessential pleiotropic transcription factor with many biological roles throughout development as well as in multiple adult tissues. Its functional heterogeneity is encoded in the range of genome-wide binding patterns that specify different regulatory networks in distinct cell types. However, STAT3 does not display remarkable DNA binding preferences that may help correlate specific motifs with individual biological functions or cell types. Therefore, achieving a detailed understanding of the regulatory mechanisms that endow STAT3 (or any other pleiotropic transcription factor) with such a rainbow of functions is not only a central problem in biology but also a fiendishly difficult one. Here we describe key genomic and computational approaches that have shed light into this question, and present the two current models of STAT3 binding (universal and cell type-specific). We also discuss the role that the local epigenetic environment plays in the selection of STAT3 binding sites.

Indexed as

bioinformaticscancerChIP-seqgenomicsinflammationJAK-STATpleiotropySTAT3transcriptional regulatory modules

Identifiers

PMID24416643
PMCPMC3876425
OpenAlexW2079761398

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.