Evidence map›Paper›PMID 20716519›Full record

ArticleNucleic acids research2010

AUF1 p42 isoform selectively controls both steady-state and PGE2-induced FGF9 mRNA decay.

Tsung-Ming Chen, Chien-Hui Hsu, Shaw-Jenq Tsai, H Sunny Sun

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Effect of lentivirus-mediated miR-182 targeting FGF9 on hallux valgus.International journal of medical sciences · 2021
    Article
  5. AUF1 regulation of coding and noncoding RNA.Wiley interdisciplinary reviews. RNA · 2017
    Review
  6. Review
  7. Hallmarks of cancer and AU-rich elements.Wiley interdisciplinary reviews. RNA · 2017
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
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

4 authors at 3 institutions in 3 countries.

Tsung-Ming ChenInstitute of Basic Medical Sciences, National Cheng Kung University Medical College, Tainan, Taiwan.
Chien-Hui Hsu
Shaw-Jenq Tsai
H Sunny Sun
National Cheng Kung University · TWInstitute of Basic Medical Sciences of the Chinese Academy of Medical SciencesInstitute of Molecular Medicine · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor 9 (FGF9) is an autocrine/paracrine growth factor that plays vital roles in many physiologic processes including embryonic development. Aberrant expression of FGF9 causes human diseases and thus it highlights the importance of controlling FGF9 expression; however, the mechanism responsible for regulation of FGF9 expression is largely unknown. Here, we show the crucial role of an AU-rich element (ARE) in FGF9 3'-untranslated region (UTR) on controlling FGF9 expression. Our data demonstrated that AUF1 binds to this ARE to regulate FGF9 mRNA stability. Overexpression of each isoform of AUF1 (p37, p40, p42 and p45) showed that only the p42 isoform reduced the steady-state FGF9 mRNA. Also, knockdown of p42(AUF1) prolonged the half-life of FGF9 mRNA. The induction of FGF9 mRNA in prostaglandin (PG) E(2)-treated human endometrial stromal cells was accompanied with declined cytoplasmic AUF1. Nevertheless, ablation of AUF1 led to sustained elevation of FGF9 expression in these cells. Our study demonstrated that p42(AUF1) regulates both steady-state and PGE(2)-induced FGF9 mRNA stability through ARE-mediated mRNA degradation. Since almost half of the FGF family members are ARE-containing genes, our findings also suggest that ARE-mediated mRNA decay is a common pathway to control FGFs expression, and it represents a novel RNA regulon to coordinate FGFs homeostasis in various physiological conditions.

Indexed as

3' Untranslated RegionsAdenineBase SequenceBinding SitesDinoprostoneFibroblast Growth Factor 9HEK293 CellsHeterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HumansMolecular Sequence DataProtein IsoformsRNA InterferenceRNA, MessengerRNA StabilityUracil3' Untranslated RegionsAdenineDinoprostoneFGF9 protein, humanFibroblast Growth Factor 9Heterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HNRNPD protein, humanProtein IsoformsRNA, MessengerUracil

Identifiers

PMID20716519
PMCPMC3001084
OpenAlexW2156933957

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Registered trials

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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.