Evidence map›Paper›PMID 18319260›Full record

ArticleThe Journal of biological chemistry2008

GLI2-specific transcriptional activation of the bone morphogenetic protein/activin antagonist follistatin in human epidermal cells.

Thomas Eichberger, Alexandra Kaser, Claudia Pixner, Carmen Schmid, Stefan Klingler, Martina Winklmayr, Cornelia Hauser-Kronberger, Fritz Aberger, Anna-Maria Frischauf

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. 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
1.8field-weighted citation impact, top 16% 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, 38 citations in OpenAlex.

  1. Article
  2. STAT3 Partly Inhibits Cell ProliferationFrontiers in genetics · 2021
    Article
  3. Review
  4. Article
  5. Conserved role of Sonic Hedgehog in tonotopic organization of the avian basilar papilla and mammalian cochlea.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  6. Low-affinity transcription factor binding sites shape morphogen responses and enhancer evolution.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. [Basal cell carcinoma and stem cell markers : Contribution to possible histogenesis?].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2011
    Review
  14. The hedgehog/Gli signaling paradigm in prostate cancer.Expert review of endocrinology & metabolism · 2011
    Article
  15. Article
  16. Hedgehog signaling and gastrointestinal cancer.Biochimica et biophysica acta · 2010
    Review
  17. Article
  18. Article
  19. Article
  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

9 authors at 2 institutions in 1 country.

Thomas EichbergerDepartment of Molecular Biology, University of Salzburg, Hellbrunnerstrasse 34, Austria.
Alexandra Kaser
Claudia Pixner
Carmen Schmid
Stefan Klingler
Martina Winklmayr
Cornelia Hauser-Kronberger
Fritz Aberger
Anna-Maria Frischauf
University of Salzburg · ATParacelsus Medical University · AT

Funding

Austrian Science Fund FWF P 16518
6 · The paper itself

Abstract

Hedgehog (HH) signaling in the epidermis is primarily mediated by the zinc finger transcription factors GLI1 and GLI2. Exquisite regulation of HH/GLI signaling is crucial for proper specification of the epidermal lineage and development of its derivatives, whereas dysregulation of HH/GLI signaling disrupts tissue homeostasis and causes basal cell carcinoma (BCC). Similarly, bone morphogenetic proteins (BMPs) and activins have been described as key signaling factors in the complex regulation of epidermal fate decisions, although their precise interplay with HH/GLI is largely elusive. Here we show that, in human epidermal cells, expression of the activin/BMP antagonist follistatin (FST) is predominantly up-regulated by the HH effector GLI2. Consistently, we found strong FST expression in the outer root sheath of human hair follicles and BCC. Detailed promoter analysis showed that two sequences with homology to the GLI consensus binding site are required for GLI2-mediated activation. Interestingly, activation of the FST promoter is highly GLI2-specific, because neither GLI1 nor GLI3 can significantly increase FST transcription. GLI2 specificity requires the presence of a 518-bp fragment in the proximal FST promoter region. On the protein level, sequences C-terminal to the zinc finger are responsible for GLI2-specific activation of FST transcription, pointing to the existence of GLI-interacting cofactors that modulate GLI target specificity. Our results reveal a key role of GLI2 in activation of the activin/BMP antagonist FST in response to HH signaling and provide new evidence for a regulatory interaction between HH and activin/BMP signaling in hair follicle development and BCC.

Indexed as

Epidermal CellsTranscriptional ActivationActivinsAnimalsBasal Cell CarcinomaBase SequenceBinding SitesBone Morphogenetic Protein 4Bone Morphogenetic ProteinsCells, CulturedEpidermisFollistatinGene Expression Regulation, NeoplasticHair FollicleHumansKeratinocytesActivinsBMP4 protein, humanBmp4 protein, mouseBone Morphogenetic Protein 4Bone Morphogenetic ProteinsFollistatinGLI2 protein, humanKruppel-Like Transcription FactorsNuclear ProteinsRNA, MessengerZinc Finger Protein Gli2

Identifiers

PMID18319260
PMCPMC2430996
OpenAlexW1990996419

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.