Evidence map›Paper›PMID 19219074›Full record

ArticleOncogene2009

Cooperation between GLI and JUN enhances transcription of JUN and selected GLI target genes.

S Laner-Plamberger, A Kaser, M Paulischta, C Hauser-Kronberger, T Eichberger, A M Frischauf

Abstract read
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In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

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  16. GLI1 upregulates C-JUN through a specific 130-kDa isoform.International journal of oncology · 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

6 authors at 2 institutions in 1 country.

S Laner-PlambergerDepartment of Molecular Biology, University of Salzburg, Salzburg, Austria.
A Kaser
M Paulischta
C Hauser-Kronberger
T Eichberger
A M Frischauf
University of Salzburg · ATParacelsus Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sustained Hedgehog (HH) signaling is implicated in basal cell carcinoma of the skin and other types of cancer. Here we show that GLI1 and GLI2, the main transcriptional activators of the HH pathway, directly regulate expression of the activator protein 1 (AP-1) family member JUN, a transcription factor controlling keratinocyte proliferation and skin homeostasis. Activation of the JUN promoter by GLI is dependent on a GLI-binding site and the AP-1 sites known to be involved in self-activation of JUN. Transcription of JUN is greatly enhanced in the presence of GLI and requires activated JUN protein. GLI2act is a more potent activator than GLI1 in these experiments and physical interaction with phosphorylated JUN was only detected for GLI2act. The synergistic effect of GLI and JUN extends to the activation of further GLI target genes as shown by shRNA-mediated knockdown of JUN in human keratinocytes. Some of these cooperatively activated genes are involved in cell-cycle progression, which is consistent with a significant reduction of the proliferative potential of GLI in the absence of JUN. These results suggest a novel connection between HH/GLI pathway activity and JUN, which may contribute to the oncogenic activity of HH/GLI signaling in skin.

Indexed as

Genes, cdcTranscription, GeneticBase SequenceBinding SitesCell ProliferationCells, CulturedHedgehog ProteinsHumansKeratinocytesPhosphorylationPromoter Regions, GeneticProtein BindingProtein KinasesProto-Oncogene Proteins c-junSignal TransductionTranscription FactorsGLI1 protein, humanHedgehog ProteinsProtein KinasesProto-Oncogene Proteins c-junTranscription FactorsZinc Finger Protein GLI1

Identifiers

PMID19219074
OpenAlexW1998299754

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.