Evidence map›Paper›PMID 19164581›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

The coactivator CRTC1 promotes cell proliferation and transformation via AP-1.

Gianluca Canettieri, Sonia Coni, Michele Della Guardia, Valentina Nocerino, Laura Antonucci, Laura Di Magno, Robert Screaton, Isabella Screpanti, Giuseppe Giannini, Alberto Gulino

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

  1. Regulation of Sleep Amount by CRTC1 via Transcription ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Molecular Mechanisms of Carcinogenesis in Pediatric Airways Tumors.International journal of molecular sciences · 2023
    Review
  7. Contribution of the Transcription Factors Sp1/Sp3 and AP-1 toInternational journal of molecular sciences · 2021
    Article
  8. Article
  9. Article
  10. Targeting Notch and EGFR signaling in human mucoepidermoid carcinoma.Signal transduction and targeted therapy · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  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

10 authors at 2 institutions in 2 countries.

Gianluca CanettieriDepartment of Experimental Medicine and Pasteur Institute, Cenci Bolognetti Foundation, Sapienza University, Rome, Italy.
Sonia Coni
Michele Della Guardia
Valentina Nocerino
Laura Antonucci
Laura Di Magno
Robert Screaton
Isabella Screpanti
Giuseppe Giannini
Alberto Gulino
Istituto Pasteur · ITChildren's Hospital of Eastern Ontario · CA

Funding

Telethon GGP07118
6 · The paper itself

Abstract

Regulation of gene expression in response to mitogenic stimuli is a critical aspect underlying many forms of human cancers. The AP-1 complex mediates the transcriptional response to mitogens, and its deregulation causes developmental defects and tumors. We report that the coactivator CRTC1 cyclic AMP response element-binding protein (CREB)-regulated transcription coactivator 1 is a potent and indispensable modulator of AP-1 function. After exposure of cells to the AP-1 agonist 12-O-tetradecanoylphorbol-13-acetate (TPA), CRTC1 is recruited to AP-1 target gene promoters and associates with c-Jun and c-Fos to activate transcription. CRTC1 consistently synergizes with the proto-oncogene c-Jun to promote cellular growth, whereas AP-1-dependent proliferation is abrogated in CRTC1-deficient cells. Remarkably, we demonstrate that CRTC1-Maml2 oncoprotein, which causes mucoepidermoid carcinomas, binds and activates both c-Jun and c-Fos. Consequently, ablation of AP-1 function disrupts the cellular transformation and proliferation mediated by this oncogene. Together, these data illustrate a novel mechanism required to couple mitogenic signals to the AP-1 gene regulatory program.

Indexed as

Cell ProliferationCell Transformation, NeoplasticDNA-Binding ProteinsHeLa CellsHumansImmunoprecipitationNuclear ProteinsPromoter Regions, GeneticProto-Oncogene MasProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junReverse Transcriptase Polymerase Chain ReactionRNA InterferenceTetradecanoylphorbol AcetateTrans-ActivatorsTranscriptional ActivationCRTC1 protein, humanDNA-Binding ProteinsMAML2 protein, humanMAS1 protein, humanNuclear ProteinsProto-Oncogene MasProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junTetradecanoylphorbol AcetateTrans-ActivatorsTranscription Factor AP-1Transcription Factors

Identifiers

PMID19164581
PMCPMC2635810
OpenAlexW2013579158

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.