Evidence map›Paper›PMID 29269871›Full record

ArticleScientific reports2017

CRTC1 mediates preferential transcription at neuronal activity-regulated CRE/TATA promoters.

Arnaldo Parra-Damas, Laura Rubió-Ferrarons, Jie Shen, Carlos A Saura

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. AlteredeNeuro · 2026
    Article
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  3. AlteredbioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Regulation ofInternational journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. S-Nitrosylation of CRTC1 in Alzheimer's disease impairs CREB-dependent gene expression induced by neuronal activity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Integration of nuclear CaCellular and molecular life sciences : CMLS · 2023
    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

4 authors at 3 institutions in 2 countries.

Arnaldo Parra-DamasInstitut de Neurociències, Department de Bioquímica i Biologia Molecular, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, Barcelona, 08193, Spain.
Laura Rubió-FerraronsInstitut de Neurociències, Department de Bioquímica i Biologia Molecular, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, Barcelona, 08193, Spain.
Jie ShenCenter for Neurologic Diseases, Department of Neurology, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Carlos A SauraInstitut de Neurociències, Department de Bioquímica i Biologia Molecular, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, Barcelona, 08193, Spain. carlos.saura@uab.es.
Universitat Autònoma de Barcelona · ESCentro de Investigación Biomédica en Red · ESHarvard University · US

Funding

Role of Presenilins in the SynapseR01NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI Jie Shen · 2001 to 2026
$10.6M
Presenilin and APP in the BrainRF1NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2021 to 2021
$2.7M
NINDS NIH HHS R01 NS041783NINDS NIH HHS RF1 NS041783
6 · The paper itself

Abstract

Gene expression mediated by the transcription factor cAMP-responsive element-binding protein (CREB) is essential for a wide range of brain processes. The transcriptional coactivartor CREB-regulated transcription coactivator-1 (CRTC1) is required for efficient induction of CREB target genes during neuronal activity. However, the mechanisms regulating induction of specific CREB/CRTC1-dependent genes during neuronal activity remain largely unclear. Here, we investigated the molecular mechanisms regulating activity-dependent gene transcription upon activation of the CREB/CRTC1 signaling pathway in neurons. Depolarization and cAMP signals induce preferential transcription of activity-dependent genes containing promoters with proximal CRE/TATA sequences, such as c-fos, Dusp1, Nr4a1, Nr4a2 and Ptgs2, but not genes with proximal CRE/TATA-less promoters (e.g. Nr4a3, Presenilin-1 and Presenilin-2). Notably, biochemical and chromatin immunoprecipitation analyses reveal constitutive binding of CREB to target gene promoters in the absence of neuronal activity, whereas recruitment of CRTC1 to proximal CRE/TATA promoters depends on neuronal activity. Neuronal activity induces rapid CRTC1 dephosphorylation, nuclear translocation and binding to endogenous CREB. These results indicate that neuronal activity induces a preferential binding of CRTC1 to the transcriptional complex in CRE/TATA-containing promoters to engage activity-dependent transcription in neurons.

Indexed as

Promoter Regions, GeneticTranscription, GeneticAnimalsBrainCyclic AMP Response Element-Binding ProteinGene Expression RegulationMiceNeuronsTranscription FactorsCreb1 protein, mouseCrtc1 protein, mouseCyclic AMP Response Element-Binding ProteinTranscription Factors

Identifiers

PMID29269871
PMCPMC5740062
OpenAlexW2771163889

What OpenQuestion holds

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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.