Evidence map›Paper›PMID 19644446›Full record

ArticleThe EMBO journal2009

Bipartite functions of the CREB co-activators selectively direct alternative splicing or transcriptional activation.

Antonio L Amelio, Massimo Caputi, Michael D Conkright

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Regulation ofInternational journal of molecular sciences · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. What turns CREB on? And off? And why does it matter?Cellular and molecular life sciences : CMLS · 2020
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. CRTC1/MAML2 gain-of-function interactions with MYC create a gene signature predictive of cancers with CREB-MYC involvement.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  16. Review
  17. Article
  18. Alternative splicing of human papillomavirus type-16 E6/E6* early mRNA is coupled to EGF signaling via Erk1/2 activation.Proceedings of the National Academy of Sciences of the United States of America · 2010
    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

3 authors at 2 institutions in 1 country.

Antonio L AmelioDepartment of Cancer Biology, The Scripps Research Institute, Scripps Florida, Jupiter, FL 33458, USA.
Massimo Caputi
Michael D Conkright
Scripps Research Institute · USFlorida Atlantic University · US

Funding

TORC2-dependent regulation of gluconeogensisR01DK081491 · NIDDK · SCRIPPS RESEARCH INSTITUTE, THE · PI CONKRIGHT, MICHAEL DALE · 2008 to 2012
$2.0M
Characterizing the Role of MYC-MAX Complexes in TORC1/MAML2-mediated OncogenesisF32CA134121 · NCI · SCRIPPS FLORIDA · PI AMELIO, ANTONIO LUIGI · 2008 to 2010
$155k
NCI NIH HHS CA134121NCI NIH HHS F32 CA134121NIDDK NIH HHS R01 DK081491
6 · The paper itself

Abstract

The CREB regulated transcription co-activators (CRTCs) regulate many biological processes by integrating and converting environmental inputs into transcriptional responses. Although the mechanisms by which CRTCs sense cellular signals are characterized, little is known regarding how CRTCs contribute to the regulation of cAMP inducible genes. Here we show that these dynamic regulators, unlike other co-activators, independently direct either pre-mRNA splice-site selection or transcriptional activation depending on the cell type or promoter context. Moreover, in other scenarios, the CRTC co-activators coordinately regulate transcription and splicing. Mutational analyses showed that CRTCs possess distinct functional domains responsible for regulating either pre-mRNA splicing or transcriptional activation. Interestingly, the CRTC1-MAML2 oncoprotein lacks the splicing domain and is incapable of altering splice-site selection despite robustly activating transcription. The differential usage of these distinct domains allows CRTCs to selectively mediate multiple facets of gene regulation, indicating that co-activators are not solely restricted to coordinating alternative splicing with increase in transcriptional activity.

Indexed as

Alternative SplicingTranscriptional ActivationAdenoviridaeAnimalsCell Line, TumorCyclic AMP Response Element-Binding ProteinDNA Mutational AnalysisGene Expression RegulationHepatocytesHumansModels, BiologicalRatsRNA, MessengerRNA SplicingTranscription, GeneticCyclic AMP Response Element-Binding ProteinRNA, Messenger

Identifiers

PMID19644446
PMCPMC2750025
OpenAlexW2106285571

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.