Evidence map›Paper›PMID 26866591›Full record

ArticlePloS one2016

Identification of Targets of CUG-BP, Elav-Like Family Member 1 (CELF1) Regulation in Embryonic Heart Muscle.

Yotam Blech-Hermoni, Twishasri Dasgupta, Ryan J Coram, Andrea N Ladd

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  8. Article
  9. Epitranscriptomics of cardiovascular diseases (Review).International journal of molecular medicine · 2022
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. RNA-Binding Proteins in Pulmonary Hypertension.International journal of molecular sciences · 2020
    Review
  17. Review
  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

4 authors at 3 institutions in 1 country.

Yotam Blech-HermoniDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States of America.
Twishasri DasguptaDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States of America.
Ryan J CoramDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States of America.
Andrea N LaddDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, United States of America.
Cleveland Clinic Lerner College of Medicine · USCase Western Reserve University · USUniversity School · US

Funding

GRADUATE TRAINING IN CELLULAR AND MOLECULAR BIOLOGYT32GM008056 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI DIEHL, JOHN ALAN, SNIDER, MARTIN D · 1985 to 2019
$7.1M
Role of pre-mRNA alternative splicing programs in heart and muscle developmentR01HL089376 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI LADD, ANDREA NICOLE · 2009 to 2014
$1.7M
NHLBI NIH HHS R01 HL089376NHLBI NIH HHS R01HL089376NIGMS NIH HHS T32 GM008056
6 · The paper itself

Abstract

CUG-BP, Elav-like family member 1 (CELF1) is a highly conserved RNA binding protein that regulates pre-mRNA alternative splicing, polyadenylation, mRNA stability, and translation. In the heart, CELF1 is expressed in the myocardium, where its levels are tightly regulated during development. CELF1 levels peak in the heart during embryogenesis, and aberrant up-regulation of CELF1 in the adult heart has been implicated in cardiac pathogenesis in myotonic dystrophy type 1, as well as in diabetic cardiomyopathy. Either inhibition of CELF activity or over-expression of CELF1 in heart muscle causes cardiomyopathy in transgenic mice. Nonetheless, many of the cardiac targets of CELF1 regulation remain unknown. In this study, to identify cardiac targets of CELF1 we performed cross-linking immunoprecipitation (CLIP) for CELF1 from embryonic day 8 chicken hearts. We identified a previously unannotated exon in MYH7B as a novel target of CELF1-mediated regulation. We demonstrated that knockdown of CELF1 in primary chicken embryonic cardiomyocytes leads to increased inclusion of this exon and decreased MYH7B levels. We also investigated global changes in the transcriptome of primary embryonic cardiomyocytes following CELF1 knockdown in a published RNA-seq dataset. Pathway and network analyses identified strong associations between CELF1 and regulation of cell cycle and translation. Important regulatory proteins, including both RNA binding proteins and a cardiac transcription factor, were affected by loss of CELF1. Together, these data suggest that CELF1 is a key regulator of cardiomyocyte gene expression.

Indexed as

Gene Expression Regulation, DevelopmentalAlternative SplicingAnimalsAnimals, Genetically ModifiedCELF1 ProteinCell LineChick EmbryoCross-Linking ReagentsExonsHeartHumansImmunoprecipitationIntronsMiceMyocardiumMyocytes, CardiacCELF1 ProteinCELF1 protein, mouseCross-Linking ReagentsMyosin Heavy ChainsRNA-Binding ProteinsRNA Precursors

Identifiers

PMID26866591
PMCPMC4750973
OpenAlexW2269976823

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.