Evidence map›Paper›PMID 27759042›Full record

ArticleScientific reports2016

Neonatal cardiac dysfunction and transcriptome changes caused by the absence of Celf1.

Jimena Giudice, Zheng Xia, Wei Li, Thomas A Cooper

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Epitranscriptomics of cardiovascular diseases (Review).International journal of molecular medicine · 2022
    Review
  8. Article
  9. RNA-Binding Proteins in Pulmonary Hypertension.International journal of molecular sciences · 2020
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Correction of GSK3β at young age prevents muscle pathology in mice with myotonic dystrophy type 1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  15. Review
  16. Article
  17. 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 2 institutions in 1 country.

Jimena GiudiceDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, TX, 77030, USA.
Zheng XiaDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, 77030, USA.
Wei LiDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, 77030, USA.
Thomas A CooperDepartment of Pathology and Immunology, Baylor College of Medicine, Houston, TX, 77030, USA.
Baylor College of Medicine · USUniversity of North Carolina at Chapel Hill · US

Funding

Consortium for Broad Based Disease Phenotyping of Knockout MiceU54HG006348 · NHGRI · BAYLOR COLLEGE OF MEDICINE · PI BEAUDET, ARTHUR L., PAYLOR, RICHARD E · 2011 to 2015
$17.0M
MOLECULAR PATHOGENESIS OF MYOTONIC DYSTROPHYR01AR045653 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI COOPER, THOMAS A · 1999 to 2018
$8.3M
TROPONIN T ALTERNATIVE SPLICING IN EMBRYONIC HEARTR01HL045565 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI COOPER, THOMAS A · 1996 to 2018
$5.5M
Transcriptome processing networks in skeletal muscle: mechanisms and functionsR01AR060733 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI COOPER, THOMAS A · 2011 to 2023
$4.0M
Computational and Experimental Modeling of Alternative PolyadenylationR01CA193466 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI LI, WEI · 2016 to 2025
$3.3M
Computational and Experimental Modeling of Epigenetic DNA MethylationR01HG007538 · NHGRI · UNIVERSITY OF CALIFORNIA-IRVINE · PI LI, WEI · 2014 to 2018
$1.9M
NCI NIH HHS R01 CA193466NHGRI NIH HHS R01 HG007538NHGRI NIH HHS U54 HG006348NHLBI NIH HHS R01 HL045565NIAMS NIH HHS R01 AR045653NIAMS NIH HHS R01 AR060733
6 · The paper itself

Abstract

The RNA binding protein Celf1 regulates alternative splicing in the nucleus and mRNA stability and translation in the cytoplasm. Celf1 is strongly down-regulated during mouse postnatal heart development. Its re-induction in adults induced severe heart failure and reversion to fetal splicing and gene expression patterns. However, the impact of Celf1 depletion on cardiac transcriptional and posttranscriptional dynamics in neonates has not been addressed. We found that homozygous Celf1 knock-out neonates exhibited cardiac dysfunction not observed in older homozygous animals, although homozygous mice are smaller than wild type littermates throughout development. RNA-sequencing of mRNA from homozygous neonatal hearts identified a network of cell cycle genes significantly up-regulated and down-regulation of ion transport and circadian genes. Cell cycle genes are enriched for Celf1 binding sites supporting a regulatory role in mRNA stability of these transcripts. We also identified a cardiac splicing network coordinated by Celf1 depletion. Target events contain multiple Celf1 binding sites and enrichment in GU-rich motifs. Identification of direct Celf1 targets will advance our knowledge in the mechanisms behind developmental networks regulated by Celf1 and diseases where Celf1 is mis-regulated.

Indexed as

Alternative SplicingAnimalsAnimals, NewbornCELF1 ProteinCell CycleCircadian ClocksFemaleGene Expression RegulationHeartHeart DiseasesHeart FailureHumansIon TransportMaleMiceMice, 129 StrainCELF1 ProteinRNA, Messenger

Identifiers

PMID27759042
PMCPMC5069560
OpenAlexW2538606599

What OpenQuestion holds

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LicenceCC BY
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.