Evidence map›Paper›PMID 25081566›Full record

ArticleGenetics2014

Galactokinase is a novel modifier of calcineurin-induced cardiomyopathy in Drosophila.

Teresa E Lee, Lin Yu, Matthew J Wolf, Howard A Rockman

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Attention LSTM U-Net model forBiomedical optics express · 2024
    Article
  4. Article
  5. Analysis ofAmerican journal of physiology. Heart and circulatory physiology · 2022
    Article
  6. Reduced CardiacCirculation. Cardiovascular genetics · 2017
    Article
  7. Article
  8. Review
  9. Drosophila melanogaster Models of Galactosemia.Current topics in developmental biology · 2017
    Review
  10. Journal of cardiovascular development and disease · 2016
    Review
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 1 institution in 1 country.

Teresa E LeeDepartment of Cell Biology, Duke University, Durham, North Carolina 27710.
Lin YuDepartment of Medicine, Duke University, Durham, North Carolina 27710.
Matthew J WolfDepartment of Medicine, Duke University, Durham, North Carolina 27710 Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina 27710.
Howard A RockmanDepartment of Cell Biology, Duke University, Durham, North Carolina 27710 Department of Medicine, Duke University, Durham, North Carolina 27710 Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina 27710 h.rockman@duke.edu.
Duke University · US

Funding

Identifying Cardiomyopathy Genes in Mice and DrosophilaR01HL083065 · NHLBI · DUKE UNIVERSITY · PI ROCKMAN, HOWARD A · 2006 to 2014
$3.5M
Novel pathways modulating Raf-mediated cardiac hypertrophyR01HL116581 · NHLBI · UNIVERSITY OF VIRGINIA · PI WOLF, MATTHEW J · 2013 to 2017
$2.0M
NHLBI NIH HHS HL083065NHLBI NIH HHS HL116581NHLBI NIH HHS R01 HL083065NHLBI NIH HHS R01 HL116581
6 · The paper itself

Abstract

Activated/uninhibited calcineurin is both necessary and sufficient to induce cardiac hypertrophy, a condition that often leads to dilated cardiomyopathy, heart failure, and sudden cardiac death. We expressed constitutively active calcineurin in the adult heart of Drosophila melanogaster and identified enlarged cardiac chamber dimensions and reduced cardiac contractility. In addition, expressing constitutively active calcineurin in the fly heart using the Gal4/UAS system induced an increase in heart wall thickness. We performed a targeted genetic screen for modifiers of calcineurin-induced cardiac enlargement based on previous calcineurin studies in the fly and identified galactokinase as a novel modifier of calcineurin-induced cardiomyopathy. Genomic deficiencies spanning the galactokinase locus, transposable elements that disrupt galactokinase, and cardiac-specific RNAi knockdown of galactokinase suppressed constitutively active calcineurin-induced cardiomyopathy. In addition, in flies expressing constitutively active calcineurin using the Gal4/UAS system, a transposable element in galactokinase suppressed the increase in heart wall thickness. Finally, genetic disruption of galactokinase suppressed calcineurin-induced wing vein abnormalities. Collectively, we generated a model for discovering novel modifiers of calcineurin-induced cardiac enlargement in the fly and identified galactokinase as a previously unknown regulator of calcineurin-induced cardiomyopathy in adult Drosophila.

Indexed as

AnimalsCalcineurinCardiomyopathy, DilatedDrosophila melanogasterDrosophila ProteinsFemaleGalactokinaseMaleMembrane ProteinsMyocardiumCalcineurinDrosophila ProteinsGalactokinaseMembrane Proteinstinc protein, DrosophilacalcineurincardiomyopathyDrosophila melanogastergalactokinase

Identifiers

PMID25081566
PMCPMC4196615
OpenAlexW2044788046

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.