Evidence map›Paper›PMID 25349259›Full record

ArticleThe Journal of cell biology2014

CLUH regulates mitochondrial biogenesis by binding mRNAs of nuclear-encoded mitochondrial proteins.

Jie Gao, Désirée Schatton, Paola Martinelli, Henriette Hansen, David Pla-Martin, Esther Barth, Christian Becker, Janine Altmueller, Peter Frommolt, Marco Sardiello and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

85 citing papers in PubMed, 155 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. TheProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. RNA-binding proteins as versatile metabolic regulators.npj metabolic health and disease · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Elimination of virus-like particles reduces protein aggregation and extends replicative lifespan inProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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

11 authors at 5 institutions in 3 countries.

Jie GaoInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany Institute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany.
Désirée SchattonInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany.
Paola MartinelliInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany.
Henriette HansenInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany.
David Pla-MartinInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany.
Esther BarthInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany.
Christian BeckerInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany.
Janine AltmuellerInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany.
Peter FrommoltInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany.
Marco SardielloDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030 Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030.
Elena I RugarliInstitute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany Institute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany Institute for Genetics, Center for Molecular Medicine, Cologne Center for Genomics, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50923 Cologne, Germany Elena.Rugarli@uni-koeln.de.
Institute of Genetics · HUCenter for Molecular Medicine and Immunology · USCologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DEBaylor College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial function requires coordination of two genomes for protein biogenesis, efficient quality control mechanisms, and appropriate distribution of the organelles within the cell. How these mechanisms are integrated is currently not understood. Loss of the Clu1/CluA homologue (CLUH) gene led to clustering of the mitochondrial network by an unknown mechanism. We find that CLUH is coregulated both with genes encoding mitochondrial proteins and with genes involved in ribosomal biogenesis and translation. Our functional analysis identifies CLUH as a cytosolic messenger ribonucleic acid (RNA; mRNA)-binding protein. RNA immunoprecipitation experiments followed by next-generation sequencing demonstrated that CLUH specifically binds a subset of mRNAs encoding mitochondrial proteins. CLUH depletion decreased the levels of proteins translated by target transcripts and caused mitochondrial clustering. A fraction of CLUH colocalizes with tyrosinated tubulin and can be detected close to mitochondria, suggesting a role in regulating transport or translation of target transcripts close to mitochondria. Our data unravel a novel mechanism linking mitochondrial biogenesis and distribution.

Indexed as

AnimalsChlorocebus aethiopsCOS CellsGene Expression RegulationMiceMitochondriaMitochondrial ProteinsProtein BiosynthesisRNA-Binding ProteinsRNA, MessengerTubulinMitochondrial ProteinsRNA-Binding ProteinsRNA, MessengerTubulin

Identifiers

PMID25349259
PMCPMC4210445
OpenAlexW2119762929

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.