Evidence map›Paper›PMID 32960481›Full record

ArticleThe EMBO journal2020

Linc-MYH configures INO80 to regulate muscle stem cell numbers and skeletal muscle hypertrophy.

Christian Schutt, Alix Hallmann, Salma Hachim, Ina Klockner, Melissa Valussi, Ann Atzberger, Johannes Graumann, Thomas Braun, Thomas Boettger

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2020. 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
1.7field-weighted citation impact, top 16% 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, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Delivery of A Chemically Modified Noncoding RNA Domain Improves Dystrophic Myotube Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  5. Article
  6. Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
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  16. Article
  17. Article
  18. Article
  19. Article
  20. Nucleolar stress: Friend or foe in cardiac function?Frontiers in cardiovascular medicine · 2022
    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

9 authors at 1 institution in 1 country.

Christian SchuttDepartment of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.
Alix HallmannDepartment of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.
Salma HachimDepartment of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.
Ina KlocknerDepartment of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.
Melissa ValussiDepartment of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.
Ann AtzbergerMax Planck Institute for Heart- and Lung Research, FACS Service Group, Bad Nauheim, Germany.
Johannes GraumannMax Planck Institute for Heart- and Lung Research, Mass Spectrometry Service Group, Bad Nauheim, Germany.ORCID 0000-0002-3015-5850
Thomas BraunDepartment of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.ORCID 0000-0002-6165-4804
Thomas BoettgerDepartment of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.ORCID 0000-0003-4280-8449
Max Planck Institute for Heart and Lung Research · DE

Funding

Deutsche Forschungsgemeinschaft (DFG) RTG2355Deutsche Forschungsgemeinschaft (DFG) TRR267Deutsche Forschungsgemeinschaft (DFG) TRR81Loewe Network Medical RNomicsMax-Planck-Gesellschaft (MPG)
6 · The paper itself

Abstract

Chromatin remodeling complexes have functions in transcriptional regulation and chromosome maintenance, but it is mostly unknown how the function of these normally ubiquitous complexes is specified in the cellular context. Here, we describe that the evolutionary conserved long non-coding RNA linc-MYH regulates the composition of the INO80 chromatin remodeler complex in muscle stem cells and prevents interaction with WDR5 and the transcription factor YY1. Linc-MYH acts as a selective molecular switch in trans that governs the pro-proliferative function of the ubiquitous INO80 complex but does not affect its role in maintaining genomic stability. The molecular switch is essential for restricting generation of quiescent MuSCs and proliferation of myoblasts in homeostasis and regeneration. Since linc-MYH is expressed in proliferating myoblasts but not in quiescent MuSCs, we reason that the extent of myoblast proliferation has decisive effects on the size of the quiescent MuSC pool.

Indexed as

AnimalsATPases Associated with Diverse Cellular ActivitiesCell ProliferationChromatinDNA-Binding ProteinsDNA GlycosylasesEpigenomicsGene Expression Regulation, EnzymologicHumansHypertrophyMaleMiceMice, KnockoutMuscle, SkeletalMyoblastsRegenerationATPases Associated with Diverse Cellular ActivitiesChromatinDNA-Binding ProteinsDNA GlycosylasesINO80 protein, humanINO80 protein, mousemutY adenine glycosylaseRNA, Long NoncodingRNA, UntranslatedYy1 protein, mouseYY1 Transcription FactorChromatin remodelerlincRNAmuscle stem cell proliferationnon-coding RNA functionsatellite cell

Identifiers

PMID32960481
PMCPMC7667881
OpenAlexW3087253861

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.