Evidence map›Paper›PMID 35676269›Full record

ArticleNature communications2022

Control of CRK-RAC1 activity by the miR-1/206/133 miRNA family is essential for neuromuscular junction function.

Ina Klockner, Christian Schutt, Theresa Gerhardt, Thomas Boettger, Thomas Braun

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024
    Review
  12. Review
  13. Genes · 2023
    Review
  14. NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023
    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

5 authors at 1 institution in 1 country.

Ina KlocknerMax Planck Institute for Heart- and Lung Research, Department of Cardiac Development and Remodelling, Ludwigstr. 43, D-61231, Bad Nauheim, Germany.
Christian SchuttMax Planck Institute for Heart- and Lung Research, Department of Cardiac Development and Remodelling, Ludwigstr. 43, D-61231, Bad Nauheim, Germany.
Theresa GerhardtMax Planck Institute for Heart- and Lung Research, Department of Cardiac Development and Remodelling, Ludwigstr. 43, D-61231, Bad Nauheim, Germany.
Thomas BoettgerMax Planck Institute for Heart- and Lung Research, Department of Cardiac Development and Remodelling, Ludwigstr. 43, D-61231, Bad Nauheim, Germany. thomas.boettger@mpi-bn.mpg.de.ORCID 0000-0003-4280-8449
Thomas BraunMax Planck Institute for Heart- and Lung Research, Department of Cardiac Development and Remodelling, Ludwigstr. 43, D-61231, Bad Nauheim, Germany. thomas.braun@mpi-bn.mpg.de.ORCID 0000-0002-6165-4804
Max Planck Institute for Heart and Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Formation and maintenance of neuromuscular junctions (NMJs) are essential for skeletal muscle function, allowing voluntary movements and maintenance of the muscle tone, thereby preventing atrophy. Generation of NMJs depends on the interaction of motor neurons with skeletal muscle fibers, which initiates a cascade of regulatory events that is essential for patterning of acetylcholine receptor (AChR) clusters at specific sites of the sarcolemma. Here, we show that muscle-specific miRNAs of the miR-1/206/133 family are crucial regulators of a signaling cascade comprising DOK7-CRK-RAC1, which is critical for stabilization and anchoring of postsynaptic AChRs during NMJ development and maintenance. We describe that posttranscriptional repression of CRK by miR-1/206/133 is essential for balanced activation of RAC1. Failure to adjust RAC1 activity severely compromises NMJ function, causing respiratory failure in neonates and neuromuscular symptoms in adult mice. We conclude that miR-1/206/133 serve a specific function for NMJs but are dispensable for skeletal muscle development.

Indexed as

MicroRNAsAnimalsMiceMuscle Fibers, SkeletalMuscle, SkeletalNeuromuscular JunctionProto-Oncogene Proteins c-crkReceptors, CholinergicCrk protein, mouseMicroRNAsProto-Oncogene Proteins c-crkReceptors, Cholinergic

Identifiers

PMID35676269
PMCPMC9178026
OpenAlexW4281963899

What OpenQuestion holds

Textmetadata
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.