Evidence map›Paper›PMID 24860983›Full record

ArticleThe FEBS journal2014

Muscle lim protein isoform negatively regulates striated muscle actin dynamics and differentiation.

Elizabeth Vafiadaki, Demetrios A Arvanitis, Vasiliki Papalouka, Gerasimos Terzis, Theodoros I Roumeliotis, Konstantinos Spengos, Spiros D Garbis, Panagiota Manta, Evangelia G Kranias, Despina Sanoudou

Open access · bronzeAbstract read
In one paragraph

Article in The FEBS journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Genomics of pediatric cardiomyopathy.Pediatric research · 2025
    Review
  3. Article
  4. Role of Muscle LIM Protein in Mechanotransduction Process.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Article
  7. Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Slow-twitch skeletal muscle defects accompany cardiac dysfunction in transgenic mice with a mutation in the myosin regulatory light chain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  17. Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017
    Review
  18. Article
  19. Review
  20. 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

10 authors at 3 institutions in 3 countries.

Elizabeth VafiadakiMolecular Biology Division, Biomedical Research Foundation of the Academy of Athens, Greece.
Demetrios A Arvanitis
Vasiliki Papalouka
Gerasimos Terzis
Theodoros I Roumeliotis
Konstantinos Spengos
Spiros D Garbis
Panagiota Manta
Evangelia G Kranias
Despina Sanoudou
Biomedical Research Foundation of the Academy of Athens · GRNational and Kapodistrian University of Athens · GRAcademy of Athens · GR

Funding

Cardiac Sarcoplasmic Reticulum Calcium Cycling ProteinsR01HL064018 · NHLBI · UNIVERSITY OF CINCINNATI · PI KRANIAS, EVANGELIA G · 2000 to 2017
$6.8M
TARGETED ABLATION AND ALTERATION OF MOUSE PHOSPHOLAMBANR01HL026057 · NHLBI · UNIVERSITY OF CINCINNATI · PI KRANIAS, EVANGELIA G · 1985 to 2017
$5.3M
NHLBI NIH HHS R01 HL026057NHLBI NIH HHS R01 HL064018
6 · The paper itself

Abstract

Muscle lim protein (MLP) has emerged as a critical regulator of striated muscle physiology and pathophysiology. Mutations in cysteine and glycine-rich protein 3 (CSRP3), the gene encoding MLP, have been directly associated with human cardiomyopathies, whereas aberrant expression patterns are reported in human cardiac and skeletal muscle diseases. Increasing evidence suggests that MLP has an important role in both myogenic differentiation and myocyte cytoarchitecture, although the full spectrum of its intracellular roles has not been delineated. We report the discovery of an alternative splice variant of MLP, designated as MLP-b, showing distinct expression in neuromuscular disease and direct roles in actin dynamics and muscle differentiation. This novel isoform originates by alternative splicing of exons 3 and 4. At the protein level, it contains the N-terminus first half LIM domain of MLP and a unique sequence of 22 amino acids. Physiologically, it is expressed during early differentiation, whereas its overexpression reduces C2C12 differentiation and myotube formation. This may be mediated through its inhibition of MLP/cofilin-2-mediated F-actin dynamics. In differentiated striated muscles, MLP-b localizes to the sarcomeres and binds directly to Z-disc components, including α-actinin, T-cap and MLP. The findings of the present study unveil a novel player in muscle physiology and pathophysiology that is implicated in myogenesis as a negative regulator of myotube formation, as well as in differentiated striated muscles as a contributor to sarcomeric integrity.

Indexed as

ActinsAlternative SplicingAmino Acid SequenceAnimalsCell DifferentiationCell LineHumansLIM Domain ProteinsMiceMuscle DevelopmentMuscle ProteinsMuscle, SkeletalMuscle, StriatedMyoblastsNeuromuscular DiseasesProtein IsoformsActinscysteine and glycine-rich protein 3LIM Domain ProteinsMuscle ProteinsProtein IsoformsisoformMLPmyotube differentiationsarcomereskeletal myopathy

Identifiers

PMID24860983
PMCPMC4416226
OpenAlexW2063779850

What OpenQuestion holds

Textmetadata
LicenceTDM
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.