Evidence map›Paper›PMID 27307584›Full record

ArticleMolecular biology of the cell2016

The N-terminal tropomyosin- and actin-binding sites are important for leiomodin 2's function.

Thu Ly, Natalia Moroz, Christopher T Pappas, Stefanie M Novak, Dmitri Tolkatchev, Dayton Wooldridge, Rachel M Mayfield, Gregory Helms, Carol C Gregorio, Alla S Kostyukova

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Localization and functional exploration of leiomodin-2's C-terminal binding sites.Biochimica et biophysica acta. Proteins and proteomics · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. CaProtein science : a publication of the Protein Society · 2022
    Article
  8. The Mechanisms of Thin Filament Assembly and Length Regulation in Muscles.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Role of intrinsic disorder in muscle sarcomeres.Progress in molecular biology and translational science · 2019
    Review
  16. Article
  17. Structural destabilization of tropomyosin induced by the cardiomyopathy-linked mutation R21H.Protein science : a publication of the Protein Society · 2018
    Article
  18. Article
  19. Article
  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 2 institutions in 1 country.

Thu LyVoiland School of Chemical Engineering and Bioengineering, Washington State University, Pullman, WA 99164-6515.
Natalia MorozVoiland School of Chemical Engineering and Bioengineering, Washington State University, Pullman, WA 99164-6515.
Christopher T PappasDepartment of Cellular and Molecular Medicine, Sarver Molecular Cardiovascular Research Program, University of Arizona, Tucson, AZ 85721.
Stefanie M NovakDepartment of Cellular and Molecular Medicine, Sarver Molecular Cardiovascular Research Program, University of Arizona, Tucson, AZ 85721.
Dmitri TolkatchevVoiland School of Chemical Engineering and Bioengineering, Washington State University, Pullman, WA 99164-6515.
Dayton WooldridgeVoiland School of Chemical Engineering and Bioengineering, Washington State University, Pullman, WA 99164-6515.
Rachel M MayfieldDepartment of Cellular and Molecular Medicine, Sarver Molecular Cardiovascular Research Program, University of Arizona, Tucson, AZ 85721.
Gregory HelmsCenter for NMR Spectroscopy, Washington State University, Pullman, WA 99164-4630.
Carol C GregorioDepartment of Cellular and Molecular Medicine, Sarver Molecular Cardiovascular Research Program, University of Arizona, Tucson, AZ 85721.
Alla S KostyukovaVoiland School of Chemical Engineering and Bioengineering, Washington State University, Pullman, WA 99164-6515 alla.kostyukova@wsu.edu.
Washington State University · USUniversity of Arizona · US

Funding

TRAINING IN BIOTECHNOLOGY: EMPHASIS ON PROTEIN CHEMISTRYT32GM008336 · NIGMS · WASHINGTON STATE UNIVERSITY · PI CALL, DOUGLAS R. · 1989 to 2023
$8.9M
Deciphering the role of Lmod2 in thin filament length regulation and dilated cardiomyopathyR01HL123078 · NHLBI · UNIVERSITY OF ARIZONA · PI Carol C Gregorio, Shashank Shekhar · 2015 to 2026
$5.6M
Deciphering the role of the RNA-binding protein, FXR1, in cardiac muscle assemblyR01HL108625 · NHLBI · UNIVERSITY OF ARIZONA · PI GREGORIO, CAROL C · 2012 to 2015
$1.9M
Factors influencing regulation of the dynamics of the actin filament pointed endR01GM081688 · NIGMS · WASHINGTON STATE UNIVERSITY · PI KOSTYUKOVA, ALLA S. · 2009 to 2013
$1.6M
Determining the role of Fragile X proteins in the heartF31HL117520 · NHLBI · UNIVERSITY OF ARIZONA · PI NOVAK, STEFANIE · 2013 to 2016
$134k
NHLBI NIH HHS F31 HL117520NHLBI NIH HHS R01 HL108625NHLBI NIH HHS R01 HL123078NIGMS NIH HHS R01 GM081688NIGMS NIH HHS T32 GM008336
6 · The paper itself

Abstract

Leiomodin is a potent actin nucleator related to tropomodulin, a capping protein localized at the pointed end of the thin filaments. Mutations in leiomodin-3 are associated with lethal nemaline myopathy in humans, and leiomodin-2-knockout mice present with dilated cardiomyopathy. The arrangement of the N-terminal actin- and tropomyosin-binding sites in leiomodin is contradictory and functionally not well understood. Using one-dimensional nuclear magnetic resonance and the pointed-end actin polymerization assay, we find that leiomodin-2, a major cardiac isoform, has an N-terminal actin-binding site located within residues 43-90. Moreover, for the first time, we obtain evidence that there are additional interactions with actin within residues 124-201. Here we establish that leiomodin interacts with only one tropomyosin molecule, and this is the only site of interaction between leiomodin and tropomyosin. Introduction of mutations in both actin- and tropomyosin-binding sites of leiomodin affected its localization at the pointed ends of the thin filaments in cardiomyocytes. On the basis of our new findings, we propose a model in which leiomodin regulates actin poly-merization dynamics in myocytes by acting as a leaky cap at thin filament pointed ends.

Indexed as

Actin CytoskeletonActinsAmino Acid SequenceAnimalsBinding SitesCarrier ProteinsChickensCytoskeletal ProteinsMiceMicrofilament ProteinsMuscle ProteinsMyocytes, CardiacProtein BindingProtein DomainsSarcomeresTropomodulinActinsCarrier ProteinsCytoskeletal Proteinsleiomodin protein, mouseMicrofilament ProteinsMuscle ProteinsTropomodulinTropomyosin

Identifiers

PMID27307584
PMCPMC4985258
OpenAlexW2423246202

What OpenQuestion holds

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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.