Evidence map›Paper›PMID 23644458›Full record

ArticleNature2013

Lamin A/C and emerin regulate MKL1-SRF activity by modulating actin dynamics.

Chin Yee Ho, Diana E Jaalouk, Maria K Vartiainen, Jan Lammerding

Open access · greenAbstract read
In one paragraph

Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 281 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
281citing papers in PubMed, 1 pooled it
20.8field-weighted citation impact, top 1% 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

281 citing papers in PubMed, 1 synthesis or guideline pooled it, 456 citations in OpenAlex.

  1. Pooled it
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  15. Stress transmission towards the nucleus of the cell.Frontiers in cell and developmental biology · 2026
    Review
  16. Review
  17. Article
  18. Article
  19. Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 3 countries.

Chin Yee HoCornell University, Weill Institute for Cell and Molecular Biology/Department of Biomedical Engineering, Ithaca, New York 14853, USA.
Diana E Jaalouk
Maria K Vartiainen
Jan Lammerding
American University of Beirut · LBBrigham and Women's Hospital · USUniversity of Helsinki · FI

Funding

Nuclear mechanics and mechanotransduction in muscular laminopathiesR01HL082792 · NHLBI · CORNELL UNIVERSITY · PI LAMMERDING, JAN · 2007 to 2023
$4.8M
Nuclear-cytoskeletal coupling in muscular laminopathiesR01NS059348 · NINDS · CORNELL UNIVERSITY · PI LAMMERDING, JAN · 2007 to 2011
$1.3M
NCI NIH HHS BC102152NHLBI NIH HHS R01 HL082792NINDS NIH HHS R01 NS059348
6 · The paper itself

Abstract

Laminopathies, caused by mutations in the LMNA gene encoding the nuclear envelope proteins lamins A and C, represent a diverse group of diseases that include Emery-Dreifuss muscular dystrophy (EDMD), dilated cardiomyopathy (DCM), limb-girdle muscular dystrophy, and Hutchison-Gilford progeria syndrome. Most LMNA mutations affect skeletal and cardiac muscle by mechanisms that remain incompletely understood. Loss of structural function and altered interaction of mutant lamins with (tissue-specific) transcription factors have been proposed to explain the tissue-specific phenotypes. Here we report in mice that lamin-A/C-deficient (Lmna(-/-)) and Lmna(N195K/N195K) mutant cells have impaired nuclear translocation and downstream signalling of the mechanosensitive transcription factor megakaryoblastic leukaemia 1 (MKL1), a myocardin family member that is pivotal in cardiac development and function. Altered nucleo-cytoplasmic shuttling of MKL1 was caused by altered actin dynamics in Lmna(-/-) and Lmna(N195K/N195K) mutant cells. Ectopic expression of the nuclear envelope protein emerin, which is mislocalized in Lmna mutant cells and also linked to EDMD and DCM, restored MKL1 nuclear translocation and rescued actin dynamics in mutant cells. These findings present a novel mechanism that could provide insight into the disease aetiology for the cardiac phenotype in many laminopathies, whereby lamin A/C and emerin regulate gene expression through modulation of nuclear and cytoskeletal actin polymerization.

Indexed as

ActinsActive Transport, Cell NucleusAnimalsCell NucleusCells, CulturedCytoskeletonFibroblastsGene Expression RegulationHeartLamin Type AMaleMembrane ProteinsMiceMutationMyocardiumNuclear ProteinsActinsemerinlamin CLamin Type AMembrane ProteinsMrtfa protein, mouseNuclear ProteinsSerum Response FactorTrans-Activators

Identifiers

PMID23644458
PMCPMC3666313
OpenAlexW2119110453

What OpenQuestion holds

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Registered trials

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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.