ReviewNucleus (Austin, Tex.)2018
Mechanotransduction, nuclear architecture and epigenetics in Emery Dreifuss Muscular Dystrophy: tous pour un, un pour tous.
Review in Nucleus (Austin, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Emerin acts as a mechanosensor linking force transmission and disease.Frontiers in oncology · 2026Review
- Nuclear mechanosignaling in striated muscle diseases.Frontiers in physiology · 2023Review
- The Nuclear Lamina.Cold Spring Harbor perspectives in biology · 2022Review
- Genetic basis of cardiovascular aging is at the core of human longevity.The journal of cardiovascular aging · 2022Article
- Alterations to Genome Organisation in Stem Cells, Their Differentiation and Associated Diseases.Results and problems in cell differentiation · 2022Article
- Role ofBiomolecules · 2021Article
- The shifting shape of genomes: dynamics of heterochromatin interactions at the nuclear lamina.Current opinion in genetics & development · 2021Review
- Nuclear Mechanotransduction in Skeletal Muscle.Cells · 2021Review
- Case Reports: Emery-Dreifuss Muscular Dystrophy Presenting as a Heart Rhythm Disorders in Children.Frontiers in cardiovascular medicine · 2021Article
- The Nuclear Lamina: Protein Accumulation and Disease.Biomedicines · 2020Review
- Novel candidate alleles associated with gene regulation for Emery-Dreifuss muscular dystrophy.EBioMedicine · 2020Article
- The role of lamin A/C in mesenchymal stem cell differentiation.Journal of physiology and biochemistry · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The alteration of the several roles that Lamin A/C plays in the mammalian cell leads to a broad spectrum of pathologies that - all together - are named laminopathies. Among those, the Emery Dreifuss Muscular Dystrophy (EDMD) is of particular interest as, despite the several known mutations of Lamin A/C, the genotype-phenotype correlation still remains poorly understood; this suggests that the epigenetic background of patients might play an important role during the time course of the disease. Historically, both a mechanical role of Lamin A/C and a regulative one have been suggested as the driving force of laminopathies; however, those two hypotheses are not mutually exclusive. Recent scientific evidence shows that Lamin A/C sustains the correct gene expression at the epigenetic level thanks to the Lamina Associated Domains (LADs) reorganization and the crosstalk with the Polycomb Group of Proteins (PcG). Furthermore, the PcG-dependent histone mark H3K27me3 increases under mechanical stress, finally pointing out the link between the mechano-properties of the nuclear lamina and epigenetics. Here, we summarize the emerging mechanisms that could explain the high variability seen in Emery Dreifuss muscular dystrophy.
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Registered trials
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 Socratic graph.