ArticleDevelopmental cell2013
Lamina-associated polypeptide-1 interacts with the muscular dystrophy protein emerin and is essential for skeletal muscle maintenance.
Article in Developmental cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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.
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.
Who cites it
63 citing papers in PubMed.
- Emerin loss of function inhibits MyoD-driven differentiation of human iPSCs into skeletal myotubes.bioRxiv : the preprint server for biology · 2026Article
- Elevation of the mechanically-sensitive protein emerin links nuclear mechanotransduction to tau-induced cytoskeletal remodeling in neurons.bioRxiv : the preprint server for biology · 2025Article
- Development of Emerin mRNA Lipid Nanoparticles to Rescue Myogenic Differentiation.International journal of molecular sciences · 2025Article
- Role of Nuclear Envelope Proteins in the Structure and Function of the Neuromuscular Junction: Focus on Subsynaptic Nuclei.Sub-cellular biochemistry · 2025Review
- LAP1 Interactome Profiling Provides New Insights into LAP1's Physiological Functions.International journal of molecular sciences · 2024Article
- Quantitative proteome analysis of LAP1-deficient human fibroblasts: A pilot approach for predicting the signaling pathways deregulated in LAP1-associated diseases.Biochemistry and biophysics reports · 2024Article
- Article
- Emerin deficiency does not exacerbate cardiomyopathy in a murine model of Emery-Dreifuss muscular dystrophy caused by an LMNA gene mutation.The journal of physiological sciences : JPS · 2023Article
- Acute downregulation of emerin alters actomyosin cytoskeleton connectivity and function.Biophysical journal · 2023Article
- Review
- Eutherian-Specific Functions of BetaM Acquired throughLife (Basel, Switzerland) · 2023Article
- Nuclear mechanosignaling in striated muscle diseases.Frontiers in physiology · 2023Review
- Loss of function of the nuclear envelope protein LEMD2 causes DNA damage-dependent cardiomyopathy.The Journal of clinical investigation · 2022Article
- Loss of the Nuclear Envelope Protein LAP1B Disrupts the Myogenic Differentiation of Patient-Derived Fibroblasts.International journal of molecular sciences · 2022Article
- Hepatocytes Deficient in Nuclear Envelope Protein Lamina-associated Polypeptide 1 are an Ideal Mammalian System to Study Intranuclear Lipid Droplets.Journal of lipid research · 2022Article
- Shared and Distinctive Neighborhoods of Emerin and Lamin B Receptor Revealed by Proximity Labeling and Quantitative Proteomics.Journal of proteome research · 2022Article
- Molecular Pathology of Laminopathies.Annual review of pathology · 2022Review
- Nuclear Envelope Alterations in Myotonic Dystrophy Type 1 Patient-Derived Fibroblasts.International journal of molecular sciences · 2022Article
- The LEM-ESCRT toolkit: Repair and maintenance of the nucleus.Frontiers in cell and developmental biology · 2022Review
- Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
X-linked Emery-Dreifuss muscular dystrophy is caused by loss of function of emerin, an integral protein of the inner nuclear membrane. Yet emerin null mice are essentially normal, suggesting the existence of a critical compensating factor. We show that the lamina-associated polypeptide1 (LAP1) interacts with emerin. Conditional deletion of LAP1 from striated muscle causes muscular dystrophy; this pathology is worsened in the absence of emerin. LAP1 levels are significantly higher in mouse than human skeletal muscle, and reducing LAP1 by approximately half in mice also induces muscle abnormalities in emerin null mice. Conditional deletion of LAP1 from hepatocytes yields mice that exhibit normal liver function and are indistinguishable from littermate controls. These results establish that LAP1 interacts physically and functionally with emerin and plays an essential and selective role in skeletal muscle maintenance. They also highlight how dissecting differences between mouse and human phenotypes can provide fundamental insights into disease mechanisms.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.