ArticleHuman molecular genetics2015
Disruption of the lamin A and matrin-3 interaction by myopathic LMNA mutations.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- SAF-A/HNRNPU regulates euchromatin dynamics and is required for nuclear envelope integrity.bioRxiv : the preprint server for biology · 2026Article
- Mechanistic and Epigenetic Partitioning of Lamina-Associated Chromatin Revealed by a Genome-Wide Imaging Screen.bioRxiv : the preprint server for biology · 2025Article
- SMAP3-ID for Identification of Endogenous Protein-Protein Interactions Reveals Regulation of Mitochondrial Activity by Lamins.JACS Au · 2025Article
- Differential Expression of Lamins and Modulation of Chromatin Architecture in Carcinogenesis: tous pour un et un pour tous.Sub-cellular biochemistry · 2025Review
- The role of Matrin-3 in physiology and its dysregulation in disease.Biochemical Society transactions · 2024Review
- Analyzing the interactome of human CK2β in prostate carcinoma cells reveals HSP70-1 and Rho guanin nucleotide exchange factor 12 as novel interaction partners.FASEB bioAdvances · 2023Article
- Native lamin A/C proteomes and novel partners from heart and skeletal muscle in a mouse chronic inflammation model of human frailty.Frontiers in cell and developmental biology · 2023Article
- Molecular determinants and modifiers of Matrin-3 toxicity, condensate dynamics, and droplet morphology.iScience · 2022Article
- A hub-and-spoke nuclear lamina architecture in trypanosomes.Journal of cell science · 2021Article
- Matrin 3 in neuromuscular disease: physiology and pathophysiology.JCI insight · 2021Review
- An APEX2 proximity ligation method for mapping interactions with the nuclear lamina.The Journal of cell biology · 2021Article
- Role of RNA Binding Proteins with prion-like domains in muscle and neuromuscular diseases.Cell stress · 2020Review
- Chromosome territories and the global regulation of the genome.Genes, chromosomes & cancer · 2019Review
- Biotinylation by antibody recognition-a method for proximity labeling.Nature methods · 2018Article
- Induced Pluripotent Stem Cells to Study Mechanisms of Laminopathies: Focus on Epigenetics.Frontiers in cell and developmental biology · 2018Review
- Exploring the Crosstalk BetweenFrontiers in genetics · 2018Review
- Nuclear poly(A) binding protein 1 (PABPN1) and Matrin3 interact in muscle cells and regulate RNA processing.Nucleic acids research · 2017Article
- Identification of novel nesprin-1 binding partners and cytoplasmic matrin-3 in processing bodies.Molecular biology of the cell · 2016Article
- Diseases of the Nucleoskeleton.Comprehensive Physiology · 2016Review
- ALS: Recent Developments from Genetics Studies.Current neurology and neuroscience reports · 2016Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The nuclear face of the nuclear membrane is enriched with the intermediate filament protein lamin A. Mutations in LMNA, the gene encoding lamin A, lead to a diverse set of inherited conditions including myopathies that affect both the heart and skeletal muscle. To gain insight about lamin A protein interactions, binding proteins associated with the tail of lamin A were characterized. Of 130 nuclear proteins found associated with the lamin A tail, 17 (13%) were previously described lamin A binding partners. One protein not previously linked to lamin A, matrin-3, was selected for further study, because like LMNA mutations, matrin-3 has also been implicated in inherited myopathy. Matrin-3 binds RNA and DNA and is a nucleoplasmic protein originally identified from the insoluble nuclear fraction, referred to as the nuclear matrix. Anti-matrin-3 antibodies were found to co-immunoprecipitate lamin A, and the lamin-A binding domain was mapped to the carboxy-terminal half of matrin-3. Three-dimensional mapping of the lamin A-matrin-3 interface showed that the LMNA truncating mutation Δ303, which lacks the matrin-3 binding domain, was associated with an increased distance between lamin A and matrin-3. LMNA mutant cells are known to have altered biophysical properties and the matrin-3-lamin A interface is positioned to contribute to these defects.
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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 OpenQuestion graph.