ArticlePloS one2015
Subcellular Localization of Matrin 3 Containing Mutations Associated with ALS and Distal Myopathy.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Matrin-3 forms spherical and wormlike assemblies that are modulated by RNA binding and ALS/FTD-associated mutations.Molecular cell · 2025Article
- The role of Matrin-3 in physiology and its dysregulation in disease.Biochemical Society transactions · 2024Review
- MATR3 P154S knock-in mice do not exhibit motor, muscle or neuropathologic features of ALS.Biochemical and biophysical research communications · 2023Article
- Integrative identification of hub genes in development of atrial fibrillation related stroke.PloS one · 2023Article
- Molecular determinants and modifiers of Matrin-3 toxicity, condensate dynamics, and droplet morphology.iScience · 2022Article
- Matrin-3 dysfunction in myopathy and motor neuron degeneration.Neural regeneration research · 2022Article
- Inner nuclear protein Matrin-3 coordinates cell differentiation by stabilizing chromatin architecture.Nature communications · 2021Article
- Matrin 3 in neuromuscular disease: physiology and pathophysiology.JCI insight · 2021Review
- First Family ofFrontiers in neurology · 2021Article
- Matrin3: Disorder and ALS Pathogenesis.Frontiers in molecular biosciences · 2021Review
- Selective neuronal degeneration in MATR3 S85C knock-in mouse model of early-stage ALS.Nature communications · 2020Article
- Dysregulation of RNA-Binding Proteins in Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2020Article
- Case Report: Early-Onset Behavioral Variant Frontotemporal Dementia in Patient With Retrotransposed Full-Length Transcript ofFrontiers in neurology · 2020Article
- N-terminal sequences in matrin 3 mediate phase separation into droplet-like structures that recruit TDP43 variants lacking RNA binding elements.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Chromosome territories and the global regulation of the genome.Genes, chromosomes & cancer · 2019Review
- Molecular Mechanisms of TDP-43 Misfolding and Pathology in Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2019Review
- Relation Between Stress Granules and Cytoplasmic Protein Aggregates Linked to Neurodegenerative Diseases.Current neurology and neuroscience reports · 2018Review
- RNA-Binding Proteins in Amyotrophic Lateral Sclerosis.Molecules and cells · 2018Review
- Matrin 3-dependent neurotoxicity is modified by nucleic acid binding and nucleocytoplasmic localization.eLife · 2018Article
- Genetics of Amyotrophic Lateral Sclerosis.Cold Spring Harbor perspectives in medicine · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutations in Matrin 3 [MATR3], an RNA- and DNA-binding protein normally localized to the nucleus, have been linked to amyotrophic lateral sclerosis (ALS) and distal myopathies. In the present study, we have used transient transfection of cultured cell lines to examine the impact of different disease-causing mutations on the localization of Matrin 3 within cells.
resultsUsing CHO and human H4 neuroglioma cell models, we find that ALS/myopathy mutations do not produce profound changes in the localization of the protein. Although we did observe variable levels of Matrin 3 in the cytoplasm either by immunostaining or visualization of fluorescently-tagged protein, the majority of cells expressing either wild-type (WT) or mutant Matrin 3 showed nuclear localization of the protein. When cytoplasmic immunostaining, or fusion protein fluorescence, was seen in the cytoplasm, the stronger intensity of staining or fluorescence was usually evident in the nucleus. In ~80% of cells treated with sodium arsenite (Ars) to induce cytoplasmic stress granules, the nuclear localization of WT and F115C mutant Matrin 3 was not disturbed. Notably, over-expression of mutant Matrin 3 did not induce the formation of obvious large inclusion-like structures in either the cytoplasm or nucleus.
conclusionsOur findings indicate that mutations in Matrin 3 that are associated with ALS and myopathy do not dramatically alter the normal localization of the protein or readily induce inclusion formation.
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