ArticleActa neuropathologica2016
ALS mutant SOD1 interacts with G3BP1 and affects stress granule dynamics.
Article in Acta neuropathologica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 101 citations in OpenAlex.
- Stress granules at the crossroads of the proteostasis network.RNA biology · 2026Review
- FAM120A - a protein inserted in the ALS disease network.Scientific reports · 2026Article
- NEDD8, stress granules, and amyotrophic lateral sclerosis: unveiling the therapeutic potential of the NEDP1 protease.Essays in biochemistry · 2025Review
- SOD1, A Crucial Protein for Neural Biochemistry: Dysfunction and Risk of Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2025Review
- Local Protein Synthesis at Synapses: A Driver for Synapse Diversification.Journal of neurochemistry · 2025Review
- Defective Ribosome Recycling: A Bridge Between Translation Fidelity, Organelle Dysfunction, and Diseases: Exploring How Flawed Ribosome Recycling Factors Impact Ribosome Metabolism and Organelle Homeostasis, Leading to Human Diseases.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Stress granules: emerging players in neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Perillaldehyde Improves Parkinson-Like Deficits by Targeting G3BP Mediated Stress Granule Assembly in Preclinical Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Using ALS to understand profilin 1's diverse roles in cellular physiology.Cytoskeleton (Hoboken, N.J.) · 2025Review
- Modeling biomolecular condensates across scales: Atomistic, coarse-grained, and data-driven approaches.Advances in physics: X · 2025Article
- Molecular hallmarks of ageing in amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2024Review
- Rapid and Robust Multi-Phenotypic Assay System for ALS Using Human iPS Cells with Mutations in Causative Genes.International journal of molecular sciences · 2023Article
- Article
- A Zn-dependent structural transition of SOD1 modulates its ability to undergo phase separation.The EMBO journal · 2023Article
- Stress granule assembly in vivo is deficient in the CNS of mutant TDP-43 ALS mice.Human molecular genetics · 2023Article
- Intracellular energy controls dynamics of stress-induced ribonucleoprotein granules.Nature communications · 2022Article
- BDNF-dependent modulation of axonal transport is selectively impaired in ALS.Acta neuropathologica communications · 2022Article
- Stressful steps: Progress and challenges in understanding stress-induced mRNA condensation and accumulation in stress granules.Molecular cell · 2022Review
- cGAS and DDX41-STING mediated intrinsic immunity spreads intercellularly to promote neuroinflammation in SOD1 ALS model.iScience · 2022Article
- Alteration of Mitochondrial Integrity as Upstream Event in the Pathophysiology of SOD1-ALS.Cells · 2022Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease. Mutations in Cu/Zn superoxide dismutase (SOD1) are responsible for approximately 20 % of the familial ALS cases. ALS-causing SOD1 mutants display a gain-of-toxicity phenotype, but the nature of this toxicity is still not fully understood. The Ras GTPase-activating protein-binding protein G3BP1 plays a critical role in stress granule dynamics. Alterations in the dynamics of stress granules have been reported in several other forms of ALS unrelated to SOD1. To our surprise, the mutant G93A SOD1 transgenic mice exhibited pathological cytoplasmic inclusions that co-localized with G3BP1-positive granules in spinal cord motor neurons. The co-localization was also observed in fibroblast cells derived from familial ALS patient carrying SOD1 mutation L144F. Mutant SOD1, unlike wild-type SOD1, interacted with G3BP1 in an RNA-independent manner. Moreover, the interaction is specific for G3BP1 since mutant SOD1 showed little interaction with four other RNA-binding proteins implicated in ALS. The RNA-binding RRM domain of G3BP1 and two particular phenylalanine residues (F380 and F382) are critical for this interaction. Mutant SOD1 delayed the formation of G3BP1- and TIA1-positive stress granules in response to hyperosmolar shock and arsenite treatment in N2A cells. In summary, the aberrant mutant SOD1-G3BP1 interaction affects stress granule dynamics, suggesting a potential link between pathogenic SOD1 mutations and RNA metabolism alterations in ALS.
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