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Updated: Feb 5, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Dysfunctional RNA binding proteins and stress granules in multiple sclerosis
Hannah E Salapa1, Chloe Johnson2, Catherine Hutchinson3
1Department of Anatomy and Cell Biology, University of Saskatchewan, Saskatoon, SK, Canada; Cameco Multiple Sclerosis Neuroscience Research Center, University of Saskatchewan, Saskatoon, SK, Canada.
Dysfunctional RNA binding protein hnRNP A1 is implicated in multiple sclerosis (MS) pathogenesis. Interferon-γ induced hnRNP A1 mislocalization and stress granule formation in neurons, mirroring findings in MS patient brains.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Heterogeneous nuclear ribonuclear protein A1 (hnRNP A1) dysfunction is linked to neurodegenerative diseases.
- The role of hnRNP A1 in multiple sclerosis (MS) pathogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the involvement of hnRNP A1 dysfunction in the pathogenesis of multiple sclerosis.
- To determine if interferon-γ affects hnRNP A1 localization and function in neuronal cells.
Main Methods:
- Utilized a neuronal cell line treated with interferon-γ.
- Examined hnRNP A1 localization (nuclear vs. cytoplasmic) and its presence in stress granules (SGs).
- Analyzed neurons from the brain of a multiple sclerosis patient.
Main Results:
- Interferon-γ induced hnRNP A1 mislocalization from the nucleus to the cytoplasm in neuronal cells.
- hnRNP A1 colocalized with stress granules (SGs) and translation was inhibited in treated cells.
- MS patient neurons exhibited pathogenic hnRNP A1 dysfunction, including nuclear depletion, cytoplasmic mislocalization, and SG colocalization.
Conclusions:
- Dysfunctional hnRNP A1 plays a role in the pathogenesis of multiple sclerosis.
- hnRNP A1 mislocalization and SG formation are potential mechanisms contributing to MS.
- These findings highlight hnRNP A1 as a potential therapeutic target in MS.
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