AI Article Synopsis
- Interferon-stimulated genes (ISGs) are crucial for the body's immune defenses, but when overactive, they can contribute to inflammatory diseases and interfere with normal immune function.* -
- Research on MATRIN3 (MATR3), a protein linked to familial ALS, shows that disrupting MATR3 increases ISG expression, revealing a potential pathway related to ALS development.* -
- The findings suggest that this pathway, involving cGAS-STING activation, could lead to new diagnostic and treatment strategies for certain cases of ALS.*
Article Abstract
Interferon-stimulated genes (ISGs) comprise a program of immune effectors important for host immune defense. When uncontrolled, ISGs play a central role in interferonopathies and other inflammatory diseases. The mechanisms responsible for turning on ISGs are not completely known. By investigating MATRIN3 (MATR3), a nuclear RNA-binding protein mutated in familial ALS, we found that perturbing MATR3 results in elevated expression of ISGs. Using an integrative approach, we elucidate a pathway that leads to activation of cGAS-STING. This outlines a plausible mechanism for pathogenesis in a subset of ALS, and suggests new diagnostic and therapeutic approaches for this fatal disease.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11071297 | PMC |
| http://dx.doi.org/10.1101/2024.04.01.587645 | DOI Listing |
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