ArticleRedox biology2026
Alexander disease mutations differentially sensitize glial fibrillary acidic protein (GFAP) to posttranslational modifications and network disruption by oxidants.
Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Corrections and comments
- Erratum issued
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8 authors.
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Abstract
The type III intermediate filament protein glial fibrillary acidic protein (GFAP) plays a key role in astrocyte and brain homeostasis. Mutations in GFAP can result in Alexander's disease (AxD), a severe neurodegenerative disease. Studies on AxD models indicate that oxidative stress may be an important pathogenic factor. Cellular expression of certain GFAP AxD mutants can provoke oxidative stress and contribute to a pathogenic cycle, as GFAP itself is an important oxidant target. To understand the molecular mechanisms involved, we have carried out a detailed LC-MS/MS characterization of posttranslational modifications formed on recombinant GFAP wild-type and AxD-relevant mutants (R79C, R239C and E373K) in response to in vitro treatment with hydrogen peroxide (H
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