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Alexander disease mutations differentially sensitize GFAP to oxidative damage and network disruption

ABSTRACT: The type III intermediate filament protein GFAP plays key roles in astrocyte and brain homeostasis. Mutations in GFAP can result in Alexander’s disease (AxD), a severe neurodegenerative disease. Studies in AxD models indicate that oxidative stress may be an important pathogenic factor. Expression of certain GFAP AxD mutants in cells can provoke oxidative stress and potentially contribute to a pathogenic cycle since GFAP itself is an important target of oxidants. In order 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 mutants (R79C, R239C and E373K), in response to in vitro treatment with the biologically-relevant oxidants H2O2, HOCl and ONOOH.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Per Hägglund

LAB HEAD: Per Hägglund

PROVIDER: PXD069155 | Pride | 2026-03-23

REPOSITORIES: Pride

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			Action	DRS
	C294S_combined_modified_peptide_Cysox.tsv	Tabular
	E373K_combined_modified_peptide_Cysox.tsv	Tabular
	GFAP_C294S_H2O2_GB2_01_26572.d.zip	Other
	GFAP_C294S_H2O2_GB3_01_26573.d.zip	Other
	GFAP_C294S_H2O2_GB4_01_26574.d.zip	Other

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