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• W2073757527 endingPage "AN20130032" @default.
• W2073757527 startingPage "AN20130032" @default.
• W2073757527 abstract "IF (intermediate filament) proteins can be cleaved by caspases to generate proapoptotic fragments as shown for desmin. These fragments can also cause filament aggregation. The hypothesis is that disease-causing mutations in IF proteins and their subsequent characteristic histopathological aggregates could involve caspases. GFAP (glial fibrillary acidic protein), a closely related IF protein expressed mainly in astrocytes, is also a putative caspase substrate. Mutations in GFAP cause A×D (Alexander disease). The overexpression of wild-type or mutant GFAP promotes cytoplasmic aggregate formation, with caspase activation and GFAP proteolysis. In this study, we report that GFAP is cleaved specifically by caspase 6 at VELD 225 in its L12 linker domain in vitro. Caspase cleavage of GFAP at Asp 225 produces two major cleavage products. While the C-GFAP (C-terminal GFAP) is unable to assemble into filaments, the N-GFAP (N-terminal GFAP) forms filamentous structures that are variable in width and prone to aggregation. The effect of N-GFAP is dominant, thus affecting normal filament assembly in a way that promotes filament aggregation. Transient transfection of N-GFAP into a human astrocytoma cell line induces the formation of cytoplasmic aggregates, which also disrupt the endogenous GFAP networks. In addition, we generated a neo-epitope antibody that recognizes caspase-cleaved but not the intact GFAP. Using this antibody, we demonstrate the presence of the caspase-generated GFAP fragment in transfected cells expressing a disease-causing mutant GFAP and in two mouse models of A×D. These findings suggest that caspase-mediated GFAP proteolysis may be a common event in the context of both the GFAP mutation and excess." @default.
• W2073757527 created "2016-06-24" @default.
• W2073757527 creator A5006497097 @default.
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• W2073757527 creator A5080356197 @default.
• W2073757527 creator A5091055322 @default.
• W2073757527 date "2013-11-11" @default.
• W2073757527 modified "2023-09-24" @default.
• W2073757527 title "Caspase Cleavage of GFAP Produces an Assembly-Compromised Proteolytic Fragment that Promotes Filament Aggregation" @default.
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• W2073757527 doi "https://doi.org/10.1042/an20130032" @default.
• W2073757527 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3833455" @default.
• W2073757527 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24102621" @default.
• W2073757527 hasPublicationYear "2013" @default.
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