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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: In vivo induction of membrane damage by β-amyloid peptide oligomers

Fig. 1

Membrane repair model. This model is based on the mechanism for repair of plasma membrane (PM) pores created in mammalian cells by exposure to the bacterial pore-forming toxin SLO [32]. ASM is acidic spingomyelinase that is stored in lysosomes, which fuse to the PM in response to an influx of Ca2+ through the pore created by SLO (Step 1), thereby releasing ASM at the cell surface (Step 2). The localized release of ASM cleaves off the phosphoryl head group of sphingomyelinase in the vicinity of the pore to generate ceramide in that area (Step 3). Consequently, the PM around the pore undergoes inward curvature and endocytosis such that the pore is removed from the PM (Step 4)

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