Draeger, Annette; Babiychuk, Eduard B. (2013). Ceramide in Plasma Membrane Repair. In: Gulbins, Erich; Petrache, Irina (eds.) Sphingolipids in Disease. Handbook of Experimental Pharmacology: Vol. 216 (pp. 341-353). Vienna: Springer 10.1007/978-3-7091-1511-4_17
Full text not available from this repository.The perforation of the plasmalemma by pore-forming toxins causes an influx of Ca2+ and an efflux of cytoplasmic proteins. In order to ensure cellular survival, lesions have to be identified, plugged and removed from the membrane. The Ca2+-driven fusion of lysosomes with the plasma membrane leads to hydrolysis of sphingomyelin by acid sphingomyelinase and a formation of ceramide platforms in the outer leaflet of the lipid bilayer. We propose that the negative curvature, promoted by tighter packing of lipids in the outer layer, leads to an inward vesiculation of the damaged area for its endocytotic uptake and internal degradation. In contrast, the activation of neutral sphingomyelinase triggers the production of ceramide within the inner leaflet of the lipid bilayer, thereby promoting an outward curvature, which enables the cell to shed the membrane-containing toxin pore into the extracellular space. In this process, ceramide is supported by members of the annexin protein family which act as Ca2+ sensors and as membrane fusion agents.
Item Type: |
Book Section (Book Chapter) |
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Division/Institute: |
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy > Cell Biology 04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy |
UniBE Contributor: |
Draeger, Annette, Babiichuk, Eduard |
Subjects: |
600 Technology > 610 Medicine & health |
ISBN: |
978-3-7091-1511-4 |
Series: |
Handbook of Experimental Pharmacology |
Publisher: |
Springer |
Language: |
English |
Submitter: |
Annette Draeger |
Date Deposited: |
15 Apr 2014 09:37 |
Last Modified: |
02 Mar 2023 23:24 |
Publisher DOI: |
10.1007/978-3-7091-1511-4_17 |
URI: |
https://boris.unibe.ch/id/eprint/50038 |