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- W2040687198 endingPage "712" @default.
- W2040687198 startingPage "703" @default.
- W2040687198 abstract "Plasmalemmal injury is a frequent event in the life of a cell. Physical disruption of the plasma membrane is common in cells that operate under conditions of mechanical stress. The permeability barrier can also be breached by chemical means: pathogens gain access to host cells by secreting pore-forming toxins and phospholipases, and the host's own immune system employs pore-forming proteins to eliminate both pathogens and the pathogen-invaded cells. In all cases, the influx of extracellular Ca(2+) is being sensed and interpreted as an immediate danger signal. Various Ca(2+)-dependent mechanisms are employed to enable plasma membrane repair. Extensively damaged regions of the plasma membrane can be patched with internal membranes delivered to the cell surface by exocytosis. Nucleated cells are capable of resealing their injured plasmalemma by endocytosis of the permeabilized site. Likewise, the shedding of membrane microparticles is thought to be involved in the physical elimination of pores. Membrane blebbing is a further damage-control mechanism, which is triggered after initial attempts at plasmalemmal resealing have failed. The members of the annexin protein family are ubiquitously expressed and function as intracellular Ca(2+) sensors. Most cells contain multiple annexins, which interact with distinct plasma membrane regions promoting membrane segregation, membrane fusion and--in combination with their individual Ca(2+)-sensitivity--allow spatially confined, graded responses to membrane injury." @default.
- W2040687198 created "2016-06-24" @default.
- W2040687198 creator A5025157687 @default.
- W2040687198 creator A5034116797 @default.
- W2040687198 creator A5044330077 @default.
- W2040687198 date "2011-03-01" @default.
- W2040687198 modified "2023-10-18" @default.
- W2040687198 title "Plasma membrane repair and cellular damage control: The annexin survival kit" @default.
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