作者: Sheldon S. Shen , Ward C. Tucker , Edwin R. Chapman , Richard A. Steinhardt
关键词: Intracellular 、 Cell biology 、 Signal transduction 、 Biology 、 Synaptotagmins 、 Synaptotagmin 1 、 Synaptotagmin I 、 Mutant 、 Vesicle fusion 、 Vesicle
摘要: Membrane resealing in mammalian cells after injury depends on Ca2+-dependent fusion of intracellular vesicles with the plasma membrane. When are wounded twice, subsequent is generally faster. Physiological and biochemical studies have shown initiation two different repair signaling pathways, which termed facilitated potentiated responses. The response dependent generation recruitment new vesicles, whereas not. Here, we report that responses can be differentially defined molecularly. Using recombinant fragments synaptobrevin-2 synaptotagmin C2 domains were able to dissociate molecular requirements vesicle exocytosis for initial membrane was blocked by C2B domain VII. Both also Although not C2AB I or C2A VII, inhibited. We used Ca2+ binding mutant show effects synaptotagmins Ca2+-dependent. pattern inhibition observed cannot specify a compartment, such as lysosomes, repair.