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Abstract
Calcium ion is required at various concentrations for vesicular recycling in the presynaptic terminal. Although calmodulin (CaM) is the most abundant Ca 2+-binding protein and has a submicromolar affinity for Ca 2+, it is not the Ca 2+ sensor for vesicular fusion because this process requires Ca 2+ concentrations above 1 μM. Several lines of evidence, however, suggest that CaM mediates the regulation of vesicular recycling by submicromolar Ca 2+ via novel protein–protein interactions. In this review, we discuss recent findings on how CaM regulates synaptic vesicle recycling by controlling the SNARE mechanism, which is the molecular machinery that mediates exocytosis.
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