ArticleCommunications biology2026
ATPase N-ethylmaleimide-sensitive factor mediated calcium dependent fusion pore closure and endocytosis.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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11 authors.
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Abstract
For a long time, it remained an unresolved question how the fusion pore is regulated to close after fusion occurs during kiss-and-run. Our study focuses on the physiological function of NSF in modulating single vesicle fusion events in live cells, using whole-cell capacitance recording coupled with live-cell confocal imaging. Our results demonstrates that in both male Sprague-Dawley rat adrenal chromaffin endocrine cells and dorsal root ganglion neurons, inhibiting or diminishing the ATPase activity of NSF significantly impedes fusion pore closure, inhibits various forms of endocytosis, and disrupts the replenishment of readily releasable pool. Interestingly, NSF is exclusively required for calcium-dependent exo-endocytosis but not for the calcium-independent process. In response to calcium influx, NSF disassembles the trans-SNARE complex intermediate via its ATPase activity, which regulates fusion pore closure and subsequently mediates slow, fast, and overshoot endocytosis. Our findings revealed a key mechanism for fusion pore regulation in calcium-evoked exo-endocytosis coupling.
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