Calcium-dependent secretion activator 1 is a protein that in humans is encoded by the CADPS gene.

CADPS encodes a novel neural/endocrine-specific cytosolic and peripheral membrane protein required for the Ca2+-regulated exocytosis of secretory vesicles. CADPS acts at a stage in exocytosis that follows ATP-dependent priming, which involves the essential synthesis of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2). Alternative splicing has been observed at this locus and three variants, encoding distinct isoforms, are described.
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[[Ischemic stroke]] triggers a cascade of events that facilitates [[neuroprotection]] and spontaneous [[recovery]], which accounts for a major part of [[functional recovery]]. Despite the cellular and molecular facilitations on neural protection, the molecular mechanisms of [[spontaneous recovery]] have not been fully understood. Ca2+ -dependent activator protein for secretion 1 (CAPS1), a member of the CAPS family, plays a major role in synaptic transmission and synaptic effectiveness by regulating [[vesicle]] [[exocytosis]]. 
The molecular mechanism of CAPS1 in spontaneous recovery after ischemic stroke was studied. In this study, transient left [[middle cerebral artery occlusion]] (MCAO) was used as the [[ischemic stroke model]]. The whole brain magnetic resonance imaging (MRI) and neurological score analysis showed decreased infarct volume and neurological scores at 7 days compared to 1 day after MCAO, suggesting spontaneous recovery. Western blot analysis showed elevated BDNF and CAPS1 expression levels in the bilateral hippocampus at both 1 day and 3 days after MCAO. Then, inhibition of CAPS1 by adeno-associated virus (AAV) microinjection in the hippocampus attenuated the spontaneous recovery of both motor and memory impairment induced by MCAO. In addition, elevated p-TrkB levels were detected after MCAO, which were reduced by CAPS1-AAV microinjection, indicating that CAPS1 could induce BDNF secretion after ischemic stroke.
Moreover, they found the elevated combination of CAPS1 with dense core vesicles (DCV) in the hippocampus at both 1 day and 3 days after MCAO, which could also be inhibited by CAPS1-AAV microinjection, indicating the potential mechanism of CAPS1 in regulating BDNF release after MCAO. Finally, we found that CAPS1/BDNF signaling could influence neurogenesis in the hippocampus after MCAO. In conclusion, CAPS1 regulates [[neurogenesis]] by upregulating [[BDNF]] release in the [[hippocampus]], which finally facilitates spontaneous recovery after ischemic stroke
((Liu D, Zheng Y, Chen Y, Jiang Y, Wang H, Li L, Ma L. Ca2+ -dependent activator protein for secretion 1 promotes spontaneous recovery in ischemic stroke by regulating BDNF secretion. J Neurochem. 2023 Mar 14. doi: 10.1111/jnc.15808. Epub ahead of print. PMID: 36916413.))