Scgn, or secretagogin, is a calcium sensor protein enriched in neuroendocrine cells. It regulates synaptic transmission, interacts with the SNARE complex for vesicle fusion, and is involved in pathways like oxytocin signaling, immune responses, and insulin secretion [1,2,4]. Genetic models such as gene knockout (KO) in zebrafish or mice have been crucial in studying its functions.

Deletion of Scgn in zebrafish or mice leads to autism-like behaviors, impairs brain development, disrupts oxytocin signaling, and abnormally activates inflammation, suggesting its role in autism spectrum disorder (ASD) [1]. In mice, Scgn deficiency also results in impaired hormone release and susceptibility to DSS-induced colitis, indicating its link to colitis susceptibility [2]. Additionally, in islet β-cells, lipotoxicity-induced down-regulation of Scgn promotes NLRP3-mediated β-cell pyroptosis, highlighting its role in type 2 diabetes [3].

In conclusion, Scgn plays essential roles in synaptic function, hormone release, and immune-related processes. Studies using KO mouse models have revealed its significance in diseases such as ASD, colitis, and type 2 diabetes, providing insights into disease mechanisms and potential therapeutic targets.