Sh2d3c, also known as NSP3, is an adaptor protein. It contains both the SH2 domain and a domain similar to guanine nucleotide exchange factor domains of Ras family GTPases. Sh2d3c is involved in the regulation of adhesion, migration, tissue organization, and immune response, and has been associated with pathways related to immune and inflammatory responses [4].

In Mn-exposed N2a cells, lncRNA Sh2d3c was significantly increased, and its knockdown increased cell viability and inhibited apoptosis, suggesting it promotes manganese-induced neuronal apoptosis through the mmu-miR-675-5p/Chmp4b/Bax axis [1]. In lung cancer, NSP3 (SH2D3C) is associated with advanced stage and poor prognoses, and may promote tumor immune evasion. Organosulfur compounds from Allium sativum show potential to target it [2]. In mice, Sh2d3c-deficient mice had reduced marginal zone B (MZB) cells, and the remaining MZB cells had impaired function, while T-cell development and function were largely normal. This led to a diminished humoral immune response against thymus-independent type 2 Ags [3].

In conclusion, Sh2d3c plays important roles in various biological processes and disease conditions. In the context of Mn-induced neurotoxicity, lung cancer, and B-cell-related immune responses, research on Sh2d3c using gene-knockout mouse models has provided insights into its functions. These studies help us understand its role in disease mechanisms and may offer potential targets for treatment.