Recombinant Human ZnT8 [His]

Zinc transporter 8 (ZNT8) is a transmembrane transporter protein in humans encoded by the SLC30A8 gene and consists of 369 amino acids. As an essential trace element, zinc deficiency can lead to various diseases with poor prognosis, such as diabetes, cancer, and Alzheimer's disease. In the human insulin synthesis pathway, zinc is required for the processing of proinsulin and the packaging of insulin. ZNT8 is primarily responsible for transporting Zn2+ from the cytoplasm to insulin vesicles, ensuring high levels of zinc accumulation within insulin secretory granules (ISGs). Consequently, ZNT8 expression is restricted to the insulin secretory granules of pancreatic β-cells.

Dysfunction of ZNT8 is associated with autoimmune diseases, particularly type 1 (T1DM) and type 2 diabetes (T2DM). When the immune system is dysregulated, immune cells (such as B cells) may mistakenly recognize and attack the ZNT8 protein in islet cells, leading to abnormal insulin secretion and affecting blood glucose balance. Furthermore, the immune system's attack on ZNT8 can trigger an inflammatory response, further impairing the function and structure of insulin-producing cells, and exacerbating the pathological process of diabetes. ZNT8 has been identified as a major autoantigen in type 1 diabetes, and the corresponding autoantibodies against ZNT8 (ZnT8A) have emerged as a promising biomarker for diagnosing T1DM. ZnT8A often appears earlier than clinical symptoms, making it a valuable tool for early diagnosis and risk stratification. Data indicate that approximately 70% of young T1DM patients can be detected with ZnT8A.

However, ZNT8 may play different roles in T1DM and T2DM. Certain loss-of-function mutations in the ZNT8 gene (such as the R325W mutation) result in decreased ZNT8 activity, but their impact on insulin secretion is not always negative. Researchers have identified 12 rare loss-of-function mutations caused by truncation of ZNT8 that can reduce abnormal insulin secretion or improve insulin function, thereby reducing the risk of T2DM by 65%. These findings suggest that moderate regulation of ZNT8 function may be a new strategy for preventing and treating type 2 diabetes.

Recombinant Human Zinc Transporter 8
Recombinant Human SLC30A8
Recombinant Human ZnT8 Protein