Insulin-degrading enzyme (IDE) is a zinc-metalloprotease primarily known for its role in metabolizing insulin and amyloid-β peptides, linking it to diabetes and Alzheimer’s disease (AD). Discovered in 1949. IDE is a 110-kDa protein encoded by the *IDE* gene, expressed ubiquitously but enriched in the liver, brain, and kidneys. Its dual substrate specificity positions it as a critical regulator of glucose homeostasis and neurodegenerative processes.
IDE antibodies are essential tools for studying its expression, localization, and function. Research using these antibodies has revealed IDE’s cytoplasmic localization under normal conditions, though it can be secreted or associate with membranes in specific contexts. In AD models, IDE antibodies help track its interaction with amyloid-β, highlighting reduced IDE levels in affected brains, which may contribute to amyloid plaque accumulation. In diabetes, they aid in analyzing insulin degradation dynamics and IDE’s potential role in insulin resistance.
IDE-targeting therapies, such as small-molecule activators or monoclonal antibodies, are under exploration. However, IDE antibodies themselves have limitations, including cross-reactivity with unrelated proteins, necessitating rigorous validation. Their application spans Western blotting, immunohistochemistry, and functional assays in both cellular (e.g., HepG2 cells) and animal models.
Overall, IDE antibodies remain pivotal in elucidating IDE’s pathophysiological roles and its therapeutic potential in metabolic and neurodegenerative disorders.