Recombinant Human RETN protein

**Background of RETN Recombinant Protein**

The RETN gene encodes resistin, a cysteine-rich secretory adipokine initially linked to insulin resistance in mice, where it is predominantly expressed in adipose tissue. In humans, resistin is primarily produced by macrophages and monocytes, playing roles in inflammation, metabolic regulation, and immune responses. Its name derives from its association with insulin resistance, particularly in obesity and type 2 diabetes, though its mechanisms remain debated. Resistin interacts with Toll-like receptor 4 (TLR4) and other receptors, influencing pathways like NF-κB to modulate cytokine production and metabolic signaling.

Recombinant RETN protein is generated using biotechnological methods, such as cloning the RETN gene into bacterial (e.g., *E. coli*) or mammalian expression systems, followed by purification. This engineered protein retains the native structure, often forming homooligomers (trimers or hexamers), critical for its bioactivity. It serves as a vital tool for studying resistin's role in metabolic disorders, inflammatory diseases, and cancer, enabling *in vitro* and *in vivo* experiments to dissect its signaling pathways.

Research applications include elucidating resistin's contribution to atherosclerosis, insulin resistance, and adipose-immune crosstalk. It is also explored as a potential therapeutic target; inhibitors or neutralizing antibodies against resistin may mitigate metabolic syndromes. However, species-specific differences—such as divergent expression patterns between mice and humans—complicate translational interpretations. Despite challenges, recombinant resistin remains pivotal in advancing understanding of metabolic and inflammatory diseases, offering insights into diagnostics and targeted therapies.