FCN3 (F9E8J) Rabbit Monoclonal Antibody #63132

The complement system plays a critical role in the innate immune response to infection (1-3). Three distinct pathways, the classical, alternative, and lectin pathways, work to regulate complement (2). In humans, there are four recognition proteins in the lectin pathway: mannose-binding lectin (MBL) and 3 ficolin proteins, FCN1, FCN2, and FCN3 (1,2). Ficolin-3 (FCN3) was originally identified as the Hakata antigen, a macroglycoprotein that showed reactivity with serum from systemic lupus erythematosus (SLE) patients (1,5,6). FCN3 contains an N-terminal collagen-like domain that mediates oligomerization, and a C-terminal fibrinogen-like domain that binds to N-acetyl compounds found on the surfaces of microorganisms, resulting in complement activation (2). This activation generates complexes that disrupt and destroy abnormal cells. Complement fragments interact with immune cells, such as macrophages, neutrophils, and dendritic cells; these interactions enhance chemotaxis, phagocytic capacity, and antigen-presentation, boosting adaptive immunity (2,3). Accordingly, dysregulation in complement pathways has been shown to correlate with susceptibility to infection and autoimmunity (3-6). FCN3 is highly expressed in the lung and liver. Recent work has focused on the role of FCN3 in cancers (7-9). FCN3 is downregulated in lung and esophageal tumors (7,8). In analysis of FCN3 in serum from hepatocellular carcinoma (HCC) patients, low expression was associated with poor prognosis (9).