Recombinant Mouse LSECtin/CLEC4G Protein, CF

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LSECtin (liver and lymph node sinusoidal endothelial cell C-type lectin), also known as C-type lectin superfamily 4 member G (CLEC4G), is a member of subgroup II of the C-type (Ca2+-dependent) lectin superfamily (1). The protein was named LSECtin because its initial expression was described to be restricted to liver and lymph node sinusoidal endothelial cells (1). However, LSECtin has also been detected in peripheral blood and thymic dendritic cells isolated ex vivo, and in monocyte-derived macrophages and dendritic cells at the RNA and protein level (2). Mouse LSECtin is a type II transmembrane glycoprotein that includes an N-terminal cytoplasmic tail (aa 1-30), a 21 aa transmembrane region, and a 243 aa extracellular domain (ECD). Within the ECD, mouse LSECtin shares 66% and 85% aa sequence identity with human and rat LSECtin, respectively. LSECtin binds to mannose, GlcNAc, and fucose in a Ca2+-dependent manner (1-3). In addition, LSECtin has the ability to bind to surface glycoproteins of enveloped viruses (3, 4). In particular, interaction of LSECtin with the surface glycoproteins of severe acute respiratory syndrome (SARS) coronavirus and Ebola virus has been described, and LSECtin-mediated infection of cells by Ebola virus has been demonstrated (3, 4). LSECtin is highly expressed on tumor-associated macrophages (TAMs) and enhances stemness of breast cancer cells (BCCs) (9). We identified BTN3A3, a B7 family member with previously unknown functions as the receptor for LSECtin on BCCs responsible for stemness-promoting effect of LSECtin (9). In mice bearing human tumor xenografts, either macrophage-specific ablation of LSECtin or silencing of BTN3A3 in BCCs decreased CSC frequency and tumor growth (9). Administration of LSECtin-positive macrophages increased the tumorigenic activity of BCCs dependent on BTN3A3 (9). Disruption of the LSECtin-BTN3A3 axis with BTN3A3-Fc or anti-BTN3A3 mAb has a therapeutic effect on breast cancer (9). These findings define a juxtacrine signaling mechanism by which TAMs promote cancer stemness (9). Targeting this axis in the CSC niche may provide potential therapies to breast cancer (9).

Array 10363-CL

• LSECtin/CLEC4G Antibodies
• LSECtin/CLEC4G Protein
• LSECtin/CLEC4G Proteins and Enzymes