Fig. 7
From: Siglec-E retards atherosclerosis by inhibiting CD36-mediated foam cell formation
Schematic diagram illustrating Siglec-E-induced negative signaling on CD36-mediated oxLDL uptake on macrophages. Siglec-E physically interacts with CD36 through their polypeptides in resting state. When oxLDL binds to CD36, oxLDL-CD36 complex elicits the recruitment of a putative surface protein containing sialoglycan to interact with Siglec-E and activate Siglec-E/SHP-1 axis, which in turn inhibits CD36 downstream signaling for oxLDL uptake