9.B.39.1.4
Putative fatty acid translocase, CD36 glycoprotein (FA translocase; FAT/CD36/SR-B2; Collagen type I receptor; thrombospondin receptor) (Glatz and Luiken 2017; Zhang et al. 2017).  It is a leukocyte differentiation antigen and adhesin of 472 aas protein with 2 TMSs, one N-terminal and one C-terminal (Schwenk et al. 2010). Studies have shown that TMS 1 plays a role in formation of a homodimeric structure which may be involved in regulating signal transduction (Wei et al. 2017). Uptake of long chain unsaturated fatty acids, eicosapentaenoic acid and docosahexaenoic acid, is facilitated by CD36/SR-B2 (Glatz and Luiken 2017). Glycosylation, ubiquitination and palmitoylation are involved in regulating CD36 stability, while phosphorylation at extracellular sites affects the rate of fatty acid uptake (Luiken et al. 2016). CD36 may facilitate fatty acid uptake by an indirect mechanism (Jay and Hamilton 2016), but fatty acid uptake studies in breast cancer cells are consistent with its role in transport (Zhao et al. 2017). CD36 is also a co-receptor that enhances the response to MICs of Toxoplasma gondii (Costa Mendonça-Natividade et al. 2019). CD36 is expressed in multiple cell types, mediates lipid uptake, immunological recognition, inflammation, molecular adhesion, and apoptosis. CD36 is a transmembrane glycoprotein that contains several posttranslational modification sites and binds to diverse ligands, including apoptotic cells, thrombospondin-1 (TSP-1), and fatty acids (FAs) (Wang and Li 2019). CD36 is responsible for several metabolic disorders. It is a multifunctional scavenger receptor mediating uptake of long-chain fatty acids. Akachar et al. 2021 determined whether Lys164, exposed to the protein surface, played roles in fatty acid uptake. Conformational changes involved Lys164 which influenced the folding, utility, solubility, and stability of the protein. It also provided the structural basis for forming an opening near the principal portal for the dissociation of palmitic acid (Akachar et al. 2021). How CD36 regulates the tumor microenvironment has been reviewed (Liao et al. 2022). CD36 mediates SARS-CoV-2-envelope-protein-induced platelet activation and thrombosis by direct binding (Tang et al. 2023). It is a skeletal muscle protein, involved in fatty acid transport, that influences fatty acid oxidation rates (Maunder et al. 2023). CD36 preferentially mediates intestinal absorption of dietary Z-astaxanthin (Zhang et al. 2024).  Downregulation of CD36 alleviates IgA nephropathy by promoting autophagy and inhibiting extracellular matrix accumulation in mesangial cells (Zhang et al. 2025).  CD36 can transport into cells: fatty acids, lipids, proteins, proteolipids, lipoproteins, PROTAC (proteolysis-targeting chimeras, such as ARV110 which targets prostate cancer, etc (Jin et al. 2020; He et al. 2025).