The antibody is validated for multiple techniques, with specific applications highlighted below:
Target Cells: Platelets, macrophages, microglia, adipocytes, and PBMCs.
Usage: Detection of CD36 expression on cell surfaces.
Protocol: Typically used at ≤0.25 µg/million cells in 100 µL volume .
Tissue Targets: Liver, adipose tissue, brain (microglia), and atherosclerotic plaques.
Neutralization: CD36-blocking antibodies inhibit ligand binding (e.g., oxidized LDL, β-amyloid) and downstream signaling (e.g., TLR2/IRF7 pathways) .
CD36 facilitates recognition of pathogens and apoptotic cells. Key studies include:
Microglial Activation: CD36 mediates β-amyloid-induced reactive oxygen species (ROS) production in microglia, contributing to neuroinflammation .
TLR Signaling: CD36 interacts with TLR2 and TLR6 to amplify inflammatory responses, as shown in LPS-challenged microglia .
CD36 regulates fatty acid uptake and storage:
Fatty Acid Transport: CD36 internalization upon FA binding (e.g., oleate) delivers lipids to adipocytes via caveolae-dependent endocytosis .
Inhibition: SMS121, a CD36 inhibitor, reduces FA uptake in AML cells and decreases viability .
Atherosclerosis: CD36 binds oxidized LDL, promoting foam cell formation .
Malaria: CD36 mediates cytoadherence of Plasmodium falciparum-infected erythrocytes .
CD36 is a multifunctional glycoprotein receptor with broad ligand specificity. It binds a diverse array of ligands, including proteins such as thrombospondin, fibronectin, collagen, and amyloid-beta, as well as lipids like oxidized low-density lipoprotein (oxLDL), anionic phospholipids, long-chain fatty acids, and bacterial diacylated lipopeptides. The multivalent nature of these ligands allows for simultaneous engagement of multiple CD36 receptors, leading to receptor clustering, signal transduction, and internalization of receptor-ligand complexes. Coreceptor involvement in signaling is ligand-dependent. Cellular responses to these ligand interactions play critical roles in angiogenesis, inflammation, fatty acid metabolism, taste perception, and dietary fat processing within the intestine.
CD36 facilitates long-chain fatty acid transport into cells, impacting muscle lipid utilization, adipose energy storage, and intestinal fat absorption. In the small intestine, it contributes to the proximal absorption of dietary fatty acids and cholesterol, crucial for optimal chylomicron formation, possibly through MAPK1/3 (ERK1/2) signaling pathway activation. It also participates in oral fat perception and preference, mediating the induction of increased intracellular calcium levels in taste receptor cells upon long-chain fatty acid detection, subsequently activating gustatory neurons in the nucleus of the solitary tract. Furthermore, CD36 is involved in ventromedial hypothalamus neuronal sensing of long-chain fatty acids, regulating energy and glucose homeostasis.
CD36 functions as a receptor for thrombospondins THBS1 and THBS2, mediating their antiangiogenic effects. Acting as a coreceptor for the TLR4:TLR6 heterodimer, it promotes inflammation in monocytes/macrophages. Upon binding ligands such as oxLDL or amyloid-beta 42, it interacts with the TLR4:TLR6 heterodimer, triggering complex internalization and an inflammatory response. This leads to NF-κB-dependent production of CXCL1, CXCL2, and CCL9 cytokines (via MYD88 signaling), CCL5 cytokine (via TICAM1 signaling), and IL1B secretion (through NLRP3 inflammasome priming and activation). CD36 serves as a selective and non-redundant sensor of microbial diacylated lipopeptides that signal through the TLR2:TLR6 heterodimer, initiating cell surface signaling and NF-κB-dependent TNF production (via MYD88 signaling). Subsequently, it undergoes Golgi targeting via a lipid-raft dependent pathway. Finally, CD36 directly mediates cytoadherence of Plasmodium falciparum-parasitized erythrocytes and particle internalization independently of TLR signaling.
The following studies highlight the diverse roles and clinical implications of CD36: