Gene Information
Gene Symbol
Entrez Gene ID
Gene Name
CD36 molecule
Chromosomal Location
The protein encoded by this gene is the fourth major glycoprotein of the platelet surface and serves as a receptor for thrombospondin in platelets and various cell lines. Since thrombospondins are widely distributed proteins involved in a variety of adhesive processes, this protein may have important functions as a cell adhesion molecule. It binds to collagen, thrombospondin, anionic phospholipids and oxidized LDL. It directly mediates cytoadherence of Plasmodium falciparum parasitized erythrocytes and it binds long chain fatty acids and may function in the transport and/or as a regulator of fatty acid transport. Mutations in this gene cause platelet glycoprotein deficiency. Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Feb 2014]
RefSeq DNA
RefSeq mRNA

Gene Ontology (GO)

GO ID Ontology Function Evidence Reference
GO:0001954 Biological process Positive regulation of cell-matrix adhesion IDA 17416590
GO:0002532 Biological process Production of molecular mediator involved in inflammatory response TAS 29111364
GO:0006629 Biological process Lipid metabolic process NAS 7518447
GO:0006631 Biological process Fatty acid metabolic process TAS 29111364
GO:0006898 Biological process Receptor-mediated endocytosis IMP 18941241
Protein Information
Protein Name
Platelet glycoprotein 4, CD36 antigen (collagen type I receptor, thrombospondin receptor), CD36 molecule (thrombospondin receptor), GPIIIB, PAS IV, PAS-4 protein, cluster determinant 36, fatty acid translocase, glycoprotein IIIb, leukocyte differentiation antigen CD36, platelet glycoprotein IV, scavenger receptor class B, member 3
Multifunctional glycoprotein that acts as receptor for a broad range of ligands. Ligands can be of proteinaceous nature like thrombospondin, fibronectin, collagen or amyloid-beta as well as of lipidic nature such as oxidized low-density lipoprotein (oxLDL), anionic phospholipids, long-chain fatty acids and bacterial diacylated lipopeptides. They are generally multivalent and can therefore engage multiple receptors simultaneously, the resulting formation of CD36 clusters initiates signal transduction and internalization of receptor-ligand complexes. The dependency on coreceptor signaling is strongly ligand specific. Cellular responses to these ligands are involved in angiogenesis, inflammatory response, fatty acid metabolism, taste and dietary fat processing in the intestine (Probable). Binds long-chain fatty acids and facilitates their transport into cells, thus participating in muscle lipid utilization, adipose energy storage, and gut fat absorption (By similarity). In the small intestine, plays a role in proximal absorption of dietary fatty acid and cholesterol for optimal chylomicron formation, possibly through the activation of MAPK1/3 (ERK1/2) signaling pathway. Involved in oral fat perception and preferences. Detection into the tongue of long-chain fatty acids leads to a rapid and sustained rise in flux and protein content of pancreatobiliary secretions (By similarity). In taste receptor cells, mediates the induction of an increase in intracellular calcium levels by long-chain fatty acids, leading to the activation of the gustatory neurons in the nucleus of the solitary tract (By similarity). Important factor in both ventromedial hypothalamus neuronal sensing of long-chain fatty acid and the regulation of energy and glucose homeostasis (By similarity). Receptor for thombospondins, THBS1 and THBS2, mediating their antiangiogenic effects (By similarity). As a coreceptor for TLR4:TLR6 heterodimer, promotes inflammation in monocytes/macrophages. Upon ligand binding, such as oxLDL or amyloid-beta 42, interacts with the heterodimer TLR4:TLR6, the complex is internalized and triggers inflammatory response, leading to NF-kappa-B-dependent production of CXCL1, CXCL2 and CCL9 cytokines, via MYD88 signaling pathway, and CCL5 cytokine, via TICAM1 signaling pathway, as well as IL1B secretion, through the priming and activation of the NLRP3 inflammasome (By similarity). Selective and nonredundant sensor of microbial diacylated lipopeptide that signal via TLR2:TLR6 heterodimer, this cluster triggers signaling from the cell surface, leading to the NF-kappa-B-dependent production of TNF, via MYD88 signaling pathway and subsequently is targeted to the Golgi in a lipid-raft dependent pathway (By similarity). (Microbial infection) Directly mediates cytoadherence of Plasmodium falciparum parasitized erythrocytes and the internalization of particles independently of TLR signaling
Refseq Proteins

PPAR signaling pathway
AMPK signaling pathway
ECM-receptor interaction
Hematopoietic cell lineage
Adipocytokine signaling pathway
Insulin resistance
Fat digestion and absorption
Cholesterol metabolism


Platelet degranulation
Cross-presentation of particulate exogenous antigens (phagosomes)
ER-Phagosome pathway
MyD88:MAL(TIRAP) cascade initiated on plasma membrane
Toll Like Receptor TLR6:TLR2 Cascade
PPARA activates gene expression
Scavenging by Class B Receptors
Transcriptional regulation of white adipocyte differentiation
Intracellular metabolism of fatty acids regulates insulin secretion
MyD88 deficiency (TLR2/4)
IRAK4 deficiency (TLR2/4)
Regulation of TLR by endogenous ligand
Interleukin-4 and Interleukin-13 signaling
Neutrophil degranulation

ENSP00000223095 P05121 P05121
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Associated Diseases

Disease groupDisease NameReferences
Cardiovascular Diseases
Hypertensive disease
Myocardial Ischemia
Congenital, Hereditary, and Neonatal Diseases and Abnormalities
Platelet Glycoprotein IV Deficiency
Endocrine System Diseases
PubMed ID Associated gene/s Associated condition Genetic Mutation Diagnostic Criteria Association with PCOS Ethnicity Conclusion
12 women with asymmetric PCO, 15 primary/ secondary infertile women without endocrine disorders and 8 polycystic ovary syndrome (PCOS) with bilateral PCO 
Decrease in CD(36) mRNA may play a role in the pathogenesis of PCO by increasing the level of T and INS in follicular fluid 
Rotterdam criteria 
10 women with PCOS,10 healthy controls 
The results of this study suggest that in insulin-resistant women with PCOS, changes in CD36 and HSL expression may result in altered FFA uptake.  

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