Abstract
CD36 is a transmembrane glycoprotein of the class B scavenger receptor family. The CD36 gene is located on chromosome 7 q11.2 and is encoded by 15 exons. Defective CD36 is a likely candidate gene for impaired fatty acid metabolism, glucose intolerance, atherosclerosis, arterial hypertension, diabetes, cardiomyopathy, Alzheimer disease, and modification of the clinical course of malaria. Contradictory data concerning the effects of antiatherosclerotic drugs on CD36 expression indicate that further investigation of the role of CD36 in the development of atherosclerosis may be important for the prevention and treatment of this disease. This review summarizes current knowledge of CD36 gene structure, splicing, and mutations and the molecular, metabolic, and clinical consequences of these phenomena.
Highlights
CD36 is a type B scavenger receptor located on the surface of many types of cells
This review summarizes current knowledge of CD36 gene structure, splicing, and mutations and the molecular, metabolic, and clinical consequences of these phenomena
STRUCTURE OF THE HUMAN CD36 GENE The CD36 gene is located on chromosome 7 q11.2 [1]
Summary
CD36 is a type B scavenger receptor located on the surface of many types of cells. More than 20 mutations in the coding sequence of the CD36 gene that lead to type I receptor deficiency have been described, but the molecular basis of type II CD36 deficiency is still unclear. STRUCTURE OF THE HUMAN CD36 GENE The CD36 gene is located on chromosome 7 q11.2 [1]. The CD36 gene is encoded by 15 exons (Table 1). The 5′-untranslated region of CD36 mRNA is encoded by 3 exons. Exon 3 contains the last 89 nucleotides of the 5′-untranslated region and encodes the N-terminal cytoplasmic and transmembrane domains [2]. CD36 expression in the heart and skeletal muscles is increased by triacylglycerides (TG) and fatty acids (FA) in plasma and regulated by energy requirements of the tissue [20]
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