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If besides hemoglobin SS patients also have hemoglobin F (HbF) in their erythrocytes, it reduces the degree of aggregation and crystallization of hemoglobin S, and as a result, they tend to have fewer symptoms of sickle cell anemia or lack them completely. When the HbF levels increase, polymerization of deoxy sickle hemoglobin slows down. HbF decreases HbS concentration, and together with its mixed hybrid tetramer (?2?S?) they cannot enter the deoxy sickle hemoglobin polymer phase. The antipolymerization effect of HbF resides mainly in HBG (both ?-globin genes) residues glycine ?87 and aspartic acid ?80. Inhibition of the tendency of deoxy sickle hemoglobin to polymerize, allows sufficient HbF to thwart the cellular damage evoked by HbS polymer

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