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The hallmark of sickle cell disease is the polymerization of sickle haemoglobin due to a point mutation in the β‐globin gene (HBB). Under low oxygen saturation, sickle haemoglobin assumes the tense (T‐state) deoxygenated conformation that can form polymers, leading to rigid erythrocytes with impaired blood vessel transit, compounded or initiated by adhesion of erythrocytes to endothelium, neutrophils...
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