Finally, although the present work is concerned with Ca 2+ entry and deoxygenation-induced PS exposure in RBCs from SCD patients, it is also important to note that in RBCs from normal individuals other pathways may be significant.
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Identification of the Ca²⁺ entry pathway involved in deoxygenation-induced phosphatidylserine exposure in red blood cells from patients with sickle cell disease.
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