Data suggest that glycophorin A (Gpa) increases expression and activity of Cl-/HCO3- exchanger Ae1 that G719D mutation renders Ae1 mutant constructs GPA-unresponsive and suggests a role for Ae1 amino acids 22-28 in GPA responsiveness.
The resistance of glycophorin A knockout mice against infection with the OB1 variant of Babesia rohaini may be attributed to the effective clearance of the parasitized erythrocytes lacking GPA in the spleen.
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