Irreversible AE1 tyrosine phosphorylation leads to membrane vesiculation in G6PD deficient red cells

不可逆的 AE1 酪氨酸磷酸化导致 G6PD 缺乏的红细胞膜囊泡形成

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作者:Antonella Pantaleo, Emanuela Ferru, Franco Carta, Franca Mannu, Luigi F Simula, Amina Khadjavi, Proto Pippia, Francesco Turrini

Background

While G6PD deficiency is one of the major causes of acute hemolytic anemia, the membrane changes leading to red cell lysis have not been extensively studied. New findings concerning the mechanisms of G6PD deficient red cell destruction may facilitate our understanding of the large individual variations in susceptibility to pro-oxidant compounds and aid the prediction of the hemolytic activity of new drugs. Methodology/principal findings: Our

Significance

Collectively, our findings indicate that persistent tyrosine phosphorylation produces extensive membrane destabilization leading to the loss of vesicles which contain hemichromes. The proposed mechanism of hemolysis may be applied to other hemolytic diseases characterized by the accumulation of hemoglobin denaturation products.

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