ArticlePloS one2011
Irreversible AE1 tyrosine phosphorylation leads to membrane vesiculation in G6PD deficient red cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Imatinib augments standard malaria combination therapy without added toxicity.The Journal of experimental medicine · 2021Trial
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- Phosphoproteomics and morphology of stored human red blood cells treated by protein tyrosine phosphatases inhibitor.Blood advances · 2024Article
- Erythrocyte mitogen-activated protein kinases mediate hemolytic events under osmotic and oxidative stress and in hemolytic diseases.Cellular signalling · 2022Article
- Blood Cell-Derived Microvesicles in Hematological Diseases and beyond.Biomolecules · 2022Review
- Syk Inhibitors: New Computational Insights into Their Intraerythrocytic Action inInternational journal of molecular sciences · 2020Article
- Syk Kinase Inhibitors Synergize with Artemisinins by Enhancing Oxidative Stress inAntioxidants (Basel, Switzerland) · 2020Article
- Signaling Response to Transient Redox Stress in Human Isolated T Cells: Molecular Sensor Role of Syk Kinase and Functional Involvement of IL2 Receptor and L-Selectine.Sensors (Basel, Switzerland) · 2020Article
- Article
- Global transformation of erythrocyte properties via engagement of an SH2-like sequence in band 3.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Testosterone-dependent sex differences in red blood cell hemolysis in storage, stress, and disease.Transfusion · 2016Article
- Inhibition of an Erythrocyte Tyrosine Kinase with Imatinib Prevents Plasmodium falciparum Egress and Terminates Parasitemia.PloS one · 2016Article
- The influence of host genetics on erythrocytes and malaria infection: is there therapeutic potential?Malaria journal · 2015Review
- Particle Simulation of Oxidation Induced Band 3 Clustering in Human Erythrocytes.PLoS computational biology · 2015Article
- Circulating membrane-derived microvesicles in redox biology.Free radical biology & medicine · 2014Review
- Thalassemic erythrocytes release microparticles loaded with hemichromes by redox activation of p72Syk kinase.Haematologica · 2014Article
- The involvement of cation leaks in the storage lesion of red blood cells.Frontiers in physiology · 2014Review
- Survival of red blood cells after transfusion: processes and consequences.Frontiers in physiology · 2013Review
- Red blood cell vesiculation in hereditary hemolytic anemia.Frontiers in physiology · 2013Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWhile 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
findingsOur results show that treatment of G6PD deficient red cells with diamide (0.25 mM) or divicine (0.5 mM) causes: (1) an increase in the oxidation and tyrosine phosphorylation of AE1; (2) progressive recruitment of phosphorylated AE1 in large membrane complexes which also contain hemichromes; (3) parallel red cell lysis and a massive release of vesicles containing hemichromes. We have observed that inhibition of AE1 phosphorylation by Syk kinase inhibitors prevented its clustering and the membrane vesiculation while increases in AE1 phosphorylation by tyrosine phosphatase inhibitors increased both red cell lysis and vesiculation rates. In control RBCs we observed only transient AE1 phosphorylation. CONCLUSIONS/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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