Membrane glycoprotein modifications of G6PD deficient red blood cells
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چکیده
منابع مشابه
Irreversible AE1 Tyrosine Phosphorylation Leads to Membrane Vesiculation in G6PD Deficient Red Cells
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...
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Background: Chest X-ray is one of the examinations required for an annual health checkup. The interaction of radiation to the medium produces free radicals, which consequently causes biological changes either structural or properties of the cells. Whether the radiation from Chest X-ray upright technique affects the plasma membrane fluidity of thalassemic red blood cells (RBCs) is still unclear....
متن کاملOxidized and poorly glycosylated band 3 is selectively phosphorylated by Syk kinase to form large membrane clusters in normal and G6PD-deficient red blood cells.
Oxidative events involving band 3 (Anion Exchanger 1) have been associated with RBC (red blood cell) removal through binding of NAbs (naturally occurring antibodies); however, the underlying mechanism has been only partially characterized. In addition to inducing direct membrane protein oxidative modification, oxidative treatment specifically triggers the phosphorylation of band 3 tyrosine resi...
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Red cell enzyme deficiency disease states are reviewed to outline the requirements for transfusion therapy in the neonatal period, during spontaneous crises, drug or infection-induced crises and chronic anemia.
متن کاملStomatocytosis is absent in "stomatin"-deficient murine red blood cells.
To examine the relationship between erythrocyte membrane protein 7. 2b deficiency and the hemolytic anemia of human hereditary stomatocytosis, we created 7.2b knock-out mice by standard gene targeting approaches. Immunoblots showed that homozygous knock-out mice completely lacked erythrocyte protein 7.2b. Despite the absence of protein 7.2b, there was no hemolytic anemia and mouse red blood cel...
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ژورنال
عنوان ژورنال: European Journal of Clinical Investigation
سال: 1995
ISSN: 0014-2972,1365-2362
DOI: 10.1111/j.1365-2362.1995.tb01522.x