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V.L. Tzounakas et al.
blockade at the metabolic step catalyzed by UDP-N- acetylglucosamine phosphorylase or an increased con- sumption of its product for protein O-GlcNAcylation (post-translational attachment of O-linked N-acetylglu- cosamine moieties to serine and threonine residues).
B
C
Figure 4. Main metabolic differences between control and beta thalassemia minor donors in circulating red blood cells. (A) Glycolysis. (B) Pentose phosphate pathway (PPP) metabolites. (C) Glutathione oxidation. (D) Purine metabolism. (E) Arginine metabolism. SAM: S-adenosyl methionine. *P<0.05, **P<0.01, #P<0.001, †P<0.0001.
UMP, acetyl-glucosamine, acetyl-glucosamine phosphate) were significantly higher in bThal+ RBC at all storage time points, while the final product of this pathway – uridine diphosphate (UDP) N-acetyl-glucosamine was significant- ly lower in bThal+ RBC (Figure 6C), suggestive of either a
A
D
E
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