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Mutations associated with chronic hemolysis tend to cluster in the vicinity of the NADP-binding domain of the G6PD gene and cause more severe deficiency, whereas those associated with acute intermittent hemolysis or no hemolysis are scattered throughout the gene

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Remarkably, this cell-based mechanism appears to be the most relevant, and the PC formed after BBB crossed appeared more stable, perhaps due to the cellular removal of a portion of PC proteins, leading to a stronger binding of the residual ones

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