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As a consequence, GDH flux (Figure 1, ) increases [5] supplying anaplerosis as malate exits the cycle forming pyruvate which in turn supports citrate formation (Figure 2)

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Once the fatty acids arrive inside the mitochondria, they are oxidized (burned)

Individuals with deficiency are more susceptible to oxidative stress which leads to the classical, acute hemolytic anemia (favism)

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Therefore, this in silico mutational analysis reinforces the key role of the transient residue Gly 376 for maintaining the GTP-induced inhibition dynamics