FigureĀ 1.
Amino acid metabolism in AML and relevant therapeutic strategies. Schematic representation showing the cellular uptake and utilization of select amino acids and their downstream intermediates. Enzymes with demonstrated relevance to AML pathophysiology are highlighted in blue. Inhibitory compounds or proteins are highlighted in red. Biological outputs and metabolic pathways are highlighted in pink. ADI, arginine deaminase; ASL, arginosuccinate lyase; ASN, asparagine; ASS1, arginosuccinate synthetase 1; NO, nitric oxide; OAA, oxaloacetic acid; OTC, ornithine transcarbamylase; PSAT1, phosphoserine aminotransferase 1; PSPH, phosphoserine phosphatase; 3-PG, 3-phosphoglycerate; 3-PHP, 3-phosphohydroxypyruvate; 3-PS, 3-phosphoserine; THF, tetrahydrofolate; 5,10-mTHF, 5,10-methylenetetrahydrofolate.

Amino acid metabolism in AML and relevant therapeutic strategies. Schematic representation showing the cellular uptake and utilization of select amino acids and their downstream intermediates. Enzymes with demonstrated relevance to AML pathophysiology are highlighted in blue. Inhibitory compounds or proteins are highlighted in red. Biological outputs and metabolic pathways are highlighted in pink. ADI, arginine deaminase; ASL, arginosuccinate lyase; ASN, asparagine; ASS1, arginosuccinate synthetase 1; NO, nitric oxide; OAA, oxaloacetic acid; OTC, ornithine transcarbamylase; PSAT1, phosphoserine aminotransferase 1; PSPH, phosphoserine phosphatase; 3-PG, 3-phosphoglycerate; 3-PHP, 3-phosphohydroxypyruvate; 3-PS, 3-phosphoserine; THF, tetrahydrofolate; 5,10-mTHF, 5,10-methylenetetrahydrofolate.

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