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. 2019 Jun;189(6):1241–1255. doi: 10.1016/j.ajpath.2019.02.008

Figure 1.

Figure 1

Diagram of the tyrosine catabolic pathway and experimental design. A: Loss of fumarylacetoacetate hydrolase (FAH) led to accumulation of fumarylacetoacetate and toxic metabolites. Fah deficiency was ameliorated by 2-(2-nitro-4-trifluoro-methylbenzoyl)-1,3-cyclo-hexanedione (NTBC) treatment or loss of homogentisate 1,2-dioxygenase (HGD). B: Schematic of experiments presented herein. HPD, 4-hydroxyphenylpyruvate dioxygenase; LKO, liver-specific E2f7/E2f8 double knockout; MAI, maleylacetoacetate isomerase; TAT, tyrosine aminotransferase.