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. Author manuscript; available in PMC: 2021 Feb 3.
Published in final edited form as: Oncogene. 2020 Nov 18;40(3):618–632. doi: 10.1038/s41388-020-01554-y

Fig 7. Two distinct metabolic phenotypes in BAP1 mutant UM.

Fig 7.

Summary figure showing two different metabolic phenotypes in BAP1 mutant UM. The glycolytic phenotype has a high OXPHOS gene signature and primarily relies on glucose utilization, which can upregulate oxidative PPP. This phenotype is specifically sensitive to glycolysis or nucleotide synthesis inhibitors. The second subtype has low OXPHOS gene expression and is more dependent on FAO. This subtype is vulnerable to either OXPHOS or FAO-specific inhibitors. FA; fatty acid, GLUT; glucose transporter, HK; hexokinase, G6PD; glucose-6-phosphate dehydrogenase, TKT; transketolase, LCFA; long chain fatty acid, CPT1; carnitine palmitoyltransferase1, 6-AN; 6-aminonicotinamide and ETO; etomoxir.