Fig. 1.

[¹⁸F]CFA accumulation is primarily dCK-dependent whereas [¹⁸F]F-AraG uptake primarily reflects dGK activity. (A) Potential mechanisms for accumulation of CFA and F-AraG in cells. (B) Western blot analysis of dCK and dGK expression in dCK-deficient CEM-R cells engineered to express EYFP (negative control), or dCK, or truncated human dGK (ΔdGK) lacking the mitochondrial sorting N-terminal sequence. (C) [³H]dC (18.5 kBq), (D) [³H]dG (18.5 kBq), (E) [¹⁸F]CFA (18.5 kBq), and (F) [¹⁸F]F-AraG (18.5 kBq) uptake assays using the isogenic panel of cells shown in B. [³H]dC and [¹⁸F]CFA uptake assays were performed in the presence or absence of DI-82 (1 µM), a small molecule inhibitor of dCK (C and E). N.S., nonsignificant; *P < 0.05; **P < 0.01; ***P < 0.001. (G) Western blot analysis of dCK expression in CEM WT cells and in CEM-R cells engineered to express EYFP or low, medium, and high dCK levels. (H) [³H]CFA (18.5 kBq) uptake, ± DI-82 (1 µM), in the isogenic panel of CEM-R cell lines shown in A. **P < 0.01; ***P < 0.001. All results are representative of three independent experiments (n = 3 for each experiment).