Extended Data Fig. 7. PNP inhibitor forodesine blocks ¹³C incorporation from [¹³C₅]-ribose-inosine into central metabolites but has little effect on [¹³C₆]-glucose catabolism.

The same experiment as in Fig. 4 was performed using active human T cells with or without Foro in the presence of [¹³C₅]-Ino or [¹³C₆]-Glc for 24 h. The polar extracts from both tracer experiments were analyzed by 1D HSQC NMR for ¹³C abundance (spectra as shown). Selected metabolites were quantified as ¹³C μmole/g protein using the N-methyl resonance of phosphocholine (NMe-PCholine) as an internal standard, which are shown as bar graphs for the [¹³C₅]-Ino (a) and [¹³C₆]-glucose tracer (b) experiments. Values are average ± SEM (n=3). Sample size (n) represents biologically independent samples. Dashed line denotes the expected peak position of the H1-glucose resonance of glycogen. The proton resonances used for quantification were: ¹³C₃-Lac/Ala – the H3 resonances of lactate/Ala; ¹³C-Gluta – the H4-Glu resonance of GSH + GSSG with minor contribution of H2,5 resonance of citrate; ¹³C-Ino, ¹³C-Glu, ¹³C-Asp, ¹³C-AXP, and ¹³C-UXP – H1’, H4, H3, and H1’ resonances of inosine, glutamate, aspartate, and adenine/uracil nucleotides, respectively.

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