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. 2013 Aug 12;110(35):14336–14341. doi: 10.1073/pnas.1221740110

Fig. 8.

Fig. 8.

Dissociation of HK from mitochondria impairs proliferation and the rapid engagement of glycolysis in (IL-15) TM cells after activation. (A) Western blot analysis for HK I and II in IL-15 TM cells incubated ± CLT for 2 h; GAPDH and prohibitin I are loading controls for cytosolic and mitochondrial fractions, respectively; representative of two experiments. (B) OCR and ECAR of IL-15 TM cells stimulated with PMA/iono in the presence of control or HK-1 peptide (10 μM) or CLT (25 μM); mean ± SEM, representative of ≥2 experiments. IL-15 TM cells were stimulated with anti-CD3/28 and proliferation ± CLT; representative of five experiments (C), or with control or HK-1 peptide (10 μM); representative of two experiments, is shown (D). (E and F) TM cells from LmOVA-infected mice. Proliferation after anti-CD3/28 ± CLT; control is same as Fig. 6G and 7A, from one experiment (E); OCR and ECAR after PMA/iono ± CLT and exposed to oligo (1 μM) plus FCCP (1.5 μM), and rotenone (100 nM) plus antimycin A (1 µM); mean ± SEM and representative of two experiments; control is the same as Fig. 6C and Fig. S7 (F).