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. Author manuscript; available in PMC: 2014 Dec 11.
Published in final edited form as: Nature. 2014 May 14;510(7505):397–401. doi: 10.1038/nature13264

Figure 4. Inhibition of ATP synthase by α-KG causes conserved decrease in TOR pathway activity.

Figure 4

a, Decreased phosphorylation of mTOR substrates in U87 cells treated with octyl α-KG or oligomycin. Similar results were obtained in HEK-293, normal human fibroblasts, and MEFs (not shown). b, Increased autophagy in animals treated with α-KG or RNAi for atp-2 or CeTOR. c, GFP::LGG-1 puncta quantitated using ImageJ (Methods). 2–3 independent experiments. Bars indicate the mean. ****P < 0.0001; n.s., not significant (t-test, two-tailed, two-sample unequal variance). d, α-KG levels are increased in starved worms. **P < 0.01 (t-test, two-tailed, two-sample unequal variance). Mean ± s.d. is plotted. e, Model of α-KG-mediated longevity.