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. Author manuscript; available in PMC: 2011 Aug 9.
Published in final edited form as: Mol Cell. 2006 Feb 17;21(4):521–531. doi: 10.1016/j.molcel.2006.01.010

Figure 3. AMPK suppresses mTOR activity under hypoxia.

Figure 3

(A–C) Serum-starved HEK293 cells were pretreated with 2 or 10 μM AMPK inhibitor compound C for 30 min before exposure to 2-DG (A), or 21% or 1.5% O2 for 1 or 3 hr (B–C).

(D) Serum replete HEK293 cells were preincubated with 10 mM methylpyruvate (MP) for 2 hr prior to 2-DG or 1.5% O2 (20 hr) treatment. Phosphorylation of eEF2, 4EBP1, and rpS6 are indicated.

(E–F) Kinase-inactive AMPK α2 mutant suppresses hypoxic mTOR inhibition. HEK293 cells were transfected with empty vector, wild-type AMPK-α2 (AMPK-WT), or kinase inactive K45R mutant (AMPK-DN). Clones expressing similar levels of AMPK protein were selected.

(E) Levels of AMPK protein in selected clones.

(F) Phosphorylation of p70S6K and rpS6 in cells exposed to 1.5% O2 for 0–20 hr.