Skip to main content
. 2005 Jul;25(14):5834–5845. doi: 10.1128/MCB.25.14.5834-5845.2005

FIG. 2.

FIG. 2.

Signaling to mTOR substrates is dysregulated in REDD1−/− cells following AMPK, but not AKT, activation. (A) Downregulation of S6K (T389) and 4E-BP1 (T70) phosphorylation is defective in REDD1−/− cells following AMPK activation. Primary MEFs were serum starved (SS) for 24 h and then treated as indicated (S, serum) for 90 min prior to Western blot analysis. The phosphorylation forms of 4E-BP1 are indicated by convention as α, β, and γ (bottom panel) (19). Note in particular the absence of the α 4E-BP1 form in REDD1−/− cells (lane 5 versus 10). (B) Reconstitution of REDD1 expression restores S6K (T389) and 4E-BP1 (T70) dephosphorylation following AMPK activation (lanes 4 and 8). Primary REDD1−/− MEFs were infected with control or REDD1-expressing retrovirus prior to treatment as in panel A for 90 min. (C) REDD1 reconstitution restores 4E-BP1 (T70) dephosphorylation following ATP depletion. Primary REDD1−/− MEFs were retrovirally infected as in panel B and then treated with 2DG as indicated for 4 h.