Fig. 2: mTORC2 increases ATF4 transcription independently of AKT. | Cell Death Discovery

Fig. 2: mTORC2 increases ATF4 transcription independently of AKT.

From: Elucidation of an mTORC2-PKC-NRF2 pathway that sustains the ATF4 stress response and identification of Sirt5 as a key ATF4 effector

Fig. 2

A Western blot analysis of WCL from MDA-MB-231 cells treated with menadione (50 μM) for 2 h. Blots are representative of two independent experiments. B Western blot analysis of WCL from MDA-MB-231 cells treated with CB-839 (1 μM) for 24 h. Blots are representative of three independent experiments. C, D Western blot analysis of WCL from MDA-MB-231 cells treated with CB-839 (1 μM) (C) or without glutamine (D)  ± Torin1 (500 nM), Rapamycin (50 nM) or MK2206 (5 μM) for 24 h. Blots are representative of three independent experiments. E, F Western blot analysis of WCL from control or sin1 KD MDA-MB-231 cells cultured in glutamine-free medium (E) or treated with CB-839 (1 μM) (F) for 24 h. Blots are representative of two independent experiments. G, H RT-qPCR quantification of ATF4 mRNA in MDA-MB-231 cells treated with CB-839 (1 μM) (G) or cultured ± glutamine (H) for 24 h with Torin1 (500 nM), Rapamycin (50 nM) or MK2206 (5 μM). Data shown are representative of three independent experiments and expressed as means ± SD for triplicate measurements. I RT-qPCR quantification of ATF4 mRNA in control or sin1 KD MDA-MB-231 cells treated with CB-839 (1 μM) or menadione (10 μM) for 24 h. Data shown are representative of two independent experiments and expressed as means ± SD for triplicate measurements.

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