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. Author manuscript; available in PMC: 2021 Feb 22.
Published in final edited form as: Antiviral Res. 2018 Jul 25;158:13–24. doi: 10.1016/j.antiviral.2018.07.015

Fig. 2. HCMV upregulates S6K activity via the PI3K/Akt/mTOR signaling pathway.

Fig. 2.

(A-B) Peripheral blood monocytes were mock or HCMV infected, or treated with GM-CSF or M-CSF for (A) 24 h or (B) 30 m. (C-D) Monocytes were pretreated with LY294002 (a PI3K inhibitor), MK, or rapamycin (a mTOR inhibitor) for 1 h. Following treatment with inhibitors, cells were mock or HCMV infected for (C) 24 h or (D) 30 min. (A-D) Levels of p-S6K (T389), and S6K were detected by immunoblotting from whole cell lysates. Membranes were then reprobed for β-actin as a loading control. Data are representative of 3–6 independent blood donors.