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. 2021 Jan 20;47:101170. doi: 10.1016/j.molmet.2021.101170

Figure 5.

Figure 5

SELENOI deficiency did not impact TCR signal strength, but led to reduced activation of metabolic-sensing protein AMPK. A time-course analyses (0–1 h) of TCR-induced activation of (A) ERK and (B–C) AKT showed no differences between WT and SELENOI KO T cells using flow cytometry. Real-time PCR was used to evaluate gene transcription downstream of TCR signaling including (D) IL-2 mRNA and (E) CD25 mRNA, with β-actin used as a housekeeping transcript for both. (F) Western blotting analyses of p-Rictor/Rictor and p-AMPK/AMPK from 0 to 5 h post-TCR activation of WT and SELENOI KO T cells. (G–H) Two repeat western blotting experiments at the 5 h time point and densitometry on three sets of results showed that SELENOI KO T cells had less phosphorylation of AMPK, but phosphorylation of Rictor was similar to WT. Means of replicates (n = 4 for A–E; n = 3 for H) were compared using Student's t test. Data represent mean ± SEM with ∗p < 0.05.