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. 2015 Dec 8;291(5):2389–2396. doi: 10.1074/jbc.M115.664995

FIGURE 3.

FIGURE 3.

Type II IFN-induced CXCL10 and IRF9 expression is Rictor-dependent. A, serum-starved Rictor+/+ and Rictor−/− MEFs were treated with mouse IFNγ as indicated. Cell lysates were prepared, proteins were resolved by SDS-PAGE, and immunoblots were probed with anti-CXCL10 antibody. B, serum-starved U937 cells transfected with control siRNA or Rictor siRNA were treated with human IFNγ for the indicated times. Cell lysates were prepared, and proteins were resolved by SDS-PAGE and then processed for immunoblotting with an anti-CXCL10 antibody. C, serum-starved Rictor+/+ and Rictor−/− MEFs were treated with mouse IFNγ as indicated. Cell lysates were prepared, proteins were resolved by SDS-PAGE, and immunoblots were probed with an anti-IRF9 antibody. The blots in the respective top panels (A–C) were probed with an anti-GAPDH antibody, as indicated, to control for protein loading. D and E, serum-starved Rictor+/+ or Rictor−/− MEFs were left untreated or treated with mouse IFNγ for 6 h, and total RNA was isolated. The mRNA expression of Cxcl10 (D) and Irf9 (E) was evaluated by quantitative real-time PCR, and Gapdh was used for normalization. Data are expressed as -fold change over control untreated cells, and error bars represent mean ± S.E. of three independent experiments.