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. Author manuscript; available in PMC: 2020 Jul 13.
Published in final edited form as: Nat Immunol. 2020 Jan 13;21(2):158–167. doi: 10.1038/s41590-019-0569-9

Figure 6: Tollip-deficiency selectively activates IRE1α, which facilitate resting-state STING protein turnover.

Figure 6:

(A) qRT-PCR analysis of basal expression of UPR genes in Tollip+/+ and Tollip−/− MEFs stably expressing an empty vector or Flag-TOLLIP. A representative experiment with 2 biological replicates is showing. Experiments were repeated three times.

(B) Immunoblot analysis of UPR proteins in Tollip+/+ and Tollip−/− MEFs treated with thapsigargin (Tg, 500 nM) for indicated amount of time (top). Red arrows denote increased IRE1α in Tollip−/− MEFs.

(C) Immunoblot analysis of Ern1+/+ and Ern1−/− MEFs stimulated with DMXAA (10 μg/ml) for indicated amount of time (top).

(D) qRT-PCR analysis of basal Tmem173 mRNA in Ern1+/+ and Ern1α−/− MEFs. A representative experiment with 2 biological replicates is showing. Experiments were repeated three times.

(E) Immunoblot analysis of Ern1+/+ and Ern1−/− MEFs after treatment with control siRNA or siTollip.

(F) Immunoblot analysis of Tollip+/+ and Tollip−/− MEFs treated with DMSO or IRE1α inhibitor 4μ8C (100 μM) overnight.

(G) Immunoblot analysis of Xbp1+/+ and Xbp1−/− MEFs treated with DMSO or 4μ8C (100 μM) overnight. Data are representative of at least three independent experiments.