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. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: Nat Microbiol. 2020 Oct 19;5(12):1576–1587. doi: 10.1038/s41564-020-00795-7

Fig. 5. INSR is the major receptor for the immunometabolic activity of SQSTM1.

Fig. 5.

(a) Heatmap of RTK phosphorylation in THP1-derived macrophages (TMs) after rSQSTM1 (100 ng/ml) stimulation for 1–24 h. (b) Western blot analysis of protein expression in TMs following treatment with rSQSTM1 (100 ng/ml) for 1–24 h. (c) GST affinity isolation analysis of the binding of SQSTM1 to INSR. (d-f) Analysis of NFKB activity (d), lactate production (e), and mRNA expression (f) in the indicated TMs following treatment with rSQSTM1 (100 ng/ml) in the absence or presence of IgG or anti-INSR monoclonal antibodies (10 μg/ml) for 24 h (n = 3 well/group; two-tailed t test, versus control rSQSTM1 group). (g-h) Indicated TMs (control or RELAKD) were stimulated with rSQSTM1 (100 ng/ml) for 24 h. The glucose uptake (g) and ECAR (h) were assayed (n = 3 well/group; two-tailed t test, versus control rSQSTM1 group). AU, arbitrary units. Data in (d), (e), (g), and (h) are presented as mean ± SD. Data in (a) is from one independent experiment. Data in (b-c) and (h) are from two independent experiments. Data in (d-g) are from three independent experiments.