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. Author manuscript; available in PMC: 2019 Apr 1.
Published in final edited form as: Cancer Res. 2018 Jan 31;78(7):1792–1804. doi: 10.1158/0008-5472.CAN-17-2774

Figure 4. EGFR promotes TRIM59 interaction with STAT3 in the nucleus.

Figure 4

A, IP and WB analyses of the association of STAT3 with ectopic HA-TRIM59 in LN229/EGFRvIII and U87/EGFRvIII GBM cells. IgG was used as a control. B, Effects of EGFRvIII overexpression on the association of STAT3 with TRIM59. C, The interaction of TRIM59 and STAT3 occurs primarily in the nucleus. Cytoplasmic and nuclear proteins from U87 GBM cells, with or without EGFRvIII overexpression, were separated and subjected to IP as indicated. The nuclear marker Lamin B1 and the cytoplasmic marker Tubulin were used to demonstrate the purity of fractions. D, TRIM59 specifically interacts with STAT3. IP/WB analyses of the association of TRIM59 with STAT1, STAT3 and STAT5 in LN229 and U87 GBM cells. E, Schematics of TRIM59WT and various TRIM59 deletion mutants. F, STAT3 interacts with TRIM59 with amino acid residues 160-280. TRIM59WT or the indicated TRIM59 mutants was transfected into U87/EGFRvIII GBM cells. Data are representative of two or three independent experiments with similar results.